Tag Archives: arrest

Down with "down" time!

A man in his 40s has a witnessed collapse and CPR is immediately started. Paramedics are on scene within 5 minutes and initiate advanced cardiac life support. He has refractory ventricular fibrillation which degenerates to asystole. He arrives in an emergency department where, with good ongoing CPR, he appears reasonably well perfused and even demonstrates some spontaneous movements and reactive pupils. He is placed on a mechanical CPR device and activation of the cardiac cath lab is requested. The patient has been in cardiac arrest now for 32 minutes. The cardiology fellow appears and asks: ‘what’s the down time?’

What’s the right answer? Would you say ‘half an hour’? ’32 minutes’?
And does it matter? Why is the cardiology fellow asking? Does she have an arbitrary cut off in mind, over which emergency coronary reperfusion will be denied?

I think there are several problems with conversations like these.
The first, is what does ‘down time’ even mean?
The second, is how relevant is a cardiac arrest time interval to prognosis in an individual patient?
The third, is what is the significance of any time interval in a patient who at the time of assessment has some signs that CPR is providing some perfusion and there is some evidence of brain function?

Let’s take the first. The definition of ‘down time’ does not appear to be standardised:
In this publication it appears to refer to the time before resuscitation is commenced, where it is demonstrated to be prognostically important.
Similarly, in this medical dictionary, it is defined as the ‘temporal duration from cardiac arrest until beginning cardiopulmonary resuscitation or advanced cardiac life support.
However, a post in Life in the Fast Lane defines it as ‘time to return of spontaneous circulation
This appears to agree with The New South Wales Government’s Intensive Care Monitoring and Coordination Unit who define it as ‘the time from when a person’s heart stops beating to the time it starts beating again
Yet another definition is used in King County, Washington, where it is defined as ‘the time interval from collapse to call 911‘.

So the first thing is to clarify what we’re talking about: “This patient received immediate bystander CPR. He has had resuscitation for 32 minutes”.

My friend in the UK, nurse resuscitationist Fernando Candal Carballido, coined the term ‘Time of Supported Circulation‘, or TOSC. I quite like this and think it could catch on.

The next question is so what? What if it was 90 minutes? At what point do we declare futility? This is where I believe the game has changed. Multiple survivors of prolonged resuscitation are springing up in the news and in the literature. Particularly in the subgroup of patients with minimal comorbidity, early CPR, and who receive circulatory support via ECMO or mechanical CPR while they undergo coronary reperfusion.

For a great example of a prolonged CPR survivor, check out paramedic Wayne Schneider’s story,
…or listen to Steven Bernard describe amazing results from ECMO used in Melbourne in the CHEER study, which includes survivors of over two hours of CPR.

So, in summary:

  • Be clear on your definitions when communicating with colleagues. ‘Down time’ does not appear to have a standard definition, so I would avoid its use.
  • Some patients without comorbidities who have had early bystander CPR may survive despite long periods of CPR (or ‘TOSC’), provided the underlying cause can be treated or is reversible.
  • ECMO and even more widely available mechanical CPR devices are extending the period in which these causes can be addressed.

Update 2016: I now use the terms ‘No Flow Time’ (time from arrest to first basic life support) and ‘Low Flow Time’ (time receiving CPR, which stops with ROSC). This is prognostically very important, with increasing numbers of reports of survivors who have had very long periods of low flow time.

Is 4 Joules per kg enough in kids?

glash-sim-paed-face-smResearchers from the Iberian-American Paediatric Cardiac Arrest Study Network challenge the evidence base behind defibrillation shock dose recommendations in children.
In a study of in-hospital pediatric cardiac arrest due to VT or VF, clinical outcome was not related to the cause or location of arrest, type of defibrillator and waveform, energy dose per shock, number of shocks, or cumulative energy dose, although there was a trend to better survival with higher doses per shock. 50% of children required more than the recommended 4J per kg and in over a quarter three or more shocks were needed to achieve defibrillation.
 
Shockable rhythms and defibrillation during in-hospital pediatric cardiac arrest
Resuscitation. 2014 Mar;85(3):387-91
[EXPAND Abstract]


OBJECTIVE: To analyze the results of cardiopulmonary resuscitation (CPR) that included defibrillation during in-hospital cardiac arrest (IH-CA) in children.

METHODS: A prospective multicenter, international, observational study on pediatric IH-CA in 12 European and Latin American countries, during 24 months. Data from 502 children between 1 month and 18 years were collected using the Utstein template. Patients with a shockable rhythm that was treated by electric shock(s) were included. The primary endpoint was survival at hospital discharge. Univariate logistic regression analysis was performed to find outcome factors.

RESULTS: Forty events in 37 children (mean age 48 months, IQR: 7-15 months) were analyzed. An underlying disease was present in 81.1% of cases and 24.3% had a previous CA. The main cause of arrest was a cardiac disease (56.8%). In 17 episodes (42.5%) ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT) was the first documented rhythm, and in 23 (57.5%) it developed during CPR efforts. In 11 patients (27.5%) three or more shocks were needed to achieve defibrillation. Return of spontaneous circulation (ROSC) was obtained in 25 cases (62.5%), that was sustained in 20 (50.0%); however only 12 children (32.4%) survived to hospital discharge. Children with VF/pVT as first documented rhythm had better sustained ROSC (64.7% vs. 39.1%, p=0.046) and survival to hospital discharge rates (58.8% vs. 21.7%, p=0.02) than those with subsequent VF/pVT. Survival rate was inversely related to duration of CPR. Clinical outcome was not related to the cause or location of arrest, type of defibrillator and waveform, energy dose per shock, number of shocks, or cumulative energy dose, although there was a trend to better survival with higher doses per shock (25.0% with <2Jkg(-1), 43.4% with 2-4Jkg(-1) and 50.0% with >4Jkg(-1)) and worse with higher number of shocks and cumulative energy dose.

CONCLUSION: The termination of pediatric VF/pVT in the IH-CA setting is achieved in a low percentage of instances with one electrical shock at 4Jkg(-1). When VF/pVT is the first documented rhythm, the results of defibrillation are better than in the case of subsequent VF/pVT. No clear relationship between defibrillation protocol and ROSC or survival has been observed. The optimal pediatric defibrillation dose remains to be determined; therefore current resuscitation guidelines cannot be considered evidence-based, and additional research is needed.

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Not finding a difference doesn't prove equivalence

Image from http://www.physio-control.com/
The recent LINC trial was a randomised controlled trial comparing a mechanical chest compression device (LUCAS) with manual CPR(1). “No significant difference” was found for any of the main outcome measures considered.
So do you think the LINC trial demonstrated that mechanical CPR using the LUCAS device is equivalent, or at least not inferior, to manual CPR?
This was an interesting and important trial for those of us who manage prehospital cardiac arrest patients. In some social media discussions, it appears to have been interpreted by some as evidence that they are equivalent resuscitative techniques or that LUCAS is not inferior to manual CPR.

LINCdata

However, unless you see a p-value less than 0.05 in the table above, (issues of multiple hypotheses testing aside) no evidence of anything was demonstrated; not of difference and certainly not of equivalence. When faced with 2-sided p values >5%, investigators often conclude that there is “no difference” between the treatments, leading to an assumption among readers that the treatments are equivalent. A better conclusion is that there is “no evidence” of a difference between treatments (see opinion piece by Sackett, 2004(2)). In order to determine if treatments are equivalent, equivalence must be tested directly.
How can we test for equivalence?
First, we must define equivalence. It is crucial that this definition is provided a priori i.e. defined before the data are examined. As the focus of the LINC study was on superiority the investigators did not offer an a priori definition of equivalence. However, the CIRC study(3), conducted some time earlier and similar in design, did. (This study examined an alternative mechanical CPR device, the Zoll AutoPulse).
When establishing equivalence between treatments, instead of the more customary null hypothesis of no difference between treatments, the hypothesis that the true difference is equal to a specified ‘delta’ (δ) is tested (4).
To analyse the LINC results to look for equivalence, we can derive our delta values from the CIRC study, which as we’ve said did offer an a priori definition of equivalence. For the purpose of illustration, we will use the risk-difference stopping boundaries calculated for the CIRC study, rather than the odds ratio based equivalence margins, on the grounds of greater simplicity and clinical appropriateness. Therefore, we set our equivalence margins at -δ=-1.4% and δ=1.6%, meaning, where LUCAS fared no worse than manual CPR by 1.4% and no better by 1.6%, we will consider the two techniques equally efficacious. Thus, we will declare equivalence between LUCAS and manual CPR if the 2-sided 95% CI for the treatment difference lies entirely within -1.4% and 1.6%, and noninferiority if the one-sided 97.5% CI for the treatment difference (equivalent to the lower limit of the two-sided 95% CI) lies above -1.4%. (5).
These concepts and how they differ from a traditional comparison are more readily appreciated graphically (Fig. 1).
Figure 1. Two one-sided test procedure and the equivalence margin in equivalence/noninferiority testing between LUCAS and manual CPR
1a Traditional comparative study, such as the LINC trial, shows results with confidence intervals that show no evidence of a difference as they encompass 0.

LINCtradcomp

1b. Using equivalence margins (-δ and δ) derived from a similar study (CIRC), we show that the LINC trial does not demonstrate that LUCAS and manual CPR are equally efficacious, since the 95% CI do not lie completely within the equivalence margins.

LINCequiv
1c. The one sided CI lies above -δ for some outcomes, allowing us to declare non-inferiority on those measures.
LINCnoninf

Conclusion
The presentation of the LINC trial’s results shows no evidence of a difference in outcomes between mechanical and manual CPR, which is not the same as showing they are equivalent or that mechanical CPR is non-inferior. However if we re-examine their data using equivalence margins (-δ, δ) derived from a similar study (CIRC), there is some evidence that the LUCAS device is not inferior to manual CPR (but not necessarily equivalent) with respect to longer term good neurological outcome.

References
1. Rubertsson S, Lindgren E, Smekal D, er al. Mechanical Chest Compressions and Simultaneous Defibrillation vs Conventional Cardiopulmonary Resuscitation in Out-of-Hospital Cardiac Arrest
JAMA. 2014 Jan 1;311(1):53-61
2. Sackett D. Superiority trials, non-inferiority trials, and prisoners of the 2-sided null hypothesis
Evid Based Med 2004;9:38-39 [Open Access]
3. Lerner EB, Persse D, Souders CM, et al. Design of the Circulation Improving Resuscitation Care (CIRC) Trial: a new state of the art design for out-of-hospital cardiac arrest research
Resuscitation. 2011 Mar;82(3):294-9
4. Dunnett CW, Gent M. Significance testing to establish equivalence between treatments, with special reference to data in the form of 2X2 tables. Biometrics. 1977 Dec;33(4):593-602
5. Piaggio G, Elbourne DR, Pocock SJ, et al. Reporting of noninferiority and equivalence randomized trials: extension of the CONSORT 2010 statement. JAMA. 2012;308(24):2594-604. [Open Access]

London Trauma Conference Day 2

London Trauma Conference 2013 – Day 2  by Dr Louisa Chan
So I find myself torn today: do I join the the main track with a Major incident theme or the Cardiac Masterclass? I never liked the thought of missing out on anything so I went to a bit of both.
 
Cardiac Masterclass
A lot of people probably think that managing cardiac arrest isn’t challenging and a bit dull because the patient is dead. But the Cardiac Masterclass would inspire you to think of a bright future for cardiac arrest management.
Mark Whitbread reminded us of how important dispatch is in the chain of survival. How much focus do we put on improving bystander CPR rates? Dispatcher assisted CPR has been shown to improve outcomes and needs to be skilfully done.
Ajay Jain pushes for all OHCA patients to be taken to a Cardiac Arrest centre for PCI. Why? Because the results he has from his centre for PCI in OHCA patients results in 77% (101/132) patients surviving to hosp discharge, 65% neurologically intact.
He also tells us that the ECG post arrest is a very poor predictor of PCI findings (although STEMI predicts a positive result) so they all should have PCI.
Lyon-survivors
 
More data from TOPCAT shows us that non survivors of OHCA are easy to cool.
 
LTC-mice
 
 
And maybe we should be cooling DURING cardiac arrest to minimise the reperfusion injury.
 
 
For persistent VF Prof Redwood says revascularisation is the key; when that doesn’t work then reducing LV volume may help so aspiration or an Impella may work. Failing that – ECMO.
 
Major Incidents
Major Incidents by their nature do not happen every day, so experience in these incidents is limited. The challenge then is how can we learn from incidents?
A standardised reporting system for a major incident database would be a good idea – www.majorincidentreporting.org – is where you will find the standard report form and open access database.
And then all I can suggest is that you need to come to the LTC and listen to the accounts of those who have been there. We heard about the Tokyo Sarin attack, Mumbai, and a very compelling story of multiple drownings from Steen Barnung.
Lessons from Tokyo – Sarin attack:

It will happen again
It will be chaos
Crowds cannot be controlled
Comms will fail
Clinical diagnosis – need a senior clinician
Treatment must be immediately available – 3min to absorb sarin
Decontamination – get naked, 90% decon with clothes removal.
Stream casualties
Empower the man on the ground.

 
Gadgets
LTC-MSUThe great thing about the London Trauma Conference is that it’s not just about the content of the tracks, there’s the networking and the opportunity to see new pieces of equipment.
The Norwegians won on the equipment front with their Mobile Stroke Unit. It’s due to go on line in 2014.
So TTFN and more from me on Day 3 of #LTC2013

London Trauma Conference 2013

FDIA_ImageOur inside reporter Dr Louisa Chan provides an update from Day One of the London Trauma Conference:
At risk of sounding like a resuscisaurus, last year was my first foray into the world of blogging. I’m proud to say that the genetic make up of most emergency physicians allows us to adapt so that others do not die! And so here I am again, making my way into the big smoke to report on the great developments of 2013.
I’ve struggled in the past to prise myself away from the main trauma track, it is after all the London Trauma Conference, which has left me curious as to the content of the Cardiac arrest symposium, this year it has been integrated, so I finally get to scratch that itch.
 
Prehospital Cardiac Arrest Management in Scotland
The conference was kicked off by Richard Lyon‘s inspirational description of his TOPCAT study.
In Scotland, of 50 cardiac arrests, 6 will survive to hospital and only 1 will survive to hospital discharge. The survival to hospital discharge in the UK is getting worse (4.8% 1995- 0.7% 2007)
Spurred on by these dreadful figures and a personal quest to improve cardiac arrest care (his father succumbed to a cardiac arrest in his forties)
All in all he has studied 400 cardiac arrest patients pre hospital. So what has he learnt?

  • Precise application of the chain of survival to your own system is vital in the delivery of Quality CPR.
  • He started in the ambulance control room analysing calls (CPR starts at step 11 so more experienced dispatchers skip thee quicker) and worked his way through the chain of survival.
  • The TOPCAT study revealed a 3 min delay to compressions where early intubation and cannulation were performed. Through an education program delivering knowledge and skills with individualised feedback they were able to increase on-chest time.
  • LEADERSHIP was a big factor. Having a clinician dedicated to managing the team improved on chest time and is now delivered by paramedics manning a car response in Edinburgh.
  • Breaks in CPR during movement are overcome by a mechanical chest compression device on carry sheet.
  • Non technical skills are monitored by camera feed
  • These changes have led to a survival to hospital discharge rate of 38% for patients in VF
  • This could translate into an extra 300 lives saved in Scotland when these changes are rolled out nationally.
  • And now there is a move to transport patients who are in VF after the third shock then straight to cath lab.

 
Echocardiography in cardiac arrest
Prof Tim Harris spoke about his passion – echocardiography in resuscitation. If you were in any doubt before then you would leave convinced.
Of course echo should not interfere with CPR so it should be done during the rhythm check with a 10 sec count down.
He covered the usual uses; PEA vs EMD in prognostication (92% sensitivity and 82% specificity to ROSC), Circulation assessment and an estimation of EF (Normal function – anterior mitral valve leaflet hits the septum or is within 5mm , EF 30-45% between 5mm- 18mm and >18mm ant mitral valve leaflets – 30% EF)
 
Cardiogenic shock after cardiac arrest
Professor Deakin: optimising cardiac function after ROSC revolves around the three elements of preload, SVR and myocardial contractility. For those who can still remember how, he recommends preload should be optimised to a LA pressure 15-20mmHg (2-12 normal) with a Swan Ganz catheter.
SVR and contractility can be manipulated thereafter using traditional vasopressors and inotropes or more novel agents like Levosimendan.
Mechanical devices such as IABP, Impella, TandemSupport are useful if available.
Where does the future lie? Perhaps synchronised pacing, hypothermia, extrathoracic ventilation and gene therapy.
LTC-BrohiOpen chest cardiac massage
Prof Karim Brohi: external chest compressions have been around since the 1960′s. Without a doubt external compressions generate a cardiac output, but is this the best way?
Over the last 10 years the priorities in traumatic cardiac arrest have changed – chest compressions are not instituted until after reversible causes have been addressed.
In non traumatic arrest how could we improve?
In canine models coronary perfusion pressure is five times better with internal cardiac massage, providing better survival rates with intact neurology.
There are a few human studies showing marked differences in cardiac index: 1.31 in the open group vs 0.61 in the closed group. In a Japanese study (1993), ROSC was achieved in 58% in open vs 1% closed.
The technique is two handed and the same as that taught in thoracotomy training. The difference is that in medical cardiac arrest you can use a smaller incision ( left lateral).
Who should we use open cardiac massage on? Perhaps in tamponade and pulmonary embolism?
How about when? When 10-15min with “standard care” has failed?
Perhaps it is time for a trial?
Post cardiac arrest syndrome and neuro protective measures
Prof Simon Redwood and Matt Thomas had overlapping talks on this . The bottom line is don’t have too much or too little CO2 or O2. The therapeutic hypothermia debate continues, what is evident is that there should be temperature control to avoid hyperthermia but what temperature? And there may be other benefits to hypothermia eg. limitation of infarct size.
What has been evident from all the speakers today is that it is an integrated system that saves lives and in order to guide the development of your system you need data and the belief that you can improve cardiac arrest outcomes.
More from me tomorrow!
Louisa Chan

Therapeutic hypothermia does not improve arrest outcome

A paper published today represents to me what’s great about science.
I am impressed with those investigators who had the wherewithall to subject previous therapeutic hypothermia studies to skeptical scrutiny and then design and conduct a robust multicentre trial to answer the question.
One of the criticisms of the original two studies was that those patients who were not actively cooled did not have their temperature tightly controlled, and therefore some were allowed to become hypERthermic, which is bad for brains.
This latest study showed no difference in survival or neurological outcome after cardiac arrest between target temperatures of 33°C and 36°C.
So controlling the temperature after cardiac arrest is still important, but cooling down to the recommended range of 32-4°C is not.
Cool.
Read the full study at the NEJM site.

Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest

NEJM November 17, 2013 Full text
[EXPAND Abstract]


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.

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Prehospital ECLS – it's happening

Patients with refractory (>30 mins) cardiac arrest underwent prehospital cannulation for extracorporeal life support in a French feasibility study. A physician-paramedic team responded by car in Paris to cardiac arrest cases that met inclusion criteria. Mechanical CPR devices (Autopulse or LUCAS) were applied during cannulation. Femoral venoarterial ECMO was instituted using a Maquet Cardiohelp system. Blood products and inotropes, echocardiography, and hypothermia were included in the prehospital management package.
Seven patients were treated, with a mean age of 42 (+/- SD of 16, no median given). ECLS was started an average 57 min (±21) after the onset of ACLS. One patient survived to discharge neurologically intact. Two brain dead patients became organ donors. The survivor had hypertrophic cardiomyopathy with refractory ventricular fibrillation.
Safety and feasibility of prehospital extra corporeal life support implementation by non-surgeons for out-of-hospital refractory cardiac arrest
Resuscitation. 2013 Nov;84(11):1525-9
[EXPAND Abstract]


BACKGROUND: Extra corporeal life support (ECLS) has been recently introduced in the treatment of refractory cardiac arrest (CA). Several studies have assessed the use of ECLS in refractory CA once the patients reach hospital. The time between CA and the implementation of ECLS is a major prognostic factor for survival. The main predictive factor for survival is ECLS access time. Pre hospital ECLS implementation could reduce access time. We therefore decided to assess the feasibility and safety of prehospital ECLS implementation (PH-ECLS) in a pilot study.

METHODS AND RESULTS: From January 2011 to January 2012, PH-ECLS implementation for refractory CA was performed in 7 patients by a PH-ECLS team including emergency and/or intensivist physicians and paramedics. Patients were included prospectively and consecutively if the following criteria were met: they had a witnessed CA; CPR was initiated within the first 5min of CA and/or there were signs of life during CPR; an PH-ECLS team was available and absence of severe comorbidities. ECLS flow was established in all patients. ECLS was started 22min (±6) after the incision, and 57min (±21) after the onset of advanced cardiovascular life support (ACLS). In one patient, ECLS was stopped for 10min due to an accidental decannulation. One patient survived without sequelae. Three patients developed brain death.

CONCLUSIONS: This pilot study suggests that PH-ECLS performed by non-surgeons is safe and feasible. Further studies are needed to confirm the time saved by this strategy and its potential effect on survival.

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Xenon – no bull?

Xenon, an inert ‘noble’ gas with proven anaesthetic properties, has possible neuroprotective properties and appears to be also cardioprotective in this small study of post-cardiac arrest patients. Its high viscosity affects airway resistance, resulting in higher peak pressures and the need for a strategy to avoid gas trapping (ie. longer expiratory times as with asthma). Apparently it’s expensive, but these results suggest further study is warranted.
Feasibility and Cardiac Safety of Inhaled Xenon in Combination With Therapeutic Hypothermia Following Out-of-Hospital Cardiac Arrest
Crit Care Med. 2013 Sep;41(9):2116-24
[EXPAND Abstract]


OBJECTIVES: Preclinical studies reveal the neuroprotective properties of xenon, especially when combined with hypothermia. The purpose of this study was to investigate the feasibility and cardiac safety of inhaled xenon treatment combined with therapeutic hypothermia in out-of-hospital cardiac arrest patients.

DESIGN: An open controlled and randomized single-centre clinical drug trial (clinicaltrials.gov NCT00879892).

SETTING: A multipurpose ICU in university hospital.

PATIENTS: Thirty-six adult out-of-hospital cardiac arrest patients (18-80 years old) with ventricular fibrillation or pulseless ventricular tachycardia as initial cardiac rhythm.

INTERVENTIONS: Patients were randomly assigned to receive either mild therapeutic hypothermia treatment with target temperature of 33°C (mild therapeutic hypothermia group, n = 18) alone or in combination with xenon by inhalation, to achieve a target concentration of at least 40% (Xenon + mild therapeutic hypothermia group, n = 18) for 24 hours. Thirty-three patients were evaluable (mild therapeutic hypothermia group, n = 17; Xenon + mild therapeutic hypothermia group, n = 16).

MEASUREMENTS AND MAIN RESULTS: Patients were treated and monitored according to the Utstein protocol. The release of troponin-T was determined at arrival to hospital and at 24, 48, and 72 hours after out-of-hospital cardiac arrest. The median end-tidal xenon concentration was 47% and duration of the xenon inhalation was 25.5 hours. The frequency of serious adverse events, including inhospital mortality, status epilepticus, and acute kidney injury, was similar in both groups and there were no unexpected serious adverse reactions to xenon during hospital stay. In addition, xenon did not induce significant conduction, repolarization, or rhythm abnormalities. Median dose of norepinephrine during hypothermia was lower in xenon-treated patients (mild therapeutic hypothermia group = 5.30 mg vs Xenon + mild therapeutic hypothermia group = 2.95 mg, p = 0.06). Heart rate was significantly lower in Xenon + mild therapeutic hypothermia patients during hypothermia (p = 0.04). Postarrival incremental change in troponin-T at 72 hours was significantly less in the Xenon + mild therapeutic hypothermia group (p = 0.04).

CONCLUSIONS: Xenon treatment in combination with hypothermia is feasible and has favorable cardiac features in survivors of out-of-hospital cardiac arrest.

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Family presence during resuscitation

CPR-iconFamilies allowed to be present during attempted cardiopulmonary resuscitation had improved psychological outcomes at ninety days.
Adult family members of adult patients were studied in this randomized study from France.
Resuscitation team member stress levels and effectiveness of resuscitation did not appear to be affected by family presence.
Family Presence during Cardiopulmonary Resuscitation
N Engl J Med. 2013 Mar 14;368(11):1008-18
[EXPAND Abstract]


BACKGROUND: The effect of family presence during cardiopulmonary resuscitation (CPR) on the family members themselves and the medical team remains controversial.

METHODS: We enrolled 570 relatives of patients who were in cardiac arrest and were given CPR by 15 prehospital emergency medical service units. The units were randomly assigned either to systematically offer the family member the opportunity to observe CPR (intervention group) or to follow standard practice regarding family presence (control group). The primary end point was the proportion of relatives with post-traumatic stress disorder (PTSD)-related symptoms on day 90. Secondary end points included the presence of anxiety and depression symptoms and the effect of family presence on medical efforts at resuscitation, the well-being of the health care team, and the occurrence of medicolegal claims.

RESULTS: In the intervention group, 211 of 266 relatives (79%) witnessed CPR, as compared with 131 of 304 relatives (43%) in the control group. In the intention-to-treat analysis, the frequency of PTSD-related symptoms was significantly higher in the control group than in the intervention group (adjusted odds ratio, 1.7; 95% confidence interval [CI], 1.2 to 2.5; P=0.004) and among family members who did not witness CPR than among those who did (adjusted odds ratio, 1.6; 95% CI, 1.1 to 2.5; P=0.02). Relatives who did not witness CPR had symptoms of anxiety and depression more frequently than those who did witness CPR. Family-witnessed CPR did not affect resuscitation characteristics, patient survival, or the level of emotional stress in the medical team and did not result in medicolegal claims.

CONCLUSIONS: Family presence during CPR was associated with positive results on psychological variables and did not interfere with medical efforts, increase stress in the health care team, or result in medicolegal conflicts.

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Traumatic cardiac arrest outcomes

simEver heard anyone spout dogma along the lines of: “it’s a traumatic cardiac arrest – resuscitation is futile as the outcome is hopeless: survival is close to zero per cent”?
I have. Less frequently in recent years, I’ll admit, but you still hear it spout forth from the anus of some muppet in the trauma team. Here’s some recent data to add to the existing literature that challenges the ‘zero per cent survival’ proponents. A Spanish study retrospectively analysed 167 traumatic cardiac arrests (TCAs). 6.6% achieved a complete neurological recovery (CNR), which increased to 9.4% if the first ambulance to arrive contained an advanced team including a physician. Rhythm and age were important: CNR was achieved in 36.4% of VFs, 7% of PEAs, and 2.7% of those in asystole; survival rate by age groups was 23.1% in children, 5.7% in adults, and 3.7% in the elderly.
Since traumatic arrest tends to affect a younger age group than medical arrests, the authors suggest:
Avoiding the potential decrease in life expectancy in this kind of patient justifies using medical resources to their utmost potential to achieve their survival
Since 2.7% of the asystolic patients achieved a CNR, the authors challenge the practice proposed by some authors that Advanced Life Support be withheld in TCA patients with asystole as the initial rhythm:
had that indication been followed, three of our patients who survived neurologically intact would have been declared dead on-scene.”
I’d like to know what interventions were making the difference in these patients. They describe what’s on offer as:


In our EMS, all TCA patients receive ALS on-scene, which includes intubation, intravenous access, fluid and drug therapy, point-of-care blood analysis, and procedures such as chest drain insertion, pericardiocentesis, or Focused Assessment with Sonography for Trauma ultrasonography to improve the treatment of the cause of the TCA.

It appears that crystalloids and colloids are their fluid therapy of choice; unlike many British and Australian physician-based prehospital services they made no mention of the administration of prehospital blood products.
Traumatic cardiac arrest: Should advanced life support be initiated?
J Trauma Acute Care Surg. 2013 Feb;74(2):634-8
[EXPAND Abstract]


BACKGROUND: Several studies recommend not initiating advanced life support in traumatic cardiac arrest (TCA), mainly owing to the poor prognosis in several series that have been published. This study aimed to analyze the survival of the TCA in our series and to determine which factors are more frequently associated with recovery of spontaneous circulation (ROSC) and complete neurologic recovery (CNR).

METHODS: This is a cohort study (2006-2009) of treatment benefits.

RESULTS: A total of 167 TCAs were analyzed. ROSC was obtained in 49.1%, and 6.6% achieved a CNR. Survival rate by age groups was 23.1% in children, 5.7% in adults, and 3.7% in the elderly (p < 0.05). There was no significant difference in ROSC according to which type of ambulance arrived first, but if the advanced ambulance first, 9.41% achieved a CNR, whereas only 3.7% if the basic ambulance first. We found significant differences between the response time and survival with a CNR (response time was 6.9 minutes for those who achieved a CNR and 9.2 minutes for those who died). Of the patients, 67.5% were in asystole, 25.9% in pulseless electrical activity (PEA), and 6.6% in VF. ROSC was achieved in 90.9% of VFs, 60.5% of PEAs, and 40.2% of those in asystole (p < 0.05), and CNR was achieved in 36.4% of VFs, 7% of PEAs, and 2.7% of those in asystole (p < 0.05). The mean (SD) quantity of fluid replacement was greater in ROSC (1,188.8 [786.7] mL of crystalloids and 487.7 [688.9] mL of colloids) than in those without ROSC (890.4 [622.4] mL of crystalloids and 184.2 [359.3] mL of colloids) (p < 0.05).

CONCLUSION: In our series, 6.6% of the patients survived with a CNR. Our data allow us to state beyond any doubt that advanced life support should be initiated in TCA patients regardless of the initial rhythm, especially in children and those with VF or PEA as the initial rhythm and that a rapid response time and aggressive fluid replacement are the keys to the survival of these patients.

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