The Biggies

TTM Trial

TTM Trial Hemodynamics

Polderman Editorial on TTM

HACA Trial (NEJM 2002;346(8):549)

Bernard RCT (NEJM 2002;346(8):557)


ILCOR Hypothermia Statement

ILCOR Post-Arrest Care Statement

Lancet Review by Kees Polderman

Nuts & Bolts Review by Kees Polderman (Crit Care Med 2009;37(3):1101-1120)

Mechanisms of Hypothermia by Kees Polderman

Study by Oddi ( )-Included Asystole and PEA

Oddi Crit Care Med 2008;36:2296. Time to ROSC, not rhythm was the best predictor.

Another PEA Asystole Included Study

Wake County implemented 2005 AHA and hypothermia and showed improved survival

role of hypothermia sr (resus 2011;82:508)

Targeted Temp Management Recs from 5 Crit Care Groups (Crit Care Med 2011;39:1113)

Survival does not improve when therapeutic hypothermia is added to post-cardiac arrest care.  Not sure why survival would improve, it is neuro intact survival that should improve. (Pfeifer et al. Resuscitation. 2011 Jun 12.)

Another study showed that neuro-intact survival did not increase with PCI in patients undergoing hypothermia, not sure why it would, it is mortality that should improve (Resuscitation 83 (2012) 699– 704)

Report from a regional network, showed survival in asystole/pea (7/7 survivors were cpc 1/2), association with delayed cooling and death (probably merely assoc.) (circulation 2011;124:206)

Another registry study showed no benefit in asystole or PEA (Circulation. 2011;123:877-886)

364 patients; 135 got hypothermia-35% of hypo group had good neuro outcome compared with 23% in non-hypo group. After multivariate was performed: OR 1.84 for favorable neuro outcome. (resus 2011;82:1162)

Meta-analysis shows, well i can’t really figure out what it shows, but I think they are saying if you evaluate all rhythms there is still equipoise for benefits of hypothermia. (Int J Card 2011;151:333)

Another study of 110 patients-VF (86) and non-VF (24); 66% of VF had CPC 1 or 2, 8% of Non-VF had CPC 1 or 2. (Am J Cardiol 2011;108:173)

Another restrospective study shows benefit in non-shockable rhythms (Resuscitation 83 (2012) 202– 207)

Meta-analysis of non-shockable rhythms (Resuscitation 83 (2012) 188– 196) show benefit

Another cohort from GB shows no neurological outcome benefit (Emerg Med J 2012;29:100-103)

ICE Preliminary Results without any multi-variate analysis showed an assoc with worse outcomes in the rapidly cooled group (Resuscitation 2011 Italian Cooling Experience Study Group PMID 22155700)

Published in the same issue, a study by Sendelbach et al. showed a delay in initiation and a delay to temp was assoc. with worse neurological outcomes (Resus 2012;83:829)

Cardiology SR shows no clear benefit from Hypothermia (Int J Cardiol 2011;151:333)

Another retrospective of spont normothermia vs. induced hypothermia (Crit Care Med 2012;40:2315)

Who Should Get It?

In one propensity matched trial, patients with time to ROSC > 15 minutes had the most benefit (Crit Care 2010;14:R155)

First Study I have seen in Asphyxia

Study for Hanging Patients (Resuscitation 80  (2009), pp. 210–212)

Didn’t work for drowning patients (Acta Anaesthesiologica Scandinavica  Volume 56, Issue 1, pages 116–123, January 2012)

Study, which was probably underpowered, showed only trend but not stat sig increase in neuro-intact survival in non-shockable (Emerg Med J 2012;29:100e103)

Review of Non-VF/VT Hypothermia use

Regionalization of Post-Arrest Care

AHA recommendations


Field Interventions

Active Comp/Decomp CPR + ITD = Better Survival (Lancet 2011;377(9762):301)

Starting Hypothermia in the Field

New Bernard trial did not show benefit with Post-arrest OOH cooling vs. at ED arrival (Circulation2010;122:737)

Intra-arrest Hypothermia

Small obs study of intra-arrest cooling

Intra-Arrest Transnasal Evaporative Cooling A Randomized, Prehospital, Multicenter Study (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness) (Circulation. 2010;122:729-736.)

Big Wake County Study showed ROSC benefit (Resus 2011;82:21)

Abstract from ACEP showed Wake County improved survival with all rhythms


From Mike Darwin

Post Arrest Treatment

Bundled Therapy after Arrest including Hypothermia Implementation of a standardized treatment protocol for post resuscitation care after out-of-hospital cardiac arrest (Resuscitation (2007) 73, 29-39)-Added EGDT to hypothermia, also aggressive PCI

Post resuscitation care What are the therapeutic alternatives and what do we know? Resus 2006;69:15

EGDT is feasible, maybe helps mortality?

New emerging therapies for the post-arrest

TH doesn’t increase pressor requirements (Resuscitation Volume 84, Issue 2, February 2013, Pages 189–193)

Are busier centers better?

Carr said maybe

Carr said yes

Callaway said maybe not


Cold simple intravenous infusions preceding special endovascular cooling for faster induction of mild hypothermia after cardiac arrest—a feasibility study (Resus Volume 64, Issue 3, March 2005, Pages 347-351) no control group: Endovascular is quicker with 2 liter cold LR. 30 cc/kg takes you down ~2 C, 40 cc/kg ~2.5. 500 cc will take you down ~0.5 C


Cold infusions alone are effective for induction of therapeutic hypothermia but do not keep patients cool after cardiac arrest Resus Volume 73, Issue 1, April 2007, Pages 46-53

Crystalloid more effective for cooling than colloids (Critical Care 2013, 17:R242)

External Cooling Can Overcool used ice packs not applicable to current methods Therapeutic hypothermia after cardiac arrest: Unintentional overcooling is common using ice packs and conventional cooling blankets Critical Care Medicine:Volume 34(12) SupplDecember 2006pp S490-S494 overcooling with ice packs and blankets. flawed by use of tympanic temps and 20% received either saline augmentation or hemofiltration


Same outcome between ice packs and endovascular, but endo was better at temp control and rewarming control


Pilot study of rapid infusion of 2 L of 4 degrees C normal saline for induction of mild hypothermia in hospitalized, comatose survivors of out-of-hospital cardiac arrest. Circ 2005;112:715 CVP and PAWP went down after infusion, EF went up


From evidence to clinical practice: Effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest Crit Care Med 2006;34:1865 good outcome 55.8 vs 25.6, even in shock pts dramatic improvement 5/17 vs 0/14


A prospective, multicenter pilot study to evaluate the feasibility and safety of using the CoolGard System and Icy catheter following cardiac arrest.(Resuscitation 2004; 62:143-150)-Overcooling occurs with catheters as well


More rapid infusion of fluids for induction (Resus 2003;56:9)

Polderman’s Fluid Induction article (CCM


My Letter comparing Rectal vs. Esophageal Temp Probes–Rectal is no good

Additional Information on Esophageal vs. Rectal Probes


How long does it take to cool a bag of saline? 2 hours in the fridge


You can probably induce and maintain but not rewarm with ice packs and iced saline

In pigs at least, IO, PIV, and Central all worked equally well for induction with iced saline

In pigs, tracheal temp was accurate


It is the post-arrest, not the iced saline that leads to poor lung function and one more using echo, and editorial


Rapid Cooling is probably better (CCM 2005;33:2744)

Patients with good outcome are harder to cool and rewarm quicker post-rosc (Resuscitation 81 (2010), pp. 867–871) and (Crit Care 2011;15:R101)



Comparison of prophylactic use of midazolam, ketamine, and ketamine plus midazolam for prevention of shivering during regional anaesthesia: a randomized double-blind placebo controlled trial British Journal of Anaesthesia 2008 101(4):557-562 ketamine blunts shivering, add midaz and it works even better.

Best review of shivering to date

Review from SCCM Critical Connections on shivering prevention pharmacology

Surface warming ameloriates shivering Crit Care Med 37(6), June 2009, pp 1893-1897

Diazepam for shivering prevention

Columbia’s anti-shivering protocol

And brand new publication of Columbia Anti-Shivering (Neurocrit Care 2011;14:389)

Great Review Article

Meta-analysis of all medications (Crit Care Med 2012;40:3070)

remember: shivering causes adrenergic release; this may be why many patient look unstable from hypothermia, we get under their threshold and they stop shivering and drop like stones

Mortality benefit from 24 hrs paralysis by multi-variate association (Resus 2013;84:1728)


No Increase in Arrhythmias during hypothermia (CCM 37(2):403-409)


Ddavp to reverse the anti-platelet effects

In Hospital

Small study on hypothermia for inpatient arrest

Largest study to date (Neurocrit Care 2012;16:06) showed neurological outcome benefit only in shockable pts, but this was retrospective before and after.

A prediction rule of neurologic outcome for in-hospital arrest (Arch Intern Med. 2012;172(12):947-953)

Post-Arrest Syndrome

Microcirculation during Cardiac Arrest


The Post-Arrest is a sepsis-like syndrome Successful Cardiopulmonary Resuscitation After Cardiac Arrest as a “Sepsis-like” Syndrome (Circ 2002;106;562-568)- it’s big time SIRS


Long Term Sequelae post-arrest


Artificially Increasing the HR is probably detrimental (J Am Coll Card 39:102)


Epinephrine is probably a big part of the cause, but when intra-arrest hypothermia is going on, epi negative effects are probably mitigated

Nuts & Bolts

How deep to place the Esophageal probe

How to interpret blood gases

And a simple approach to Alpha and Ph-Stat during Hypothermia

Maintain K > 3.0 to avoid dysrhythmia

Myocardial Stunning

Myocardial dysfunction after resuscitation from cardiac arrest: An example of global myocardial stunning JACC Volume 28, Issue 1, July 1996, Pages 232-240

Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest JACC Volume 40, Issue 12, 18 December 2002, Pages 2110-2116 J Am Coll Cardiol 28 (1996), pp. 232–240, Crit Care Med 24 (1996), pp. 992–1000.  J Am Coll Cardiol 40 (2002), pp. 2110–2116.  Resuscitation 61 (2004), pp. 199–207. Circulation 95 (1997), pp. 2610–2613.

Myocardial Dysfunction starts in hours after arrest and lasts 24 hours (JACC Volume 40, Issue 12, 18 December 2002, Pages 2110-2116)

Calcium makes things better, low calcium makes things worse, card arrest lowers calcium… in pigs at least (Resuscitation 2010;81:117)


Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis (lancet 2008;372:554)- increased survival

Editorial about Extracorporeal Life Support

Analysis and results of prolonged resuscitation in cardiac arrest patients rescued by extracorporeal membrane oxygenation J Am Coll Cardiol. 2003 Jan 15;41(2):197-203.Click here to read

Primary percutaneous coronary intervention and mild induced hypothermia in comatose survivors of ventricular fibrillation with ST-elevation acute myocardial infarction Resuscitation. 2007 Aug;74(2):227-34. Epub 2007 Mar 23


Mild therapeutic hypothermia in patients after out-of-hospital cardiac arrest due to acute ST-segment elevation myocardial infarction undergoing immediate percutaneous coronary intervention. Crit Care Med. 2008 Jun;36(6):1780-6


Extracorporeal membrane oxygenation support can extend the duration of cardiopulmonary resuscitation Crit Care Med Volume 36(9), September 2008, pp 2529-2535 incredibly impressive neurologic survival

Nagao – Japanese Study on IABP, Bypass,

Cath Study showed improved outcomes if ECMO started in patients with time to cpr of > 10 minutes (Crit Care Med 2011;39:1)

Review of Japanese Literature (Resus 2011;82:10) concludes a higher survial rate with ECMO

Propensity analysis of Out-of-Hospital (Crit Care Med 2013;41(5):1186) Better outcome, but poor overall neuro survival


ST elev on  post-arrest EKG actually represents STEMI (Ann Emerg Med. 2008;52:658-664)

Derivation of a rule to determine which ekgs should get post-arrest cath, they found ST elevations and Depressions got to 95% sens/65% spec, if they added in global wide qrs/lbbb it went to 100% sens/46% spec (Resus 2011;82:1148)

1/3 of patients without STEMI post-arrest will have acute or presumed recent cardiac lesions (Resus 2013;84:1250)


Safety of Thrombolysis during CPR (Drug Safety 2003;26(6):367) Only small incremental risk from thrombolysis post-cpr as normal thrombolysis


Safety and Efficacy of Thrombolysis for Acute Myocardial Infarction in Patients with Prolonged Out of Hospital Cardiopulmonary Resuscitation  (Am J Cardiol 73 (1994), pp. 953–955)-no increased risk, dramatic, but just under significant decrease in mortality


Thrombolytic therapy vs primary percutaneous intervention after ventricular fibrillation cardiac arrest due to acute ST-segment elevation myocardial infarction and its effect on outcome. (Am J Emerg Med. 2007 Jun;25(5):545-50)- Lysis appears as good as PCI


Thrombolytic therapy after cardiac arrest and its effect on neurological outcome. (Resuscitation. 2002 Jan;52(1):63-9)- After controlling for age,

prehospital dosage of epinephrine, and the duration of cardiac arrest we found a non significant trend towards good neurological recovery when thrombolytic therapy was given (OR 1.9, 95% CI 0.8-4.6)


More on safety of  lysis (Resuscitation (2007) 73, 189—201)

TROICA No benefit to empiric lytics in undifferentiated cardiac arrest after physicians stripped out the high-prob PE patients. No stat. sig increase in complications with lytics.


No Increased Bleeding complications for patients with lytics or pci


Propensity Prospective Analysis shows PCI after arrest improves survival (J Intens Care Med 209;24:179)


Out-of-hospital cardiac arrests in patients with acute ST elevation myocardial infarctions in the East Bohemian region over the period 2002-2004. (Cardiology. 2008;109(1):41-51.)-huge mortality difference that just missed stat. sig


Study of angiography after cardiac arrest. They claim they found a number of complete lesions without STEMI signs, but it is impossible to say if these were pre-existing clots or the cause of arrest. (NEJM 1997;336:1629)


Retrospective look at patients taking to cath after cardiac arrest. (JACC 2009;53(5):409)


More PCI data 

From Procat data, successful angioplasty with or without STEMI is associated with improved survival


Among the factors identified, diabetes and a history of coronary artery were strong predictors for a positive coronary angiography, whereas ST segment elevation was not as predictive as expected. (Eur J Emerg Med. 2011 Apr;18(2):73-6.)

Meta-Analysis: only on STEMI, dysrhytmia, hemodynamic instability (Acute coronary angiography in patients resuscitated from out-of-hospital cardiacarrest—a systematic review and meta-analysis  Resuscitation, 83 (2012), pp. 1427–1433)



TEG of effects of Hypothermia  Anesthesiology 2008;109:1465

Ddavp reverses Plt Effects of Hypothermia (Anaesthesia, 2011, 66, pages 999–1005)


Induced Normothermia

Induced Normothermia < 37.5 for 72 hours Post-Rosc or until back to baseline mental status (probably better to just say until pt doesn’t need ICU level care any longer)

Zero-Hour Prognosis

In Japan, there is no field termination, so in patients without prehospital ROSC, who survives. They found 9-factors: non-asystole, Age<65, EMS-witnessed arrest, call-to-hospital time, arrest witnessed by any layperson, physician staffed ambulance, call-to-response time < 5 minutes, prehospital shock delivery, presumed cardiac cause. Best scenarios–Non-asystole, Age<65, EMS-witnessed, and Call-to-hospital < 24 minutes got ~16% with VF/VT and 3.8% in PEA for CPC 1 or 2. (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

ED docs suck at prognosticating in the department (ED prognostication of comatose cardiac arrest patients undergoing therapeutic hypothermia is unreliableCatherine M. Wares, MDa, , , ,Alan C. Heffner, MDa, b,Shana L. Ward, MSc,David A. Pearson, MDaShow moredoi:10.1016/j.ajem.2014.12.033)

Meet 2 Criteria: No ROSC by Hospital Arrival and no Prehospital Defib had 30 day survival in only 3 of 9499 patients (Circulation 2015;131:1536)

ICU Prognosis

Most recent Guidelines

Best so Far: Structured Approach to Neuroprognosticaiton

Excellent Review Article

Most recent review 3/2013

Perman et al. reviewed 28 of 49 individuals who were assigned to poor prognosis group. 8 survived and 6 had good neurological outcome. (Crit Care Med 2012;40:719)

ED Prognosis-First attempt at rule derivation (as in not ready for prime-time) the 5-R score. (Resus Volume 83, Issue 6, June 2012, Pages 734–739)

Fantastic Review by Dave Greer et al.


SSEP Probably best means of prognostication


Neurologist 2007;13:369. Absence of brainstem at arrival did not preclude good outcome


Practice Parameters of the AAN. Lack of brainstem is not predictive in the first day, only on day 3. All bets are off if hypothermia used.


Myoclonic Status vs. Lance Adams


Very Small Data set on predicting outcome in TH patients (Neurology 2008;71:1535)


Perhaps in future CTA and CTP can predict early brain death

BIS/EEG markers of outcome


DW MRI for Prognosis beyond me but the neurocrit care folks seem to be using it


Article and two more articles (Transplant Proceedings 2007;39:16 & Neurocrit Care 2009;11:261) saying CTA and CAT/P may be good enough to establish brain death (Editorial)


Small numbers and retrospective, but this study indicates that GCS on arrival is not predictive, but no Pupils and no corneals at 72 hours is predictive of poor outcome


BIS of zero = zero prognosis in this study


Fasciculations post-brain death


Some retrospective associations, but not too helpful


Abstract from Propac II – no pupils at 72 hr and no SSEP after rewarming = no outcome


Case series of folks that looked crappy at arrival but left the hospital intact (Neurologist 2007;13(6):369)


111 patients prospectively studied, looked at factors assoc with good and bad outcome: unreactice eeg pattern was assoc with dismal neuro outcome, Incomplete brainstem recovery was 96% specific, myoclonus 93% specific, absent motor response to pain 76% specific. 2 out of 4 (incomplete brainstem, myoclonus, unreactive EEG, absent cortical SSEP) (Ann Neurol 2010;67:301) The combination of M1 or M2 and absent pupillary reactions to light and absent corneal reflexes on day 3 was present in 14.9% of patients with an unfavourable and none of the patients with a favourable outcome. None of the patients with a favourable outcome had a bilaterally absent somatosensory evoked potential of the median nerve. The value of electroencephalogram patterns in predicting outcome was low, except for reactivity to noxious stimuli.(Resuscitation 82 (2011) 696–701)

Editorial from previous article

Neuron-specific Enolase?? S-100B

Predicting Neuro Outcome Review Article (Curr Opin Crit Care 2011;17:254)

Exam at 72 hours doesn’t predict prognosis (and additional info in a letter to the editor)

Gray-white ratio < 1.2 on the CT within 24 hours of arrest predicted poor outcome despite hypothermia (Resus 2011;82:1180)

No duh!!!, but it is still good to get it in the literature. Sedation around the 72-hr exam confounds outcome prediction (Neurocrit Care 2011;15:113)

Myoclonus doesn’t predict bad outcome (Resuscitation 83 (2012) 265– 269)

Many patients were declared poor prognosis within 15 hours of normothermia–many of these patients left neurologically intact; others were made comfort care (CCM 2012;40:719)

CT scan at day 3 may turn out to be helpful (Stroke. 2011;42:985-992)

DWI MRI abnormalities were 98.5% sensitive and 46.2% specific for bad outcome meaning patients with a normal MRI should have good outcome, but an abnormal MRI doesn’t mean they won’t  (Neurocrit Care 2012;17:240)

pH and Lactate may have a role (Journal of Critical Care Volume 28, Issue 3, June 2013, Pages 317.e13–317.e20)

Meta-analysis concludes: At 72 h with TH, absence of pupillary response and absent SSEP may be the way to predict bad outcome (Intens Care Med 2013;39:1671)

Newest, best Meta-Analysis:

Golan et al pooled data from 20 studies (n = 1,845) investigating diagnostic tests to predict poor neurologic outcome or death following targeted temperature management in adult cardiac arrest survivors, and found:

  1. three tests accurately predicted poor neurologic outcome with low false-positive rates:
    • bilateral absence of pupillary reflexes more than 24 hours after a return of spontaneous circulation
      • (false-positive rate 0.02; 95% CI 0.01 to 0.06; summary positive likelihood ratio 10.45; 95% CI 3.37 to 32.43)
    • bilateral absence of corneal reflexes more than 24 hours
      • (false-positive rate 0.04; 95% CI 0.01 to 0.09; positive likelihood ratio 6.8; 95% CI 2.52 to 18.38)
    • bilateral absence of somatosensory-evoked potentials between days 1 and 7
      • (false-positive rate 0.03; 95% CI 0.01 to 0.07; positive likelihood ratio 12.79; 95% CI 5.35 to 30.62)
  2. False-positive rates were higher for a
    • Glasgow Coma Scale motor score showing extensor posturing or worse
      • (false-positive rate 0.09; 95% CI 0.06 to 0.13; positive likelihood ratio 7.11; 95% CI 5.01 to 10.08)
    • unfavorable electroencephalogram patterns
      • (false-positive rate 0.07; 95% CI 0.04 to 0.12; positive likelihood ratio 8.85; 95% CI 4.87 to 16.08)
    • myoclonic status epilepticus
      • (false-positive rate 0.05; 95% CI 0.02 to 0.11; positive likelihood ratio 5.58; 95% CI 2.56 to 12.16)
    • elevated neuron-specific enolase
      • (false-positive rate 0.12; 95% CI 0.06 to 0.23; positive likelihood ratio 4.14; 95% CI 1.82 to 9.42)
  3. the specificity of available tests improved when these were performed beyond 72 hours
  4. data on neuroimaging, biomarkers, or combination testing were limited and inconclusive

Abstract:  Golan. Predicting Neurologic Outcome After Targeted Temperature Management for Cardiac Arrest: Systematic Review and Meta-Analysis. Crit Care Med 2014;42(8):1919–1930

(From Crit Care Reviews)

Non-Convulsive Status Epilepticus (NCSE)

12% of patients had NCSE; it was associated with poor outcome (Neurocrit Care 2012;16:114)

Yield of intermittent versus continuous EEG in comatose survivors of cardiac arrest treated with hypothermia. Intermittent seems to be ok (Critical Care 2013, 17:R190)


Hypothermia blocks the effects of plavix


May be able to treat myoclonus with Keppra (Inten Care Med 2011;37:177)


Moderate hypothermia decreases Oxygen consumption and CO2 production by 50% Edema post-arrest can cause increased ICP (CCM 1993;21:104)


Cost Effectiveness

Cost-effectiveness states it is more expensive but matches QALY value of most of the other crap we do

Barriers to Adoption

Why EM and CCM claim they can’t do it

Summary Evidence

Therapeutic Hypothermia and Temperature Management 2011;1(1):10

Speed of Cooling

Early achievement of mild therapeutic hypothermia and the neurologic outcome after cardiac arrest. This study showed time to cooling had an assoc with good outcome. (Int J Cardiol. 2009 Apr 3;133(2):223-8.)

EEG for Seizures

Standard intermittent EEGs seemed as good as cEEG in a small study (Crit Care 2013, 17:R190.)


To Index

Am J Emerg Med. 2007 Jun;25(5):545-50. Links

Thrombolytic therapy vs primary percutaneous intervention after ventricular

fibrillation cardiac arrest due to acute ST-segment elevation myocardial infarction and its effect on outcome.



Richling N, Herkner H, Holzer M, Riedmueller E, Sterz F, Schreiber W.Department of Emergency Medicine, Medical University of Vienna, 1090 Vienna,


The aim of this study was to evaluate the effect of thrombolytic therapy on

neurologic outcome and mortality in patients after cardiac arrest due to acute

ST-elevation myocardial infarction and to compare this with those in patients

treated with primary percutaneous coronary intervention (PCI). We

retrospectively examined patients after they had ventricular fibrillation

cardiac arrests. To assess the effect of thrombolysis and PCI on outcome, we

used odds ratios and their 95% confidence intervals and logistic regression

modeling. Thrombolysis was applied in 101 patients (69%) and PCI in 46 patients

(31%). More patients who received thrombolysis had favorable functional

neurologic recovery (cerebral performance category 1 and 2) and survived to 6

months compared with patients with primary PCI (P = .38 and P = .13,

respectively). In patients with cardiac arrest due to ST-elevation myocardial

infarction, it may be acceptable to use thrombolysis as a reperfusion strategy.

This applies especially in hospitals where immediate PCI is not available.

Resuscitation. 2008 Feb;76(2):180-4. Epub 2007 Aug 28. Links



Out-of-hospital thrombolysis during cardiopulmonary resuscitation in patients


with high likelihood of ST-elevation myocardial infarction.



Arntz HR,

Wenzel V,

Dissmann R,

Marschalk A,

Breckwoldt J,

Müller D.

Department of Medicine, Division of Cardiology/Pulmonology, Benjamin Franklin

Medical Center, Charité, Berlin, Germany.

Up to 90% of cardiac arrests are due to acute myocardial infarction or severe

myocardial ischaemia. Thrombolysis is an effective treatment for ST-elevation

myocardial infarction (STEMI), but there is no evidence or guideline to put

forward a thrombolysis strategy during cardiopulmonary resuscitation (CPR). In

two physician-manned emergency medical service (EMS) units in Berlin, Germany,

using thrombolysis is based on an individual judgment of the EMS physician

managing the CPR attempt. In this retrospective analysis over 3 years (total

22.164 scene calls), thrombolysis was started at the scene in 50 patients during

brief intermittent phases of spontaneous circulation, and in 3 patients during

ongoing CPR. On-scene diagnosis of myocardial infarction was established in 45

patients (85%) by a 12-lead ECG, 5 (9%) patients had a left bundle branch block.

Sixteen patients (30%) died at the scene, 37 patients

(70%) were admitted to a hospital. In-hospital mortality was 35% (13 of 37

patients), with cause of death being cardiogenic shock in nine patients, hypoxic

cerebral coma in two and acute haemorrhage in two other patients. All 24 of 53

(45%) survivors were discharged with an excellent neurological recovery. CPR was

started by an EMS physician in 18 of the 24 survivals (75%) and emergency

medical technicians who arrived first in six (25%). Duration of CPR until return

of spontaneous circulation was <10 min in 13 of 24 (54%) of the survivors.

Thrombolysis was initiated during intermittent phases of spontaneous circulation

in 50 (94%) of all patients and in 23 (96%) of the 24 survivors. In conclusion,

this retrospective analysis shows excellent survival rates and neurological

outcome in selected patients with a high likelihood of myocardial infarction,

who develop cardiac arrest and are treated with thrombolysis.

Resuscitation. 2001 Jun;49(3):251-8. Links



Thrombolytic treatment of acute myocardial infarction after out-of-hospital


cardiac arrest.



Voipio V,

Kuisma M,

Alaspää A,

Mänttäri M,

Rosenberg P.

Department of Anaesthesiology and Intensive Care, Helsinki University Central

Hospital, P.O. Box 340, Helsinki, FIN-00029 HUS, Finland.

OBJECTIVE: To investigate the safety and efficacy of thrombolytic treatment

for an acute myocardial infarction (AMI) immediately after resuscitation in the

out-of-hospital setting. DESIGN: Retrospective. SETTING: A middle-sized urban

city (population 540000) served by a single emergency medical system using a

tiered response with physicians in field. PATIENTS AND METHODS: Sixty-eight

patients with an initial diagnosis of AMI who received thrombolytic treatment in

an out-of-hospital setting after cardiac arrest and cardiopulmonary

resuscitation (CPR) between January 1st 1994 and December 31st 1998. An ECG and

the myocardial enzymes (CK, CK-MB, Troponin-T) were used to diagnose AMI.

Myocardial reperfusion was assessed by resolution of the ST-segment elevation.

Side effects and complications were studied. The quality of secondary survival

was evaluated. The Utstein style was used for a uniform style of reporting the

cardiac arrest data. RESULTS: The accuracy of prehospital diagnosis was found to

be excellent. Retrospective analysis revealed that thrombolytic therapy had been

appropriately administered in 64 (94%) of the 68 patients actually treated.

Reperfusion was achieved in 71% of the patients. Haemorrhagic complications were

few, and included intracranial haemorrhage (one patient), gastrointestinal

bleeding (two patients), bleeding from the puncture site (one patient) and

epistaxis (one patient). The incidence of hypotension during streptokinase

infusion was 22%. Sixty-three (93%) of the patients were admitted alive to the

hospital, with 36 subsequently surviving to discharge. CONCLUSIONS: Thrombolytic

treatment is a safe and effective treatment in AMI even after out-of-hospital

cardiopulmonary resuscitation



empiric early abx reduced mortality in an obs trial (crit care med 2014;42(8):1749)

ph stat may be better post-arrest if you shoot for physiological ph (crit care med 2014;42:1849)




Is there recent evidence supporting NOT using paralytics during hypothermia induction and rewarming OR continuous? I have a patient whom the physician stated he did not want to paralyze due to recent evidence.

There is a growing body of evidence to avoid chemical paralysis, when possible, during targeted temperature management (TTM) or therapeutic hypothermia (TH). Neuromuscular blockade (NMB) agents have traditionally been a primary method to control shivering, which is a normal homeostatic reflex for heat production (thermogenesis). Heat is a byproduct of metabolism and NMBs reduce or eliminate the ability of the muscle to contact, thereby decreasing metabolism. Shivering should be aggressively controlled for two reasons. First, it is a barrier to achieving and maintaining a set targeted temperature. Second, there are deleterious effects of discomfort, increased oxygen consumption, increased carbon dioxide production, decreased lactate clearance, and cardiac ischemia after arrest due to the increased metabolic demand caused by elevated plasma catecholamine concentrations (Choi et al., 2011; Park et al., 2012; Lascarrou et al., 2014).

While NMB agents can be quite useful, there are known consequences. Paralytics make it difficult to assess the depth of sedation and perform a neurologic exam. A patient with inadequate sedation may have posttraumatic stress disorder if chemically paralyzed while awake. Additionally, paralytics may mask seizures, where early treatment is crucial to preserve neurological function. When paralytics are used continuously for more than 48 hours, patients are at increased risk for pneumonia, neuromyopathy, and delayed extubation (Nair et al., 2010; Choi et al., 2011; Price et al., 2012; Lascarrou et al., 2014).

Multiple alternatives to paralytics should be included in shivering protocols. A nonpharmacologic method to control shivering is counter-surface warming: wrapping the head and extremities of patients with warm blankets, or blowing warm air, to raise skin temperature while cooling the core temperature. Guidelines support that patients undergoing induced hypothermia should be on a continuous sedative and analgesic to prevent discomfort and shivering associated with TTM. Other medications available in the United States that are shown to decrease shivering include meperdine, ketamine, dexmedetomidine, magnesium to raise the shivering threshold, granisetron, and physostigmine (Park et al., 2012).

When paralytics are used for refractory shivering, steps should be taken to limit the dose and duration of paralytics, and continuous EEG should be considered to assist with neurologic monitoring (Choi et al., 2011). Consider using bolus dosing of NMB agents as an option to reduce the cumulative dose. If a continuous drip is needed, the dose can be minimized by using a target train of four of 2/4 (versus 0/4), which correlates with approximately 80% of receptors being blocked. When the target temperature is reached, the NMB agent should be discontinued because the shivering response may be suppressed.


HA Choi, SB Ko, M Presciutti, L Fernandez, AM Carpenter, C Lesch, E Gilmore, R Malhotra, SA Mayer, K Lee, J Claassen, JM Schmidt, N Badjatia. Prevention of shivering during therapeutic temperature modulation: The columbia anti-shivering protocol. Neurocrit Care 2011;14:389–394.
JB Lascarrou, A Le Gouge, J Dimet, JC Lacherade, L Martin-Lefevre, M Fiancette, I Vinatier, C Lebert, K Bachoumas, A Yehia, MH Lagarrigue, G Colin, J Reignier. Neuromuscular blockade during therapeutic hypothermia after cardiac arrest: Observational study of neurological and infectious outcomes. Resuscitation 2014;85:1257–1262.
SC Nair, Y Dargaud, M Chitlur, A Srivastava. Tests of global haemostasis and their applications in bleeding disorders. Haemophilia 2010;16 Suppl 5:85–92.
SM Park, HS Mangat, K Berger, AJ Rosengart. Efficacy spectrum of antishivering medications: Meta-analysis of randomized controlled trials. Crit Care Med 2012;40:3070–3082.
D Price, NJ Kenyon, N Stollenwerk. A fresh look at paralytics in the critically ill: Real promise and real concern. Ann Intensive Care 2012;2:43.


  1. Lisa GilmoreTo says

    Hey Scott….LOVE the podcast. I am currently the nurse educator for my Level I facility, but am also attending APRN school…and hope to practice the same way you do…critical care in the emergency department!! Would love to do some clinical time with you… :)

    I have a specific need regarding ed hypothermia. I too believe that we can easily bring patients to goal temp quickly with iced saline and cooling blankets. We have ONE Alsius unit in the house…and we are getting pressured to use this in our ED. We are busy enough–and are not a teaching center–that often my docs can’t/won’t place a central line if peripheral access is good. I feel strongly that to train 160 nurses to use one machine (maybe one time/year) is risky–they have enough trouble setting up the cooling blankets.

    Do you have any literature to support my theory that the cooling blanket and iced saline is good in the ED?

    Would appreciate any help.
    Lisa Gilmore, MSN/Ed., RN, EMT-P

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