Should Paramedics Intubate Out-of-Hospital Cardiac Arrest?

Airway management of out-of-hospital cardiac arrest is a controversial topic.  Most patients transported for OHCA have receive prehospital airway management.  However, attempts at establishing an airway can interrupt compressions, over-ventilation can decrease cerebral perfusion, and delays in airway acquisition impact transport to definitive care.

This study retrospectively evaluates the CARES surveillance group, a multi-site registry from North America, comparing neurologically intact survival after prehospital endotracheal intubation, supraglottic airway, or no advanced airway.  In the unadjusted results, survival rates were 5.4% for intubated patients, 5.2% for supraglottic airway, and 18.6% for no advanced airway.  After statistical adjustments and propensity scores, the authors report the ultimate winner is not attempting an advanced airway – and then endotracheal intubation is superior to supraglottic airway.

But, really, this study tells us nothing.  Even though the authors attempt several methods of statistical adjustment, the likely presence of massive unmeasured confounders invalidates these observations.  There is an entire host of patient-level and situational factors that impact the type of airway attempted, the number of airway attempts, and the aggressiveness of care provided both pre-hospital and in-hospital.  The profound differences in unadjusted outcomes, between those not receiving an advanced airway and those requiring one, paints the most obvious picture of the likely underlying differences in unfavorable physiology at work.

This is hardly the first observational report regarding the impact of prehospital airway management.  And, frankly, we’ve seen enough – this type of retrospective cohort does not hold the answer, unless the registry was specifically designed to answer such questions.  To the authors credit, they do not overstate the level of evidence provided – but an unsophisticated reader might draw the wrong conclusions.

“Airway management and out-of-hospital cardiac arrest outcome in the CARES registry”
http://www.ncbi.nlm.nih.gov/pubmed/24561079

No LVADs Were Harmed in the Making of This Blog Post

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.

Do not perform chest compressions on an LVAD patient in arrest is a pseudoaxiom for the 21st century. The concern is the force of the compressions will dislodge the cannula, turning a critically ill patient into a critically ill patient with an LVAD-sized hole in their left ventricle. The manufacturers staunchly warn against performing compressions at the risk of causing the sky to fall, our patient’s chest to explode, and an incredibly enraged cardiothoracic surgeon to magically appear at bedside spewing hellfire and brimstone.

Authors of this recent retrospective case series attempt to disprove this modern day axiom. This series describes 8 LVAD patients who presented to their facility, Sharp Memorial Medical Center, in arrest over a 4 year span, all of whom received external chest compression as part of the resuscitative efforts. They assessed device integrity post-arrest in two fashions, either by blood flow data from the LVAD control monitor or examination of the device itself on autopsy (a poor prognostic indicator for the patient). 7/8 patients had flow data post-arrest recorded, all of which indicated a functionally intact VAD. 3/8 had an autopsy performed, including the patient with missing flow data. All confirmed an anatomically intact VAD. The authors conclude that at least in this small case series no VADs were harmed during chest compressions. Whether they were helped is another question all together. These are complex patients with multiple variables including the function of both the VAD and the patient’s intrinsic heart. In this series, 5 out of 8 patients arrested due to pump malfunction, 4 of which were due to accidental disconnection (yikes!). Even in this cohort of a seemingly correctable malady (just plug the thing back in), only one patient had return of neurological function.

A case series of 8 patients is clearly not a large enough n to prove chest compressions are safe in the LVAD patient.  What can be said for sure is the sky did not fall and no angry cardiothoracic surgeons materialized from thin air spewing fire and brimstone. Well, at least a half a psuedoaxiom disproven…

“Chest compressions may be safe in arresting patients with left ventricular assist devices (LVADs).” www.ncbi.nlm.nih.gov/pubmed/24472494

Dantrolene: Saving Canadian Pigs in Ventricular Fibrillation

Just a quick highlight of interesting translational research, this time aimed at improving survival post-ventricular fibrillation.

These authors hypothesized that, as VF is associated with impaired intracellular calcium cycling, perhaps blockade of an intracellular pathway may reduce refractoriness to defibrillation.  The agent?  Dantrolene – which acts upon the ryanodine receptor of the sarcoplasmic reticulum.

Twenty-six Yorkshire pigs had VF induced, subsequently received dantrolene or normal saline, and finally CPR and defibrillation.  85% of dantrolene-treated pigs were successfully defibrillated compared with 39% of controls, and all dantrolene-treated pigs remained in organized rhythm.  An ex vivo rabbit-heart model also showed similar physiologic effects.

Perhaps dantrolene has a future as a component of ACLS protocols – only time, and further study, will tell.

“Dantrolene Improves Survival Following Ventricular Fibrillation by Mitigating Impaired Calcium Handling in Animal Models”
http://circ.ahajournals.org/content/early/2014/01/07/CIRCULATIONAHA.113.005443.abstract

The Optimal Blood Pressure After OHCA Is …

… normal.

This article is a lot of science for not a lot of insight.  These authors gathered 3,620 out-of-hospital cardiac arrest patients who were transported to the Emergency Department after return of spontaneous circulation.  Patients that arrived to the Emergency Department with ROSC and a normal blood pressure had the best survival, with a linear decrease in survival for patients arriving with SBP below 90 mmHg.

However, the authors take this finding to the next step and conclude patients might benefit from more aggressive post-resuscitation blood pressure management.  Yes – any subgroup association identified on retrospective data dredging may reveal a true finding – but, rather than implicitly hype the positive result, it would be more appropriate to significantly downplay the finding as of uncertain significance and only hypothesis generating for future study.  After all, chances are – sick patients are sick, and those that persist in hypotension after OHCA are declaring themselves as such.  Prehospital blood pressure management does not address the underlying pathophysiology of the arrest and, given what we know about coronary and cerebral vasoconstriction, is more likely to be deleterious than beneficial.

“The association between systolic blood pressure on arrival at hospital and outcome in adults surviving from out-of-hospital cardiac arrests of presumed cardiac aetiology.”
http://www.ncbi.nlm.nih.gov/pubmed/24333351

A Rapid Response Fantasyland

Rapid response teams sound good in theory – specifically skilled nurses as back-up providers for floor emergencies, intervening and escalating patients in times of unexpected deterioration.  However, the largest cluster-randomized trial and multiple meta-analyses have failed to show any benefit to rapid response teams.

The response to this high-quality evidence?  Irresponsible conclusions based on low-quality retrospective data.

These authors have so much enthusiasm for their product – a rapid response team that proactively rounds on patients – they’re blind to the most obvious holes in their data.  They try to retrospectively compare pre- and post-RRT implementation outcomes, despite having essentially only data on floor codes.  And, backing up their main conclusion, floor codes are lower post-RRT proactive rounding – of course, floor codes were already trending downwards at the time of implementation.

What happened when the RRT intervened?  The same thing as all other studies show – they moved patients to a higher level of care.  How did patients fare in the ICU?  A third died or were transferred to hospice.  Utterly overlooked in the discussion, in which these authors praise their product and their RRT nurses profusely, is the end result of their RRT product appears to be an unchanged mortality – a simple shuffling around the location of in-hospital deaths.  Their title implies a result that is simply demonstrated nowhere in the article, yet they continue to lavish themselves with accolades right up through the final conclusion:

“Our study demonstrates proactivity and innovation as an overall approach to inpatient cardiac arrests  ….  Innovation stems from a dedicated managerial team who routinely evaluates trends in the code data and creatively seeks ways to prevent cardiac arrest from occurring.”

Managerial buzzword self-aggrandizing nonsense.

“Proactive rounding by the rapid response team reduces inpatient cardiac arrests”
http://www.ncbi.nlm.nih.gov/pubmed/23994805

The Shock Index is a Shockingly Poor Predictor of Peri-Intubation Arrest

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.
This retrospective analysis of 410 patients undergoing RSI is a helpful reminder of how a statistically significant association does not implicitly translate into a clinically useful one.

The authors of this paper attempted to identify factors that would predict peri-intubation cardiac arrest using a cohort of patients requiring emergent intubation in a large urban emergency department. Specifically does the Shock Index accurately predict those who will suffer post-intubation cardiac arrest? The Shock Index (HR/systolic BP) is essentially an attempt to quantify a patient’s volume status and cardiac reserve into simple ratio. These same authors have examined this score’s ability to predict peri-intubation hypotension in the past and found similar predictive capabilities.

Given the pedigree of the authors (Dr. Alan Jones and company) it is no surprise their chart review methods were next to flawless. Using standardized data collection forms, a single trained extractor identified patients who underwent ED intubations over a one year period. To ensure inter-observer reliability, 10% of this data was randomly audited by a second extractor blinded to the trials hypothesis. Backwards stepwise regression was utilized to determine what factors were independently associated with peri-intubation cardiac arrest (defined as cardiac arrest up to 60 minutes after intubation).

In this cohort, the rate of cardiac arrest after intubation was 4.2%, or 17 patients. 10 out of these 17 events occurred within 10 minutes of the intubation and, in 15 of the 17 events the initial arresting rhythm was PEA.  As one would expect, patients who experienced peri-intubation cardiac arrest had faster a heart rate, lower blood pressure and more frequent incidence of pre-RSI hypotension. The only two metrics that were found to be independently associated with cardiac arrest were the patient’s body weight and pre-intubation Shock Index. The Shock index was found to have an odds ratio of 1.16 with a confidence interval ranging from 1.003 to 1.3. Put in another manner, it was found to have an AOC of 0.73, rendering it essentially clinically useless.

Given these test characteristics, if we were to use a Shock Index of 0.88 (as suggested by the authors) to determine who is at risk for peri-intubation arrest than we would be left unprepared for an unacceptable quantity of patient who will decompensate during the procedure. This should be inherently obvious, as a formula that incorporates only heart rate and systolic blood pressure is incapable of encapsulating all the many reasons a patient may code peri-intubation. Not to mention that this study does not tell us whether the patients whom the Shock Index identifies as “at risk” will actually benefit from our added vigilance and pre-intubation hemodynamic optimization. Or does the Shock Index merely highlights a spectrum of the more critically ill patients who will inevitably deteriorate despite our clairvoyant best efforts?

Tachycardic, hypotensive patients are at increased peril for peri-intubation arrest. Sicker patients, older patients, and patients with poor cardiac reserve are all at higher risk. Most importantly, the Shock Index does not accurately predict who will and will not arrest after intubation. Similar to tools meant to predict difficult airways (not accurate enough to depend on clinically), we must be prepared for peri-intubation arrest in the majority of the patients requiring emergent intubation. Once a patient reaches the critical juncture of requiring intubation, we should be aware of all the perils this procedure involves and plan accordingly.

“Incidence and Factors Associated with Cardiac Arrest Complicating Emergency Airway Management”
www.ncbi.nlm.nih.gov/pubmed/23911630

Man vs Machine: A CPR Battle to the…

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.

Presenting the LUCAS 2.0, the latest and greatest in CPR technology! The LUCAS device “provides the same quality for all patients and over time, independent of transport conditions, rescuer fatigue, or variability in the experience level of the caregiver.” Or at least that is what the manufacturer, Physio-Control Inc, will have you believe.

High quality CPR and early defibrillation have been the cornerstones of cardiac arrest management since the AHA published their “Chain of Survival”. Reducing the time off the chest is of utmost importance in the current CPR mantra. So a machine that not only performs consistent high quality CPR, but delivers countershocks without interrupting compressions was sure to show benefit in patient oriented outcomes. What follows is a Paul Bunyan-like contest of man against machine. One in which the makers of the LUCAS device strived to prove modern technology’s superiority over good old fashion manpower. In a delightful twist on the original tale the fancy new mechanical CPR device was found to be no better than traditional CPR.

The trial published in JAMA in November 2013, randomized 2,589 subjects to either traditional CPR following the 2005 European Resuscitation Council guidelines or a mechanical compressions protocol. Patients in the mechanical CPR group received traditional compressions until the device could be deployed, at which point compressions were continued mechanically. Ninety seconds after deployment the device delivered a countershock regardless of the initial rhythm. After which the rhythm was checked every 3-minutes and, if appropriate, a shock was delivered after a 90-second delay.

Despite the obvious advantages the LUCAS device provides, no difference was found in survival at 4-hours, ICU discharge, 1-month, or 6-months. The authors claim victory in a single positive endpoint that reached significance. The number of patients with a CPC score of 1 at 1-month was 2.6% in the traditional CPR vs 4.2% in the mechanical CPR group (p-value of 0.04). This is, of course, just post-hoc dredging of innumerable secondary outcomes, and nothing more than statistical noise. To the authors’ credit, they do not revisit this positive finding.

Despite their claims that the LUCAS device would free up rescuers to do other life sustaining actions, patients in the manual CPR group were defibrillated sooner, intubated faster, transported earlier, and arrived at the hospital in a swifter fashion than those in the mechanical CPR group.

The authors conclude “CPR with this mechanical device using the presented algorithm can be delivered without major complications but did not result in improved outcomes compared with manual chest compressions.” Given that there were only 7 major adverse events in the mechanical CPR group vs 3 in the tradition CPR group this does seem to be the case. Though I would caution, with the low incidence of adverse events, this trial was not powered to truly assess safety of the mechanical delivered CPR. 

“Mechanical Chest Compressions and Simultaneous Defibrillation vs Conventional Cardiopulmonary Resuscitation in Out-of-Hospital Cardiac Arrest: The LINC Randomized Trial” www.ncbi.nlm.nih.gov/pubmed/24240611

Man vs Machine: A CPR Battle to the…

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.

Presenting the LUCAS 2.0, the latest and greatest in CPR technology! The LUCAS device “provides the same quality for all patients and over time, independent of transport conditions, rescuer fatigue, or variability in the experience level of the caregiver.” Or at least that is what the manufacturer, Physio-Control Inc, will have you believe.

High quality CPR and early defibrillation have been the cornerstones of cardiac arrest management since the AHA published their “Chain of Survival”. Reducing the time off the chest is of utmost importance in the current CPR mantra. So a machine that not only performs consistent high quality CPR, but delivers countershocks without interrupting compressions was sure to show benefit in patient oriented outcomes. What follows is a Paul Bunyan-like contest of man against machine. One in which the makers of the LUCAS device strived to prove modern technology’s superiority over good old fashion manpower. In a delightful twist on the original tale the fancy new mechanical CPR device was found to be no better than traditional CPR.

The trial published in JAMA in November 2013, randomized 2,589 subjects to either traditional CPR following the 2005 European Resuscitation Council guidelines or a mechanical compressions protocol. Patients in the mechanical CPR group received traditional compressions until the device could be deployed, at which point compressions were continued mechanically. Ninety seconds after deployment the device delivered a countershock regardless of the initial rhythm. After which the rhythm was checked every 3-minutes and, if appropriate, a shock was delivered after a 90-second delay.

Despite the obvious advantages the LUCAS device provides, no difference was found in survival at 4-hours, ICU discharge, 1-month, or 6-months. The authors claim victory in a single positive endpoint that reached significance. The number of patients with a CPC score of 1 at 1-month was 2.6% in the traditional CPR vs 4.2% in the mechanical CPR group (p-value of 0.04). This is, of course, just post-hoc dredging of innumerable secondary outcomes, and nothing more than statistical noise. To the authors’ credit, they do not revisit this positive finding.

Despite their claims that the LUCAS device would free up rescuers to do other life sustaining actions, patients in the manual CPR group were defibrillated sooner, intubated faster, transported earlier, and arrived at the hospital in a swifter fashion than those in the mechanical CPR group.

The authors conclude “CPR with this mechanical device using the presented algorithm can be delivered without major complications but did not result in improved outcomes compared with manual chest compressions.” Given that there were only 7 major adverse events in the mechanical CPR group vs 3 in the tradition CPR group this does seem to be the case. Though I would caution, with the low incidence of adverse events, this trial was not powered to truly assess safety of the mechanical delivered CPR. 

“Mechanical Chest Compressions and Simultaneous Defibrillation vs Conventional Cardiopulmonary Resuscitation in Out-of-Hospital Cardiac Arrest: The LINC Randomized Trial” www.ncbi.nlm.nih.gov/pubmed/24240611

Mostly Dead is All Dead – Neuro Outcomes in OHCA Without Prehospital ROSC

A guest post by Anand Swaminathan (@EMSwami) of EM Lyceum and Essentials of EM fame.

Over the last two weeks there has been a lot of buzz around the NEJM study on targeted temperature management in out of hospital cardiac arrest (OHCA) with return of spontaneous circulation (ROSC). This blog has been no exception. This article we’re going to discuss here addresses the care of a very different population: the patient with OHCA without ROSC in the field.

Over four years, 398,121 adults with OHCA and no ROSC in the field were prospectively entered into a database. The overall survival was dismal (1.89%) with even fewer patients having a good neurologic outcome (0.49%).  Neurologic outcome was defined using the Cerebral Performance Category (CPC) scale with a CPC 1 or 2 as a good neurological outcome. Using logistic regression, the authors identified nine factors that were associated with a CPC 1 or 2 outcomes. The authors further stated that there were four critical factors predictive of a good neurological outcome in these patients: initial non-asystole rhythm; age < 65 years, EMS witnessed arrest and hospital arrival time (from call) < 24 minutes. They further broke down the outcomes by type of non-asystolic rhythm:

There are a number of interesting findings in this study. If there’s no ROSC in the field, the chance of achieving good neurologic status is minimal. Survivors were 3-4 times more likely to have a poor neurologic outcome (i.e. severe cerebral disability, coma or brain death) than a good one (1.89% vs. 0.49%). The presence of the previously mentioned four factors was associated with a higher incidence of better outcomes. In particular, a presenting rhythm of ventricular fibrillation had an adjusted OR of 9.37 for a good outcome. Additionally, this study showed, as others have in the past, that epinephrine use increased the rate of ROSC but did not increase the rate of good neurological outcomes (see also Stiell 2004, Hagihara 2012).

How does this change what we do? We’ve all been working when EMS brings in an unwtinessed arrest patient that never had ROSC. The entire ED team mobilizes to care for this patient even though we know the potential for a good outcome is miniscule. This study provides preliminary information on which patients are more likely to have a good neurologic outcome. It should be the basis of further studies looking at protocols to stop resuscitation in the field and avoid transport to the hospital.

References
Goto Y, Maeda T, Nakatsu-Goto, Y. Neurological outcomes in patients transported to hospital without prehospital return of spontaneous circulation after cardiac arrest. Critical Care 2013; 17:R274 doi: 10.1186/cc13121 [Open Access]

Stiell IG et al. ACLS in OHCA. NEJM 2004; 351: 647-56.

Hagihara A et al. Prehospital Epinephrine Use and Survival Among Patients with OHCA. JAMA 2012; 307(11): 1161-68

Mostly Dead is All Dead – Neuro Outcomes in OHCA Without Prehospital ROSC

A guest post by Anand Swaminathan (@EMSwami) of EM Lyceum and Essentials of EM fame.

Over the last two weeks there has been a lot of buzz around the NEJM study on targeted temperature management in out of hospital cardiac arrest (OHCA) with return of spontaneous circulation (ROSC). This blog has been no exception. This article we’re going to discuss here addresses the care of a very different population: the patient with OHCA without ROSC in the field.

Over four years, 398,121 adults with OHCA and no ROSC in the field were prospectively entered into a database. The overall survival was dismal (1.89%) with even fewer patients having a good neurologic outcome (0.49%).  Neurologic outcome was defined using the Cerebral Performance Category (CPC) scale with a CPC 1 or 2 as a good neurological outcome. Using logistic regression, the authors identified nine factors that were associated with a CPC 1 or 2 outcomes. The authors further stated that there were four critical factors predictive of a good neurological outcome in these patients: initial non-asystole rhythm; age < 65 years, EMS witnessed arrest and hospital arrival time (from call) < 24 minutes. They further broke down the outcomes by type of non-asystolic rhythm:

There are a number of interesting findings in this study. If there’s no ROSC in the field, the chance of achieving good neurologic status is minimal. Survivors were 3-4 times more likely to have a poor neurologic outcome (i.e. severe cerebral disability, coma or brain death) than a good one (1.89% vs. 0.49%). The presence of the previously mentioned four factors was associated with a higher incidence of better outcomes. In particular, a presenting rhythm of ventricular fibrillation had an adjusted OR of 9.37 for a good outcome. Additionally, this study showed, as others have in the past, that epinephrine use increased the rate of ROSC but did not increase the rate of good neurological outcomes (see also Stiell 2004, Hagihara 2012).

How does this change what we do? We’ve all been working when EMS brings in an unwtinessed arrest patient that never had ROSC. The entire ED team mobilizes to care for this patient even though we know the potential for a good outcome is miniscule. This study provides preliminary information on which patients are more likely to have a good neurologic outcome. It should be the basis of further studies looking at protocols to stop resuscitation in the field and avoid transport to the hospital.

References
Goto Y, Maeda T, Nakatsu-Goto, Y. Neurological outcomes in patients transported to hospital without prehospital return of spontaneous circulation after cardiac arrest. Critical Care 2013; 17:R274 doi: 10.1186/cc13121 [Open Access]

Stiell IG et al. ACLS in OHCA. NEJM 2004; 351: 647-56.

Hagihara A et al. Prehospital Epinephrine Use and Survival Among Patients with OHCA. JAMA 2012; 307(11): 1161-68