Theraputic hypothermia - new evidence of less benefit then previously thought??

Christopher

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This was just published:

http://www.nejm.org/doi/full/10.1056/NEJMoa1310519?query=featured_cardiology#t=articleTop
Nielsen et al 2013 said:
BACKGROUND
Unconscious survivors of out-of-hospital cardiac arrest have a high risk of death or poor neurologic function. Therapeutic hypothermia is recommended by international guidelines, but the supporting evidence is limited, and the target temperature associated with the best outcome is unknown. Our objective was to compare two target temperatures, both intended to prevent fever.

METHODS
In an international trial, we randomly assigned 950 unconscious adults after out-of-hospital cardiac arrest of presumed cardiac cause to targeted temperature management at either 33°C or 36°C. The primary outcome was all-cause mortality through the end of the trial. Secondary outcomes included a composite of poor neurologic function or death at 180 days, as evaluated with the Cerebral Performance Category (CPC) scale and the modified Rankin scale.

RESULTS
In total, 939 patients were included in the primary analysis. At the end of the trial, 50% of the patients in the 33°C group (235 of 473 patients) had died, as compared with 48% of the patients in the 36°C group (225 of 466 patients) (hazard ratio with a temperature of 33°C, 1.06; 95% confidence interval [CI], 0.89 to 1.28; P=0.51). At the 180-day follow-up, 54% of the patients in the 33°C group had died or had poor neurologic function according to the CPC, as compared with 52% of patients in the 36°C group (risk ratio, 1.02; 95% CI, 0.88 to 1.16; P=0.78). In the analysis using the modified Rankin scale, the comparable rate was 52% in both groups (risk ratio, 1.01; 95% CI, 0.89 to 1.14; P=0.87). The results of analyses adjusted for known prognostic factors were similar.

CONCLUSIONS
In unconscious survivors of out-of-hospital cardiac arrest of presumed cardiac cause, hypothermia at a targeted temperature of 33°C did not confer a benefit as compared with a targeted temperature of 36°C.

Hard to know WHAT works anymore. Lets see what you think.

Let's not forget this pre-hospital study out of King County published the same day in JAMA:
Kim et al 2013 said:
Importance Hospital cooling improves outcome after cardiac arrest, but prehospital cooling immediately after return of spontaneous circulation may result in better outcomes.

Objective To determine whether prehospital cooling improves outcomes after resuscitation from cardiac arrest in patients with ventricular fibrillation (VF) and without VF.

Design, Setting, and Participants A randomized clinical trial that assigned adults with prehospital cardiac arrest to standard care with or without prehospital cooling, accomplished by infusing up to 2 L of 4°C normal saline as soon as possible following return of spontaneous circulation. Adults in King County, Washington, with prehospital cardiac arrest and resuscitated by paramedics were eligible and 1359 patients (583 with VF and 776 without VF) were randomized between December 15, 2007, and December 7, 2012. Patient follow-up was completed by May 1, 2013. Nearly all of the patients resuscitated from VF and admitted to the hospital received hospital cooling regardless of their randomization.

Main Outcomes and Measures The primary outcomes were survival to hospital discharge and neurological status at discharge.

Results The intervention decreased mean core temperature by 1.20°C (95% CI, −1.33°C to −1.07°C) in patients with VF and by 1.30°C (95% CI, −1.40°C to −1.20°C) in patients without VF by hospital arrival and reduced the time to achieve a temperature of less than 34°C by about 1 hour compared with the control group. However, survival to hospital discharge was similar among the intervention and control groups among patients with VF (62.7% [95% CI, 57.0%-68.0%] vs 64.3% [95% CI, 58.6%-69.5%], respectively; P = .69) and among patients without VF (19.2% [95% CI, 15.6%-23.4%] vs 16.3% [95% CI, 12.9%-20.4%], respectively; P = .30). The intervention was also not associated with improved neurological status of full recovery or mild impairment at discharge for either patients with VF (57.5% [95% CI, 51.8%-63.1%] of cases had full recovery or mild impairment vs 61.9% [95% CI, 56.2%-67.2%] of controls; P = .69) or those without VF (14.4% [95% CI, 11.3%-18.2%] of cases vs 13.4% [95% CI,10.4%-17.2%] of controls; P = .30). Overall, the intervention group experienced rearrest in the field more than the control group (26% [95% CI, 22%-29%] vs 21% [95% CI, 18%-24%], respectively; P = .008), as well as increased diuretic use and pulmonary edema on first chest x-ray, which resolved within 24 hours after admission.

Conclusion and Relevance Although use of prehospital cooling reduced core temperature by hospital arrival and reduced the time to reach a temperature of 34°C, it did not improve survival or neurological status among patients resuscitated from prehospital VF or those without VF.

So what do we glean from this?

1. Both studies are extremely well done from a methodology standpoint.
2. Both have large numbers of patients enrolled.
3. On its own, the Nielsen et al study could appear to be biased by variability in pre-hospital care...however, when King County fails to demonstrate a difference with post-arrest TH in the field you have to figure maybe the Nielsen study isn't as biased.
4. Intra-arrest TH is the only thing left "unstudied".

Now we have to ask ourselves where these benefits from TH actually come from in some of these systems?

1. Hawthorne Effect: we're paying attention to cardiac arrest patients...the extra attention improves survival.
2. They don't get fevers: this is what the NEJM article seems to show.
3. Standardization of ICU care improves outcomes: study protocol and "Code Cool" protocols made us more efficient at post-arrest care.

In any case, I want to know:

1. Does intra-arrest TH make a difference? We currently practice this at one of my services.
2. Would post-arrest TH via another method than chilled saline change outcomes?

My takeaways:

1. Stick to CPR and defibrillation as the means to affect the greatest change in survival to discharge.
2. Work with the in-hospital staff to determine a post-arrest management plan/bundle that optimizes care with the goal of hypo- or normothermia.
 
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Av8or007

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This is more a question for my own learning (I'm new to this whole EBM thing), but why are the p-values in the NEJM study so high for most of their findings?

"RESULTS
In total, 939 patients were included in the primary analysis. At the end of the trial, 50% of the patients in the 33°C group (235 of 473 patients) had died, as compared with 48% of the patients in the 36°C group (225 of 466 patients) (hazard ratio with a temperature of 33°C, 1.06; 95% confidence interval [CI], 0.89 to 1.28; P=0.51). At the 180-day follow-up, 54% of the patients in the 33°C group had died or had poor neurologic function according to the CPC, as compared with 52% of patients in the 36°C group (risk ratio, 1.02; 95% CI, 0.88 to 1.16; P=0.78). In the analysis using the modified Rankin scale, the comparable rate was 52% in both groups (risk ratio, 1.01; 95% CI, 0.89 to 1.14; P=0.87). The results of analyses adjusted for known prognostic factors were similar."

The studies were both well done with regards to methodology like you mentioned.

What is the rate of bystander CPR in the King county study? The NEJM study had a very good bystander CPR rate (median 1 min for both groups). What was the rate of bystander CPR in the original studies?

Another one of my stupid points - what were the vent settings used/how was oxygenation managed in these patients?
What were the PaO2 values at each time-point for the TH vs 36 deg C groups? We know that hyperoxia alone +/- TH/TTM will worsen outcomes. Just wondering.

Biggest issue with complex patients like these is that we still don't know the whole picture.
 
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Christopher

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This is more a question for my own learning (I'm new to this whole EBM thing), but why are the p-values in the NEJM study so high for most of their findings?

Because the two distributions were not statistically different.

You start with a null hypothesis, apply a test to your data, and compare a calculated p-value against your significance level.

In this case, the null hypothesis is (effectively) that these two distributions are not different.

If the p-value is below your significance level (the magic "0.05" you see) you are said to "reject" the null hypothesis.

A lower p-value means either:
(a) your null hypothesis is false (roughly: the two treatments produce different outcomes)
(b) your null hypothesis is true and your findings are by chance (roughly: the two treatments are identical, but randomly your study showed they were not)

A higher p-value means:
(a) your null hypothesis is true, for the given significance.

So in this case:

The p-value >0.05 for the primary end-point shows that TH and normothermia did not result in different patient outcomes.

The p-values >0.05 for many of the sample population demographics/etc show that the two patient groups did not differ in composition.

More importantly, the study was powered appropriately to detect the differences they were looking for (20% difference). An inappropriately powered study can result in the inability to determine if your findings were significant.

In this case as well you see Hazard Ratio Confidence Intervals which overlap with Unity (1.0): basically we can't show that there is no difference in hazards with a 95% confidence.

(nb: this post is probably not completely mathematically consistent, but serves to illustrate the point without falling in the trap of oversimplifying p-values to, "your findings happened by chance")
 
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Christopher

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What is the rate of bystander CPR in the King county study? The NEJM study had a very good bystander CPR rate (median 1 min for both groups). What was the rate of bystander CPR in the original studies?

Bystander CPR rates for the original hypothermia studies were not bad, 43/49% (TH/Normo) in the Hypothermia after Cardiac Arrest Study Group's 2002 paper and 49/71% (TH/Normo) in Bernard's 2002 paper.

In the King County study 68/64% (TH/Normo) received bystander CPR in the VF/VT group and 50/53% (TH/Normo) received bystander CPR in the non-shockable group.

Perhaps the most impressive numbers in that paper...94% of VF/VT patients achieved ROSC in the field, and 90% of non-shockable patients achieved ROSC...I mean holy crap that is impressive even before looking at survival to discharge.

59% survival to discharge in the VF/VT group and 12% survival to discharge in the non-shockable group...Crazy impressive.

Another one of my stupid points - what were the vent settings used/how was oxygenation managed in these patients?
What were the PaO2 values at each time-point for the TH vs 36 deg C groups? We know that hyperoxia alone +/- TH/TTM will worsen outcomes. Just wondering.

Not listed, but presumed to be up to the clinical discretion of the intensivist.

Biggest issue with complex patients like these is that we still don't know the whole picture.

I think these two studies are about as close to controlling independent variables in a resuscitation that I've ever seen.
 
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Av8or007

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http://jama.jamanetwork.com/article.aspx?articleid=185969

Context Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic brain injury; however, clinical data are lacking.

Objective To test the hypothesis that postresuscitation hyperoxia is associated with increased mortality.

Design, Setting, and Patients Multicenter cohort study using the Project IMPACT critical care database of intensive care units (ICUs) at 120 US hospitals between 2001 and 2005. Patient inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival. Patients were divided into 3 groups defined a priori based on PaO2 on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO2 of 300 mm Hg or greater; hypoxia, PaO2 of less than 60 mm Hg (or ratio of PaO2 to fraction of inspired oxygen <300); and normoxia, not classified as hyperoxia or hypoxia.

Main Outcome Measure In-hospital mortality.

Results Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) compared with the normoxia group (532/1171 [45%; 95% CI, 43%-48%]; proportion difference, 18% [95% CI, 14%-22%]) and the hypoxia group (2297/3999 [57%; 95% CI, 56%-59%]; proportion difference, 6% [95% CI, 3%-9%]). In a model controlling for potential confounders (eg, age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2).

Conclusion Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia.

I guess the take home message is that we really don't know what is good and bad re hyperoxia post arrest. The evidence does tend to lean towards hyperoxia being bad.

The vasoconstrictive effects of oxygen and I/R injury phenomenon are well documented in various studies. What we don't know is the effect this has on some disease states (or sub-populations of patients w/ these disease states)

In other settings, hyperoxia is bad and can cause issues. Generally, you can do no harm by titrating oxygen therapy to SpO2 or ABG values, save for a few specific circumstances where HC O2 is definitely required prehospitally and in-hospital (i.e. CO poisoning).
Titrated O2 avoids any possible hyperoxia issues.
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Good discussion though.

Re therapeutic hypothermia, I wonder WHY there may not be as much of a benefit as we thought?

Although the take home message is that we do need to do SOME form of TTM, whether that is induced hypothermia or induced NORMOthermia. If one compares TTM to nothing, the TTM groups do fare better.

If fever prevention is one mechanism of TTM benefits (even for induced normothermia), do we know if pharmacological anti-pyretic agents show the same benefit as physical TTM methods?
 
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triemal04

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Perhaps the most impressive numbers in that paper...94% of VF/VT patients achieved ROSC in the field, and 90% of non-shockable patients achieved ROSC...I mean holy crap that is impressive even before looking at survival to discharge.
Actually, that means that 94% of the patient's entered into the study had a sustained ROSC; nobody is entered into the study in the first place unless they are alive. It doesn't mean that 94% of all VF arrests had ROSC.
59% survival to discharge in the VF/VT group and 12% survival to discharge in the non-shockable group...Crazy impressive.
Don't worry, someone will come along and complain about how all the numbers are lies and false data and how it's really a godawful terrible worthless county.

Not listed, but presumed to be up to the clinical discretion of the intensivist.
It's not, but the initial in hospital PAO2 and PACO2 are listed. While high, they aren't as high as some numbers I've seen, and it seems like most hospitals are usually good about titrating the FiO2 down, so I'd guess it wouldn't be that elevated eventually.

This isn't the first published study that casts doubt on prehospital therapeutic hypothermia; but it is the first that was done in the US.

About 3 years ago (I think) there was a paper out of Italy that looked at essentially the same thing, and had similar outcomes, though theirs actually showed that prehospital TH was fairly detrimental. Granted, there are differences in both the EMS systems, and routine in hospital care, so I'm glad this was finally done here. Definetly food for thought.

Christopher, I'm curious about something. The paper out of King County really was looking more at WHEN starting TH mattered; it makes note that essentially all VF arrests, no matter if they were in the study arm, or the control arm, got TH after arriving at the hospital, and as noted, the results were essentially the same.

With that being the case, if you think that intra-arrest TH would be beneficial, why do you think that?

Granted, one study doesn't prove or disprove anything, but this seems to be a very well done, randomized study with higher enrollement than most; people definetly should be taking note, especially when there were several downsides to the field TH patients.
 

triemal04

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Re therapeutic hypothermia, I wonder WHY there may not be as much of a benefit as we thought?

Although the take home message is that we do need to do SOME form of TTM, whether that is induced hypothermia or induced NORMOthermia. If one compares TTM to nothing, the TTM groups do fare better.

If fever prevention is one mechanism of TTM benefits (even for induced normothermia), do we know if pharmacological anti-pyretic agents show the same benefit as physical TTM methods?
I think part of the issue is that it's being used more and more in a way that it wasn't intended; initially it was for patient's who arrested due to a cardiac cause, AND presented in VF. That combo has the highest likelihood of actually having a cardiac cause; a PEA arrest that get's enrolled due to post-arrest ST-elevation may not have a coronary lesion; just post-arrest ischemia. Even the initial study you posted used "a presumed cardiac cause" as the sole criteria. Without looking at the specific protocol for entry, that can be a very diverse group of people.

Christopher mentioned the other part; TH isn't that easy to maintain properly; there are several things that go into it, so the extra attention paid to those patients may be paying off.

It's always interesting to watch what happens when people start taking a deeper look at a treatment pathway that was pounced upon as the next best thing.
 

medicsb

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So now all the "progressive" services inducing hypothermia are suddenly not so progressive (at least in this aspect). I think the next step in assessing field use will be the relation to transport times. Obviously, if the you're a certain distance from the nearest hospital capable of inducing hypothermia, there may be a benefit. I imagine that transport times are generally short in King County.

As far as induced therapeutic hypothermia, it is not necessarily debunked, but there is a lot to consider, especially the role of a fever in contributing to bad outcomes. If you can reliably ward off a fever without cold saline or the cooling suits, would that be just as good? Would tylenol, motrin, or steroids be just as good? Is active cooling needed to reliably keep a fever from occuring?

Good stuff.
 

Christopher

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Actually, that means that 94% of the patient's entered into the study had a sustained ROSC; nobody is entered into the study in the first place unless they are alive. It doesn't mean that 94% of all VF arrests had ROSC.

Good catch. This is what happens when you compare tables for studies with different inclusion criteria :)

This isn't the first published study that casts doubt on prehospital therapeutic hypothermia; but it is the first that was done in the US.

It is also the first that was appropriately powered to detect differences that mattered.

About 3 years ago (I think) there was a paper out of Italy that looked at essentially the same thing, and had similar outcomes, though theirs actually showed that prehospital TH was fairly detrimental. Granted, there are differences in both the EMS systems, and routine in hospital care, so I'm glad this was finally done here. Definetly food for thought.

That was the ICE Study (Italian Cooling Experiment), and it wasn't the best study methodologically, but was certainly worth considering. We paid close attention to it locally.

Christopher, I'm curious about something. The paper out of King County really was looking more at WHEN starting TH mattered; it makes note that essentially all VF arrests, no matter if they were in the study arm, or the control arm, got TH after arriving at the hospital, and as noted, the results were essentially the same.

With that being the case, if you think that intra-arrest TH would be beneficial, why do you think that?

My main reason is a means of breaking VF without antiarrhythmics (or in conjunction with lidocaine), plus some cardio/neuroprotection...and I'd enjoy giving nitrates alongside all of this.

I was pretty sold on TH as a strategy based on the earlier studies and work out of some of the labs, and the animal data is fairly persuasive that the earlier it begins has a larger benefit.

It seems in practice this may not be the case.

Granted, one study doesn't prove or disprove anything, but this seems to be a very well done, randomized study with higher enrollement than most; people definetly should be taking note, especially when there were several downsides to the field TH patients.

We're taking a very close look at things...but the momentum is against change haha.
 

triemal04

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That was the ICE Study (Italian Cooling Experiment), and it wasn't the best study methodologically, but was certainly worth considering. We paid close attention to it locally.
How the :censored::censored::censored::censored: did you find that? I spent over an hour looking and didn't come close.

My main reason is a means of breaking VF without antiarrhythmics (or in conjunction with lidocaine), plus some cardio/neuroprotection...and I'd enjoy giving nitrates alongside all of this.
I don't know about using it as a means to break vf; I will admit I've never heard that before though.

I think that if this continues to play out the way it sounds like it will (apparently it was a very eye-opening presentation to the AHA) that intraarrest TH will be the next thing to be looked at in much greater detail.

But...unless it does help to terminate vf faster (which would only make it useful in a small subset of arrests) I don't think it will have that much benefit. Again, in the King County study, there was no difference in starting TH late versus early; I think that it's worth looking at, but starting it even earlier doesn't make the most sense. And while some of the downsides (pulmonary edema) might not show up that rapidly (or it very well could), the TH arm did have a higher incidence of rearresting; maybe not a good sign to start on someone who's still in arrest or periarrest.

That does remain to be seen though. And if there are benefits other than neuroprotection or maybe cardio protection then it might be somewhat beneficial.

Now...if a better and more efficient way of cooling patients prehospitally than cold fluid could be devised that might help to alleviate some of the downsides.
 

mycrofft

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We sometimes try too hard to control for outliers of all sorts in these statistical exercises. This leads us to overgeneralize. There are many subtle and unsubtle differences between people re their reaction to something. Some of these are historic (pt had been defibrillated in the field on three occasions), contemporary (pt was a heavy drinker and/or was very intoxicated on ETOH at the time), sometimes genetic, and often just we can't figure it out yet (why anthology samples are kept for so damn long).

Reading the comments above shows that not all prehospital EMS workers slept through a cram course and printed their own certificates.
 

Brandon O

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I will just say that it's a bit hard to draw complete conclusions from this given that the endpoints (moderate hypothermia versus enforced normothermia) aren't really what people are extrapolating to (enforced normothermia versus no temperature management). For that we'd probably need a new study. Or one with three arms, but that would just dilute the numbers more...
 

Christopher

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How the :censored::censored::censored::censored: did you find that? I spent over an hour looking and didn't come close.
khFfu.gif

Annnd a ridiculous library of papers...

I don't know about using it as a means to break vf; I will admit I've never heard that before though.

Animal models have shown that in mild to moderate hypothermia, VF may spontaneously quit, or that defibrillation itself is much easier (impedence is usually lower too). Limited human data precludes making this statement stronger.

Arredondo MT, et al. Effect of body hypothermia on transventricular simple-capacitor-discharge defibrillation thresholds. Am J Physiol Heart Circ Physiol 1980 May;238:H675-H681.

Ujhelyi MR, et al. Defibrillation energy requirements and electrical heterogeneity during total body hypothermia. Crit Care Med 2001 May;29(5):1006-11.

Gilbert NF, et al. Effects of hypothermia on myocardial substrate selection. Ann Thorac Surg 2002 Oct;74(4):1208-12.

Rhee BJ, et al. Effect of hypothermia on transthoracic defibrillation in a swine model. Resus 2005 Apr;65(1):79-85.

Boddicker KA, et al. Hypothermia Improves Defibrillation Success and Resuscitation Outcomes From Ventricular Fibrillation. Circ 2005; 111:3195-3201.

Kämäräinen A, et al. Spontaneous defibrillation after cessation of resuscitation in out-of-hospital cardiac arrest: a case of Lazarus phenomenon. Resus 2007 Dec;75(3):543-6.

Harada M, et al. Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation. Am J Physiol Heart Circ Physiol. 2008 Apr;294(4):H1896-905. doi: 10.1152/ajpheart.00986.2007

Sorrell VL, et al. Mild hypothermia delays the development of stone heart from untreated sustained ventricular fibrillation - a cardiovascular magnetic resonance study. J Cardiovasc Magn Reson 2011; 13(1):17.
 

triemal04

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Animal models have shown that in mild to moderate hypothermia, VF may spontaneously quit, or that defibrillation itself is much easier (impedence is usually lower too). Limited human data precludes making this statement stronger.
Interesting. I do think that is what the next study needs to look at, but I'm willing to place bets now that intra-arrest hypothermia itself won't be a game changer; if there is a heavier focus on providing proper compressions and ventilations and limiting hands off time then things might change, but I doubt it will soley because of a temp change.

Also worth remembering that SEVERE hypothermia may cause the heart to stay in vf.

Part of the reason that I have doubt about this because of how little the temps in the King County study actually changed; if you look at the supplement, the patient's on average went from about 36C to 35C; while still much cooler than normal, that's really pretty minimial. And given that the average patient had about 20 minutes to reach that point...how much do you think you'll drop their temp while still on scene?
 

Christopher

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Interesting. I do think that is what the next study needs to look at, but I'm willing to place bets now that intra-arrest hypothermia itself won't be a game changer; if there is a heavier focus on providing proper compressions and ventilations and limiting hands off time then things might change, but I doubt it will soley because of a temp change.

Also worth remembering that SEVERE hypothermia may cause the heart to stay in vf.

Part of the reason that I have doubt about this because of how little the temps in the King County study actually changed; if you look at the supplement, the patient's on average went from about 36C to 35C; while still much cooler than normal, that's really pretty minimial. And given that the average patient had about 20 minutes to reach that point...how much do you think you'll drop their temp while still on scene?

We do intraarrest TH in our service area, and usually reach ~35 by hospital arrival. We've halted cooling in a few patients who have reached 33 in the field (one was on a dentist's office table and was 34.something upon EMS arrival).
 

triemal04

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We do intraarrest TH in our service area, and usually reach ~35 by hospital arrival. We've halted cooling in a few patients who have reached 33 in the field (one was on a dentist's office table and was 34.something upon EMS arrival).
That's my point. What you guys should be looking at is what the temp of these patient's are AT ROSC. Not when they reach the hospital, but how cool did they actually get before their heart started beating.
 
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