Category Archives: Cardiac Arrest

Thrombolytic treatment of cardiac arrest or periarrest due to suspected pulmonary embolism

I recently saw a case in the department that led to me thinking about the role of thrombolytics in cardiac arrest patients — particularly for the purpose of trying to treat arrest from suspected PE. Thrombolytics in out-of-hospital cardiac arrest patients is something I’ve seen considerable inter-attending variability on in practice, and heard conflicting things about from the things that I’ve read and heard in podcasts. So, naturally when there are no podcasts readily accessible on the matter, I turned to PubMed and came across an excellent review article on the subject from Logan et al., “Evidence-based diagnosis and thrombolytic treatment of cardiac arrest or periarrest due to suspected pulmonary embolism”, published four years ago in AJEM.

As they write in the introduction, “This article discusses clinical features consistent with the presumptive diagnosis of PE, provides an overview of thrombolytic agents, and presents a detailed review of the literature supporting the use of thrombolysis as a treatment option for patients in cardiac arrest or periarrest due to suspected PE.” The authors do an excellent job summarizing the available (as of 2014, at least, or 2012 — this being the latest publication included) evidence and discuss strategies for considering whether to push lyrics in the cardiac arrest patient you think might have a pulmonary embolism. Note that this is a different question from lytics in patients with cardiac arrest due to coronary occlusion — though it is likely that many of those showed up in the reviewed trials of lytics in undifferentiated cardiac arrest, or PEA arrest that wasn’t necessarily thought to be secondary to an MI.

What does it boil down to?

“The above literature review shows that unstable or arresting patients experiencing massive PE will likely benefit from thrombolytic therapy. Studies with a retrospective design generally demonstrated the best outcomes, as was expected, due to the patient population having a known or high risk for PE, and possibly publication bias of positive results. Trials with a prospective design had more variation because these trials generally included a heterogeneous patient population in cardiac arrest and illustrates the potential difficulty of applying this intervention in real-time clinical practice. Analysis of the subgroup population of patients with PE in the prospective trials showed possible improved outcome after thrombolytic therapy, although these studies were not powered to look specifically at this group. This disparity emphasizes the importance of patient selection when evaluating for the efficacy of thrombolytic therapy.”

They said it best, so I won’t try to restate their conclusions — one thing I did find particularly interesting was a clinical decision making rule evaluated  in both a retrospective and a prospective trial which found the following triad to be associated with cardiac arrest secondary to massive PE: witnessed cardiac arrest, age less than 65 to 70 years, and PEA as the initial rhythm. This study found that 50% of the (admittedly fairly small n of 48) patients with this triad had a PE, which improved the diagnostic likelihood of PE when compared with the previously discussed sensitivity of 36% when only assessing for PEA rhythm in unexplained cardiac arrest.

There are robust data supporting the use of lytics in patients with hemodynamic compromise in the setting of diagnosed pulmonary embolism. Do these same data, or the data presented in this review and since support the use of it in all undifferentiated cardiac arrest patients, or in any subset of cardiac arrests? I agree with the authors — the data suggests that if the arrest is due to massive PE, lytics may benefit them and are probably worth trying, especially early on if your suspicion is high. But in the undifferentiated cardiac arrest patient, even one in PEA, I think there are many other things to consider like bedside ultrasound, duration of arrest, initial  rhythm, witnessed/unwitnessed, and cormorbid conditions / premorbid quality of life to consider before using an expensive, non-FDA-approved (for this indication) medication that has significant risks.

My next question that I still don’t have a good answer for yet, is whether someone can and should go to the cath lab after ROSC in the setting of the use of thrombolytics? And does this answer hinge on whether the lytics were given for a high suspicion of pulmonary embolism as the precipitating event? Is there ever a role for lytics in cardiac arrest where your suspicion isn’t high for PE as the etiology, but the patient is “too unstable” to go to catheterization? As I said in the last post, definitely more to come.


Logan JK1, Pantle H2, Huiras P3, Bessman E2, Bright L4. Evidence-based diagnosis and thrombolytic treatment of cardiac arrest or periarrest due to suspected pulmonary embolism. Am J Emerg Med. 2014 Jul;32(7):789-96. PMID: 24856738. [PubMed] [Read by QxMD]

Post-Arrest Prognostication

While I want to focus this blog on things relevant to practice in the Emergency Department, I have an academic interest (and maybe a career interest long-term) in critical care. I also feel that cardiac arrest is a particular area in critical care should be something that EPs are expert in — it’s also an area in which there is considerable nihilism which may lead in sub-optimal patient care, or early withdrawal of efforts before such withdrawal is justifiable.

What do I mean by nihilism? I mean that we in the ED rarely see good outcomes in out-of-hospital cardiac arrest (OOHCA) patients (and when we do, they’re often comatose and whisked away to the ICU, which means that even if they *do* have a good clinical outcome we do not see it happen and rarely even hear about it), and this leads to a sentiment that any cardiac arrest patient is bound for either death or a meaningless life due to neurologic injury.

Everyone in in the department, from patient care assistants and techs and medical students to the attendings, puts a lot of energy and effort into running codes and trying to resuscitate these patients. People care a lot and do some of their best work in these stressful contexts. But at the same time, I sometimes wonder whether we would focus more on improving our process and quality of care– and perhaps thereby do even better– if we had a better sense that our interventions translated into patients who could again be alive and well because of them. This sense is difficult to come by if many of the patients that you successfully attain ROSC on have features that many people associate with a very low likelihood of meaningful recovery.

This pair of recent review articles focused on prognostication in post-cardiac arrest patients — findings on clinical exam, imaging, and other methods to try to suss out who will go onto do well and who is unlikely to ever regain meaningful neurologic function. As ICU bed availability dwindles and the incidence of cardiac arrest and survival thereof continues to increase, this will be of increasing relevance to ED docs, intensivists, and those working with these patients.

So what is a “good outcome”? As the article says, “Experts in coma prognositication defined outcome by cerebral performance categories (CPCs; CPC 1 back to baseline, CPC 2 moderate impairment, CPC 3 severe impairment, CPC 4 vegetative or comatose, CPC 5: dead).” They bifurcate these into either a good (CPC 1 or 2) or poor (CPC 3-5) outcome. Obviously the difference between “moderate” and “severe” impairment is somewhat subjective, but there are additional tools used to help with this distinction.

The old standard was clinical assessment of brainstem reflexes, the response to pain, and the absence or presence of myoclonus during the first 72 hours post-arrest. In the TTM era, this becomes trickier because temperature management and the required sedation can alter these features, though the bedside exam still has significant prognostic significance. Absence of pupillary reflexes at 72 hours is the best bedside predictor of a bad outcome, with a false positive rate (FPR) of only 0.5% — presence of pupillary reflexes however, does not confer a good outcome, given that it only has a PPV of 61% (95% CI 50-71).

What about earlier? In the first 24 hours post-arrest, particularly in hypothermic patients, ~ 8% of patients without pupillary reflexes will go on to have a good recovery — so don’t count them out. In terms of corneal reflexes, the reliability is less than that of pupillary reflexes but their absence still correlates with a poor prognosis, with an FPR of 5%.

Motor response is the most affected by sedatives, opiates, and neuromuscular blockade — all common in patients undergoing TTM, and absent or extensor responses to painful stimuli at 72 hours had a FPR of 24%. To reliably utilize this for prognostication, you need exclusion of residual effects of sedation, which can be extended beyond when the drips are simply turned off secondary to the effects of TTM and also the effects of reduced clearance due to shock liver, renal dysfunction, or both.

In terms of myoclonus, which is classically associated with poor outcomes, ~ 9% of patients with myoclonus may survive, according to the data presented here. As the article states, myoclonus is somewhat of a nebulously defined entity — “Not all so-called twitches have the same prognostic implication, rather their usefulness in predicting prognosis depends on semiology, duration, and associated EEG findings.”

I’ll skip EEG and ERPs because this is already too long, but suffice to say they’re useful after hypothermia and for ruling out sub-clinical status epilepticus, which is something we really want to avoid happening in our post-arrest patients, but is very common. More to come on this, which I feel is of particular relevance to us in the ED. Same goes for biomarkers such as neuron specific enolase and Serum S-100B, which can both be measured and trended as the “troponins of the brain”, so to speak.

In terms of imaging — CT scan of the head is recommended in patients in whom there is not another obvious cause of cardiac arrest, to evaluate for a bleed or ischemic stroke. Evaluation of gray:white ratios can predict poor outcomes, but is less reliable than clinical exam and EEG, and this is true for MRI as well, though again MRI does not add very much prognostic capability beyond what can be achieved with bedside tests and the logistics and cost associated with MRI scans of every comatose survivor of cardiac arrest make this somewhat limited in utility.
PPV for Neuro Findings

So what’s the takeaway from all this? Basically, reliable prognostication after cardiac arrest is hard, but at the same time, it isn’t– don’t do it right away, and if you do, it shouldn’t necessarily be based on your bedside neurologic exam. There are tools that can give us useful information, but rarely certainty, to guide conversations with family. And the reality is that none of them are accurate enough inside the first 48-72 hours, especially in patients who are being cooled. There is a very powerful desire to be able to give families hope, or to caution against hope in a way that changes outcomes before they’ve happened — in my very early-in-development opinion, all you can really tell them is something I heard one of my mentors say to families whose children were in the Pediatric ICU: “Prepare for the worst, and hope for the best.”

I also take away from this that nihilism is an un-useful form of prognsotication in these patients — I have seen patients myself who had unreactive pupils or myoclonic jerks, who went onto walk out of the hospital, fairly neurologically intact. This is even more true if the arrest was witnessed, was a shockable rhythm such as VT or VF, and if the patient received high-quality chest compressions and early defibrillation, preventing lengthy low/no-flow states to the brain.

The message not to take away from this post that I believe in any sense that there is no ability to meaningfully make predictions about the likely outcome of cardiac arrest patients, whether or not you’ve gotten ROSC — there are many other variables not considered in the above article  that predict do reliably predict outcomes such as comorbidities, age of the patient, how long they were down for, the initial rhythm, and an often-overlooked variable in the literature (because it’s tough to quantify): consideration of their quality of life before they suffered a cardiac arrest. I also think that the pragmatic realities of cardiac arrest care — an emotionally charged event where patients are often teetering along a line between life and death, and where decisions have real and immediate impacts on that outcome– may require a sense of somewhat-morbid realism when the outcomes are often so dismal. I just hope that when people are making decisions about termination of efforts (or withdrawal of care post-ROSC) they’re considering all of these things and more, beyond just what their clinical gestalt is.

More to come, I’m sure — I’m especially interested in what happens moving forward in terms of biomarkers, cerebral oximetry, and near-infrared brain imaging to try to determine cerebral oxygenation and metabolism without having to move patients out of the ICU.


Rossetti AO1, Rabinstein AA2, Oddo M3. Neurological prognostication of outcome in patients in coma after cardiac arrest. Lancet Neurol. 2016 Mar 23. PMID: 27017468. [PubMed] [Read by QxMD]
Sivaraju A1, Gilmore EJ, Wira CR, Stevens A, Rampal N, Moeller JJ, Greer DM, Hirsch LJ, Gaspard N. Prognostication of post-cardiac arrest coma: early clinical and electroencephalographic predictors of outcome. Intensive Care Med. 2015 Jul;41(7):1264-72. PMID: 25940963. [PubMed] [Read by QxMD]

More Low-Risk Chest Pain!

In this article published in JAMA Internal Medicine in July of last year, a group of emergency physicians reviewed 11,230 records of patients hospitalized for chest pain with 2 negative troponin tests, nonconcerning initial ED vital signs, and nonischemic, interpretable electrocardiographic findings to determine the incidence of patient-centered adverse events in the short term.

What is interesting and unique about this study is the shift from using MACE (which, as I have discussed before, includes somewhat-nebulously-patient-centered bad outcomes such as need for cardiac revascularization — this is an intervention, not a harm that occurred to a patient due to a lack of intervention) from using their more  “clinically relevant adverse cardiac events” (of course requiring a new catchy acronym, CRACE): (1) life-threatening arrhythmia (ventricular fibrillation, sustained ventricular tachycardia requiring treatment, symptomatic bradycardia or bradyasystole requiring emergent intervention, and any tachydysrhythmia treated with cardioversion); (2) inpatient STEMI; (3) cardiac or respiratory arrest; and (4) death.

Another unique aspect of this study was the enrollment of patients who were sick who met their criteria discussed above– many other studies only considered “low risk patients” to be those without significant comorbidities or CV disease histories (e.g. history of CABG, multiple stents, diabetes, hypertension, etc) . They did exclude patients with LBBB or pacemaker rhythms on EKGs, which would have made identification of ischemia perhaps more difficult.

What did they find? Only four patients out of 7266 meeting the above criteria went on to have any of the primary endpoints. Of these, two were non-cardiac and two were possibly iatrogenic. This is a rate of 0.06% (95% CI 0.02-0.14%), which is much lower than many people would likely guess, and can help inform the discussion we can have with patients when arriving at a disposition. If I am practicing in a community such as the authors’, where short-term follow up with a cardiologist can be arranged, and a patient is reliable, I feel that this data can help me feel more comfortable discharging them with that plan rather than admitting to the hospital, if the patient is comfortable with this.

As Ryan Radecki wrote, the applicability of this hinges on tightly integrated follow up, and we cannot practice “catch and release” medicine. This is also only one data set, and requires prospective validation, and we need to acknowledge that this is not a zero-miss strategy (just like any strategy). That said, there are many potential downsides associated with admission, from costs and downstream sequelae of unnecessary invasive testing to iatrogenic harms, and this study will help better inform our conversation with patients about all of these issues.


Weinstock MB1, Weingart S2, Orth F3, VanFossen D4, Kaide C5, Anderson J6, Newman DH7. Risk for Clinically Relevant Adverse Cardiac Events in Patients With Chest Pain at Hospital Admission. JAMA Intern Med. 2015 Jul;175(7):1207-12. PMID: 25985100. [PubMed] [Read by QxMD]

Can the use of tourniquets improves CPR outcomes?

In my third year of medical school, I was discussing my plan for a heart failure patient in the ED and somehow in the course of our discussion, it got brought up that once upon a time “rotating tourniquets” were used in the emergent management of acute heart failure. This method has long since been abandoned in favor of pharmacological methods of Preload reduction, but still a got me thinking on – I was trying to think about the ways in which  the application of a tourniquet affects physiology. One thought crossed my mind was that a patient with acute heart failure or hemorrhagic shock, or any other low flow state might benefit from a theoretical increase in blood perfusion to vital organs if tourniquets were applied to the limbs. The use of rotating tourniquets in the past in patients suffering from decompensated heart failure might suffice as evidence that this, at least in a time-limited fashion, what at least not be harmful (though I understand that the application of a tourniquet is quite painful, and it would  be necessary to ensure that patients were adequately sedated pain-free if we were to do this).

For some reason, this thought crossed my mind again today and I decided to do a literature search. Unsurprisingly it turns out I am not the only person who has had this idea. Last year a group of Chinese researchers published a paper in which they showed an increase in cerebral perfusion pressure and myocardial blood flow in a porcine model of cardiac arrest. Ten pigs (poor pigs, it is such bad luck that their hearts are like ours)  were assigned to receive standard CPR or  CPR augmented with tourniquets wrapped from the distal to the proximal portion of all four limbs.  Ventricular fibrillation was induced with a pacing wire, and  maintained for seven minutes of “down time” before beginning resuscitation. CPR was performed for two minutes before a dose of epinephrine was given, followed by three more minutes of CPR after which defibrillation was attempted.  There were no significant differences between the outcomes in terms of resuscitation success, number of defibrillation attempts, intra-thoracic pressure, duration of CPR, or the use of epinephrine. What did differ between the groups were measures of cerebral perfusion pressure is measured by carotid bloodflow, systolic and diastolic blood pressures during CPR, coronary perfusion pressure, and end-tidal CO2.  Survival was the same in both groups, but alas, it is difficult to measure neurologic outcome in pigs, so some important end-points were not reported. The differences in CPP were almost 10 mmHg, ETCO2 went from ~ 28 mmHg in the standard CPR pigs to ~36 mmHg in the tourniquet group, and CBF had a ~ 10 mL/min difference (this seems much less clinically-significant to me, but I’m not sure how big of an impact that is– we don’t have this monitor in our ED).

This is obviously a long way away from being ready for prime time in humans, and I’m not sure that you could use this to even get the idea past an IRB.  that said, if you really could improve both coronary and cerebral blood flow, and there were no significant harms associated with this technique I don’t really see the downside of trying– do you?  Some important limitations beyond the animal model  of this study include the relatively short “downtime”, the lack of assessment of function after the resuscitation (even if you can’t measure neurologic outcomes, you could look at cardiac function),  and the fact that there model of tourniquet usage doesn’t really match the way that we use tourniquets and human beings. This may be nitpicky, but the tourniquets were applied during fibrillation, not during CPR– it is hard to imagine that this would be an easy feat to accomplish or get buy-in for outside a setting where you have plenty of free hands. Lastly, these were presumably otherwise-healthy pigs– we really need a porcine model of a more typical cardiac arrest patient if we’re going to try to apply this to humans.

Still, I find this very interesting, who think that there may be a future in trying to use a similar technique in humans eventually. I have seen many “survivors” of cardiac arrest who may have achieved ROSC, but ultimately never made it out of the ICU– these represent the majority of those who survive in and out-of-hospital cardiac arrest– and anything that could potentially improve their most important outcomes, survival of head and heart, would be welcomed. The odds of me being able to do this RCT while in residency? Probably low. But you never know!


Yang Z1, Tang D2, Wu X3, Hu X4, Xu J5, Qian J6, Yang M7, Tang W8. A Tourniquet Assisted Cardiopulmonary Resuscitation Augments Myocardial Perfusion in a Porcine Model of Cardiac Arrest. Resuscitation. 2014 Oct 23;86C:49-53. PMID: 25447436. [PubMed] [Read by QxMD]