Category Archives: Resus

Life-saving medicine

Acute Med, All Updates, ICU, PHARM, Resus

The 'Magic Eye®' method of rhythm assessment

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Are you someone who tries to determine whether an ECG trace is ‘irregularly irregular’ by drawing little dots on a piece of paper level with the R waves to see if they are evenly spaced? I’d done that for years until I read this fantastic suggestion, which I’ve been following for over a year now.
In the 1990s there was a popular series of posters and books called ‘Magic Eye‘. These contained a ‘random dot autostereogram‘ which appeared as a mish-mash of coloured dots, but when you stared at it for a while the illusion of a 3D image would emerge. They looked a bit like this (although this one won’t work at such reduced resolution):

Image Credit: Wikimedia Commons
Image Credit: Wikimedia Commons

Dr Broughton and colleagues from Cambridge, UK, discovered that this technique, which involves forcing a divergent gaze to get repeating patterns to appear to overlap, can be applied to an ECG trace.
Stereoviewing an ECG trace causes successive QRS complexes to visually overlap and produce a new image. As Broughton and colleagues point out:
“When achieved, this will lead to one of three outcomes. Entirely regular rhythms will ‘click’ into place as a new image at fixed depth. Rhythms with only mild irregularity may be stereoviewable, and if so, will appear to show successive QRS complexes at subtly varying depths. Rhythms with marked irregularity will not be stereoviewable, instead (in our experience) merely giving the viewer sore eyes after several failed viewing attempts.”
The authors assert that this can be applied to continuous ECG monitors, although unless you are really good at stereoviewing while moving your head/eyes horizontally, you should really freeze the trace on the screen first.
The ‘Magic Eye®’ method of rhythm assessment
Anaesthesia. 2012 Oct;67(10):1170-1

Acute Med, All Updates, PHARM, Resus

Not finding a difference doesn't prove equivalence

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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]

Acute Med, All Updates, ICU, Resus, Ultrasound

Does RV enlargement on echo predict PE?

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A nice paper from Annals of Emergency Medicine showing the test characteristcs of some of the common signs we look for on basic 2D echo that suggest the presence of (sub)massive pulmonary embolism:
Right Ventricular Dilatation on Bedside Echocardiography Performed by Emergency Physicians Aids in the Diagnosis of Pulmonary Embolism
Ann Emerg Med. 2014 Jan;63(1):16-24
[EXPAND Abstract]


STUDY OBJECTIVE: The objective of this study was to determine the diagnostic performance of right ventricular dilatation identified by emergency physicians on bedside echocardiography in patients with a suspected or confirmed pulmonary embolism. The secondary objective included an exploratory analysis of the predictive value of a subgroup of findings associated with advanced right ventricular dysfunction (right ventricular hypokinesis, paradoxical septal motion, McConnell’s sign).

METHODS: This was a prospective observational study using a convenience sample of patients with suspected (moderate to high pretest probability) or confirmed pulmonary embolism. Participants had bedside echocardiography evaluating for right ventricular dilatation (defined as right ventricular to left ventricular ratio greater than 1:1) and right ventricular dysfunction (right ventricular hypokinesis, paradoxical septal motion, or McConnell’s sign). The patient’s medical records were reviewed for the final reading on all imaging, disposition, hospital length of stay, 30-day inhospital mortality, and discharge diagnosis.

RESULTS: Thirty of 146 patients had a pulmonary embolism. Right ventricular dilatation on echocardiography had a sensitivity of 50% (95% confidence interval [CI] 32% to 68%), a specificity of 98% (95% CI 95% to 100%), a positive predictive value of 88% (95% CI 66% to 100%), and a negative predictive value of 88% (95% CI 83% to 94%). Positive and negative likelihood ratios were determined to be 29 (95% CI 6.1% to 64%) and 0.51 (95% CI 0.4% to 0.7%), respectively. Ten of 11 patients with right ventricular hypokinesis had a pulmonary embolism. All 6 patients with McConnell’s sign and all 8 patients with paradoxical septal motion had a diagnosis of pulmonary embolism. There was a 96% observed agreement between coinvestigators and principal investigator interpretation of images obtained and recorded.

CONCLUSION: Right ventricular dilatation and right ventricular dysfunction identified on emergency physician performed echocardiography were found to be highly specific for pulmonary embolism but had poor sensitivity. Bedside echocardiography is a useful tool that can be incorporated into the algorithm of patients with a moderate to high pretest probability of pulmonary embolism.

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Acute Med, All Updates, ICU, Resus

Sepsis research – let's get some answers

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There’s so much debate on which components of Early Goal Directed Therapy in sepsis really make a difference. The good news is that three randomised controlled trials in the UK, Australasia, and North America, aim to answer the question, and the study design from the outset has been a collaboration that will allow the results to be pooled.
ProMISe is taking place in the UK, ProCESS in the US, and ARISE in Australasia.

sepsistrialssm

The Australasian study (ARISE) and is nearing completion. If you can recruit patients then please do. Listen to a podcast on this fantastic study with lead investigator Dr Anthony Delaney.

All Updates, ICU, PHARM, Resus, Trauma

London Trauma Conference Day 4

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London Trauma Conference Day 4 by Dr Louisa Chan
It’s the last day of the conference and new this year is the Neurotrauma Masterclass running in parallel with the main track which focuses on in-hospital care.
We heard a little from Mark Wilson yesterday. He believes we are missing a pre-hospital trick in traumatic brain injury. Early intervention is the key (he has data showing aggressive intervention for extradural haemorrhage in patients with fixed dilated pupils has good outcomes in 75%).
Today he taught us neurosurgery over lunch. If you have a spare moment over then go to his website and you too can learn how to be a brain surgeon!
Dr Gareth Davies talks about Impact Brain Apnoea. Many will not heard of this phenomenon. Clinicians rarely see patients early enough in their injury timeline to witness
Essentially this term describes the cessation of breathing after head injury. It has been described in older texts (first mentioned in 1894!) The period of apnoea increases with the severity of the injury and if non fatal will then recover to normal over a period of time. Prolonged apnoea results in hypotension.
This is a brain stem mediated effect with no structural injury.
The effect is exacerbated by alcohol and ameliorated by ventilatory support during the apnoeic phase.
Associated with this response is a catecholamine surge which exacerbates the cardiovascular collapse and he introduces the concept of Central Shock.
So how does this translate into the real world?
Well, could we be miscategorising patients that die before they reach hospital as succumbing to hypovolaemic when in fact they had central shock?
These patients essentially present with respiratory arrest, but do well with supported ventilation. Identification of these patients by emergency dispatchers with airway support could mean the difference between life and death.
Read more about this at: http://www.sciencedirect.com/science/article/pii/S0025619611642547
Prof Monty Mythen spoke on fluid management in the trauma patient after blood (not albumin, HES or colloids) and Prof Mervyn Singer explained the genetic contribution to the development of MODS after trauma.
LTC-BrohiProf Brohi gave us the lowdown on trauma laparotomies – not all are the same! With important human factors advice:
1. Task focus kills
2. Situational awareness saves lives
3. The best communication is non verbal
4. Train yourself to listen
Prof Susan Brundage is a US trauma surgeon who has been recruited into the Bart’s and the London School of Medicine and the Royal College of Surgeons of England International Masters in Trauma Sciences for her trauma expertise.
She tells us that MOOCs and FOAM are changing education. Whilst education communities are being formed, she warns of the potential pitfalls of this form of education with a proportion of participants not fully engaged.
The Masters program is growing and if you’re interested you can read more here.
This has been a full on conference, with great learning points.
Hopefully see you next year!

Acute Med, All Updates, ICU, PHARM, Resus, Trauma

London Trauma Conference Day 3

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Dr Louisa Chan reports on Day 3 of the London Trauma Conference
There was a jam-packed line up for the Pre-hospital and Air Ambulance Day which was Co-hosted by the Norwegian Air Ambulance Foundation.
 

My highlights were:

HEMS

Dr Rasmus Hesselfeldt works in Denmark where they have a pretty good EMS system with ambulances, RRV’s and PHC doctors. Road conditions are good with the longest travel distance of 114 miles. So would the introduction of a HEMS service improve outcomes? He did an observational study looking at year of data post-trial and compared this with 5 months pre-trial. Trauma patients with ISS > 15 and medical emergencies greater than 30 min by road to the Trauma Centre (TC). Primary endpoint was time to TC, secondary outcomes were number of secondary transfers and 30 day mortality.
Results: Increase in on scene time 20 min vs 28 min, time to hospital increased but time to TC was less – 218 min vs 90 min, reduced mortality, increased direct transfer to TC and fewer secondary transfers.
Full article here: A helicopter emergency medical service may allow faster access to highly specialised care. Dan Med J. 2013 Jul;60(7):A4647
 
Airway
Prof Dan Davis ran through pre-hospital intubation. It seems that this man has spent his life trying to perfect airway management. Peter Rosen was his mentor and imprinted on him that RSI is the cornerstone of airway management.
So surely pre-hospital intubation saves lives. The evidence however begs to differ, or does it? As with all evidence we need to consider the validity of the results and luckily Prof Davis has spent a lot of time thinking through the reasons why there no evidence.
During his research he opened a huge can of worms:
1. Hyperventilation was common – any EtCO2 <30mmHg lead to a doubling in mortality.
2. First pass intubation is great, but not if you let your patient become hypoxic or hypotension or worse still both!
3. Hospital practice had similar issues.
So really the RSI processes he was looking at weren’t great.
The good news is that things have improved and he can now boast higher first pass rates and lower complication rates for his EMS system. His puts this success down to training.
 
 
AIRPORT-LTCThe AIRPORT study was discussed at last years LTC. This year we have the results. 21 HEMS services in 6 countries were involved in the data collection including GSA HEMS. The headline findings are that intubation success rates are high (98%) with a complication rate of 10-12%. The more difficult airways were seen in the non-trauma group. 28.2% patients died (mainly cardiac arrest).
 
 
Matt Thomas reported on REVIVE – a pre-hospital feasibility study looking at airway management in OHCA (I-Gel vs LMA Supreme vs standard care). It was never powered to show a difference in these groups, the main aim was to see if research in this very challenging area was possible. And the answer is YES. The paramedics involved recruited more patients than expected and stuck to the protocol (prob better that docs would have!). A randomised controlled trial to look at the I-Gel vs ETT is planned.
 
(P)REBOA
ReboaLTCFinally, Pre-hospital Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) seems eminently possible – Dr Nils Petter Oveland showed us the training manikin they developed for training. Through training on this manikin they achieved an average skin to balloon time of 3.3mins. Animal data supports this procedure as a bridge to definitive care in non compressible haemorrhage.
London HEMS will be starting (P)REBOA in the New Year.
So now it’s stand up science, I’m off for my glass of wine…………….
Check out what they’re saying about the London Trauma Conference on Twitter

Acute Med, All Updates, ICU, PHARM, Resus, Trauma

London Trauma Conference Day 2

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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

Acute Med, All Updates, ICU, PHARM, Resus, Trauma

London Trauma Conference 2013

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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

Acute Med, All Updates, Guidelines, ICU, PHARM, Resus

Therapeutic hypothermia does not improve arrest outcome

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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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Acute Med, All Updates, ICU, Resus

Double balloon pump fail

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IABPicon
Two recent trials question the ongoing use of intra-aortic balloon pumps: in patients with acute myocardial infarction with cardiogenic shock undergoing revascularisation(1), and patients with poor left ventricular function undergoing coronary artery bypass surgery(2).
Editorialists Krischan D Sjauw and Jan J Piek from the Netherlands make the following commentary(3) in reference to one of the studies:
Although the results of IABP-SHOCK II question the usefulness of IABP therapy in cardiogenic shock, there still might be an indication for initial stabilisation of severely compromised patients, especially in centres without facilities for early revascularisation, as an adjunct to thrombolytic therapy, or to allow transport to specialised tertiary centres.
So retrieval specialists like me may still be up in the night transferring patients with balloon pumps, but these studies suggest this should be restricted to those with cardiogenic shock pending corrective therapy (eg. revascularisation for AMI or surgery for acute mitral valvular dysfunction). Unless the ECMO team gets to them first, of course.

1. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial
The Lancet, Volume 382, Issue 9905, Pages 1638 – 1645
[EXPAND Abstract]


BACKGROUND: In current international guidelines the recommendation for intra-aortic balloon pump (IABP) use has been downgraded in cardiogenic shock complicating acute myocardial infarction on the basis of registry data. In the largest randomised trial (IABP-SHOCK II), IABP support did not reduce 30 day mortality compared with control. However, previous trials in cardiogenic shock showed a mortality benefit only at extended follow-up. The present analysis therefore reports 6 and 12 month results.

METHODS: The IABP-SHOCK II trial was a randomised, open-label, multicentre trial. Patients with cardiogenic shock complicating acute myocardial infarction who were undergoing early revascularisation and optimum medical therapy were randomly assigned (1:1) to IABP versus control via a central web-based system. The primary efficacy endpoint was 30 day all-cause mortality, but 6 and 12 month follow-up was done in addition to quality-of-life assessment for all survivors with the Euroqol-5D questionnaire. A masked central committee adjudicated clinical outcomes. Patients and investigators were not masked to treatment allocation. Analysis was by intention to treat. This trial is registered at ClinicalTrials.gov, NCT00491036.

FINDINGS: Between June 16, 2009, and March 3, 2012, 600 patients were assigned to IABP (n=301) or control (n=299). Of 595 patients completing 12 month follow-up, 155 (52%) of 299 patients in the IABP group and 152 (51%) of 296 patients in the control group had died (relative risk [RR] 1·01, 95% CI 0·86-1·18, p=0·91). There were no significant differences in reinfarction (RR 2·60, 95% CI 0·95-7·10, p=0·05), recurrent revascularisation (0·91, 0·58-1·41, p=0·77), or stroke (1·50, 0·25-8·84, p=1·00). For survivors, quality-of-life measures including mobility, self-care, usual activities, pain or discomfort, and anxiety or depression did not differ significantly between study groups.

INTERPRETATION: In patients undergoing early revascularisation for myocardial infarction complicated by cardiogenic shock, IABP did not reduce 12 month all-cause mortality.

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2. A Randomized Controlled Trial of Preoperative Intra-Aortic Balloon Pump in Coronary Patients With Poor Left Ventricular Function Undergoing Coronary Artery Bypass Surgery
Crit Care Med. 2013 Nov;41(11):2476-83
[EXPAND Abstract]


BACKGROUND: Preoperative intra-aortic balloon pump use in high-risk patients undergoing surgical coronary revascularization is still a matter of debate. The objective of this study is to determine whether the preoperative use of an intra-aortic balloon pump improves the outcome after coronary operations in high-risk patients.

DESIGN: Single-center prospective randomized controlled trial.

SETTING: Tertiary cardiac surgery center, research hospital.

PATIENTS: One hundred ten subjects undergoing coronary operations, with a poor left ventricular ejection fraction (< 35%) and no hemodynamic instability.
INTERVENTIONS:
Patients randomized to receive preincision intra-aortic balloon pump or no intervention.

MEASUREMENTS AND MAIN RESULTS: The primary outcome measurement was postoperative major morbidity rate, defined as one of prolonged mechanical ventilation, stroke, acute kidney injury, surgical revision, mediastinitis, and operative mortality. There was no difference in major morbidity rate (40% in intra-aortic balloon pump group and 31% in control group; odds ratio, 1.49 [95% CI, 0.68-3.33]). No differences were observed for cardiac index before and after the operation; at the arrival in the ICU, patients in the intra-aortic balloon pump group had a significantly (p = 0.01) lower mean systemic arterial pressure (80.1 ± 15.1 mm Hg) versus control group patients (89.2 ± 17.9 mm Hg). Fewer patients in the intra-aortic balloon pump group (24%) than those in the control group (44%) required dopamine infusion (p = 0.043).

CONCLUSIONS: This study demonstrates that in patients undergoing nonemergent coronary operations, with a stable hemodynamic profile and a left ventricular ejection fraction less than 35%, the preincision insertion of intra-aortic balloon pump does not result in a better outcome. Given the possible complications of intra-aortic balloon pump insertion, and the additional cost of the procedure, this approach is not justified.

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3. Is the intra-aortic balloon pump leaking?
Lancet 2013;382:1616-7