Category Archives: Acute Med

Acute care of the medically sick adult

Acute Med, All Updates, ICU, PHARM, Resus

Esmolol for refractory VF

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Already well publicised on social media, the team at Hennepin County published a retrospective comparison between patients with refractory VF who received esmolol with those who did not(1). The results are impressive and I look forward to further studies on this.
I work in an ED in a hospital with no cath lab and no access to extracorporeal life support, limiting our options for patients who remain in shockable rhythms despite ACLS interventions. We now have esmolol available in our resus room. You might want to keep it in your list of options for ACLS-refractory VF, which might also include double sequential external defibrillation(2) and even stellate ganglion block.
The dose of esmolol used was: loading dose 500 mcg/kg, followed by infusions of 0, 50, or 100 mcg/kg/min
An important point to note in the esmolol study is that almost all patients received high-quality mechanical CPR with the combined use of an impedence threshold device to augment venous return and cardiac output. The authors “speculate that this additional hemodynamic support may be essential given the hypotensive effects of esmolol.”
1. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation
Resuscitation. 2014 Oct;85(10):1337-41
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INTRODUCTION: We compare the outcomes for patients who received esmolol to those who did not receive esmolol during refractory ventricular fibrillation (RVF) in the emergency department (ED).

METHODS: A retrospective investigation in an urban academic ED of patients between January 2011 and January 2014 of patients with out-of-hospital or ED cardiac arrest (CA) with an initial rhythm of ventricular fibrillation (VF) or ventricular tachycardia (VT) who received at least three defibrillation attempts, 300mg of amiodarone, and 3mg of adrenaline, and who remained in CA upon ED arrival. Patients who received esmolol during CA were compared to those who did not.

RESULTS: 90 patients had CA with an initial rhythm of VF or VT; 65 patients were excluded, leaving 25 for analysis. Six patients received esmolol during cardiac arrest, and nineteen did not. All patients had ventricular dysrhythmias refractory to many defibrillation attempts, including defibrillation after administration of standard ACLS medications. Most received high doses of adrenaline, amiodarone, and sodium bicarbonate. Comparing the patients that received esmolol to those that did not: 67% and 42% had temporary return of spontaneous circulation (ROSC); 67% and 32% had sustained ROSC; 66% and 32% survived to intensive care unit admission; 50% and 16% survived to hospital discharge; and 50% and 11% survived to discharge with a favorable neurologic outcome, respectively.

CONCLUSION: Beta-blockade should be considered in patients with RVF in the ED prior to cessation of resuscitative efforts.

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2. Double Sequential External Defibrillation in Out-of-Hospital Refractory Ventricular Fibrillation: A Report of Ten Cases.
Prehosp Emerg Care. 2015 January-March;19(1):126-130
[EXPAND Abstract]


Background. Ventricular fibrillation (VF) is considered the out-of-hospital cardiac arrest (OOHCA) rhythm with the highest likelihood of neurologically intact survival. Unfortunately, there are occasions when VF does not respond to standard defibrillatory shocks. Current American Heart Association (AHA) guidelines acknowledge that the data are insufficient in determining the optimal pad placement, waveform, or energy level that produce the best conversion rates from OOHCA with VF.

Objective. To describe a technique of double sequential external defibrillation (DSED) for cases of refractory VF (RVF) during OOHCA resuscitation.

Methods. A retrospective case series was performed in an urban/suburban emergency medical services (EMS) system with advanced life support care and a population of 900,000. Included were all adult OOHCAs having RVF during resuscitation efforts by EMS providers. RVF was defined as persistent VF following at least 5 unsuccessful single shocks, epinephrine administration, and a dose of antiarrhythmic medication. Once the patient was in RVF, EMS personnel applied a second set of pads and utilized a second defibrillator for single defibrillation with the new monitor/pad placement. If VF continued, EMS personnel then utilized the original and second monitor/defibrillator charged to maximum energy, and shocks were delivered from both machines simultaneously. Data were collected from electronic dispatch and patient care reports for descriptive analysis.

Results. From 01/07/2008 to 12/31/2010, a total of 10 patients were treated with DSED. The median age was 76.5 (IQR: 65-82), with median resuscitation time of 51minutes (IQR: 45-62). The median number of single shocks was 6.5 (IQR: 6-11), with a median of 2 (IQR: 1-3) DSED shocks delivered. VF broke after DSED in 7 cases (70%). Only 3 patients (30%) had ROSC in the field, and none survived to discharge.

Conclusion. This case series demonstrates that DSED may be a feasible technique as part of an aggressive treatment plan for RVF in the out-of-hospital setting. In this series, RVF was terminated 70% of the time, but no patient survived to discharge. Further research is needed to better understand the characteristics of and treatment strategies for RVF.

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Acute Med, All Updates, Resus

Open cardiac massage in asthmatic arrests?

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This idea was provoked by a colleague some years ago who could not achieve a palpable pulse during CPR of an arrested asthmatic child. He wondered whether the severe hyperinflation was rendering external cardiac compressions ineffective and whether he should have done a (prehospital) thoracotomy.
The literature is not strong. The 2010 AHA Guidelines rightly focus on reducing hyperinflation by disconnecting the tracheal tube from the ventilator circuit, and they mention ECMO for refractory cases, but there is no mention of open chest CPR.
I can only find two papers discussing it, both pretty old. A case series in the British Medical Journal from 1968 describes three patients with asthma who had asystolic arrests but did not achieve femoral pulses with external compressions(1). In two, open cardiac massage was performed resulting in restoration of sinus rhythm and cardiac output, and one appeared to make a neurological recovery.
A case report in 1987 describes a 32 year old man in asystolic cardiac arrest due to asthma(2):

“Ventilation required very high inflation pressures and little air movement was heard within the chest despite the administration of Adrenaline 1 mg and Aminophylline 250mg intravenously, and Adrenaline 1mg via the endotracheal tube. This was followed by an intravenous infusion of 100 ml of 8.4% Sodium Bicarbonate solution. External cardiac massage failed to produce a palpable pulse in the carotid area. The chest was, therefore, opened through a left anterolateral thoracotomy. The lungs appeared hyperinflated, bulky and tense and did not collapse when the pleural cavity was opened. The pericardium was opened and asystole confirmed, following eight to ten compressions of the heart some intrinsic activity commenced, ventilation also became much easier.”

He achieved ROSC and became haemodynamically stable but failed to wake up and treatment was withdrawn some days later.
Neither reports include mention of disconnection strategies to reduce hyperinflation. The lack of neurological recovery is not surprising given the apparent prolonged state of arrest the patients were resuscitated from. However there does appear to be a survivor who may not have made it had standard resuscitation (at the time) been continued.
Does this mean I would open the chest in an arrested asthma patient?
Not straight away, no. I would treat dynamic hyperinflation with tube disconnection and external compressions. I would correct absolute and relative hypovolaemia with crystalloid. I would treat bronchospasm (and possible anaphylaxis) with intravenous adrenaline/epinephrine. And I would exclude pneumothorax, possibly with ultrasound or more likely with bilateral open thoracostomies. If however these measures resulted in no detectable carotid flow with external cardiac compressions, ECMO was not available, and the arrest was not prolonged, I would definitely consider doing internal cardiac massage via thoracotomy.
What about you?
1. Grant IW, Kennedy WP, Malone DN
Deaths from asthma
Br Med J. 1968 May 18;2(5602):429–30
2. Diament RH, Sloan JP
Failed resuscitation in acute severe asthma: a medical indication for emergency thoracotomy?
Arch Emerg Med. 1987 Dec;4(4):233–5

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

London Cardiac Arrest Symposium 2014

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The focus of the entire day is cardiac arrest and this is the second day of the London Cardiac Arrest Symposium.

Professor Niklas Nielsen kicked off with a presentation of his Targeted Temperature Management trial.  It seems that even now there is uncertainty in the interpretation of this latest study. I take heart from the knowledge that Prof Nielsen has changed the practice of his institution to reflect the findings of his study – I have certainly changed my practice. But we need to remain aware that there is more work to be done to answer the multiple questions that remain and the need for further RCTs is recognised.

The management of Cardiac arrest after avalanche is not a clinical scenario that I imagine I’ll ever find myself in. The management is well documented in the ICAR MEDCOM guidelines 2012. Dr Peter Paal reminded us that you’re not dead until you’re rewarmed and dead unless: with asystole, CPR may be terminated (or withheld) if a patient is lethally injured or completely frozen, the airway is blocked and duration of burial >35 min, serum potassium >12 mmol L(-1), risk to the rescuers is unacceptably high or a valid do-not-resuscitate order exists.

The age old question about prognostication after cardiac arrest was tackled by Prof Mauro Oddo. He covered the evidence for clinical examination, SSPE, EEG, and neurone specific enolase. Bottom line, all of these modalities are useful but none are specific enough to be used as a stand alone test so multiple modalities are required.

SAMU is leading the way with prehospital ECMO. They have mastered the art of cannulation (in the Louvre no less!) but there haven’t enough cases to demonstrate a mortality benefit. The commencement of ECMO prehospital reduces low flow time and theoretically should improve outcomes. This is begging for a RCT.

The experience of the Italians with in hospital ECMO shoes a better survival rate for in-hospital rather than out of hospital cardiac arrests, explained Dr Tomasso Mauri. They treat patients with a no flow time of <6min and low flow rate of <45min and had a 31% ICU survival rate. If you want to learn more about ED ECMO go to http://edecmo.org.

VA-ECMO

The Douglas Chamberlain lecture this year was Selective aortic arch perfusion presented by Prof James Manning. He spoke about the use of this technique in cardiac arrest and also in trauma (where it is known to you as Zone 1 REBOA).

image-1

In cardiac arrest the aim is to improve coronary perfusion, to preserve perfusion to the heart and the brain, offer a route of rapid temperature control and offer a direct route of administration of adrenaline. Coronary perfusion is seen to be supra normal after SAAP. And the suggested place for SAAP is prior to ECMO.

image-5

It’s more familiar ground talking about SAAP in trauma. This Zone 1 occlusion preserves cerebral and cardiac perfusion while blood loss is limited and rapid fluid resuscitation can occur.

image-3

You can hear Prof Manning on SAAP over at EMCrit (of course!). 

It’s been another great conference. Put the dates for next year’s London Trauma & Cardiac Arrest Conferences in your diary: 8th-10th December 2015!

Happy Holidays & Keep Well

Louisa Chan

 

 

 

 

 

Acute Med, All Updates, ICU, Resus

Left Ventricular Assist Device for Cardiac Arrest?

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LVADguyiconAn interesting case report by Dr Heidlebaugh and colleagues from the Department of Emergency Medicine at the William Beaumont Hospital describes a 72 year old marathon runner who arrested during cardiac catheterisation. It suggests a possible novel alternative to ECMO for cardiac arrest.
The patient became bradycardic then asystolic during catheterisation of his right coronary artery. High quality CPR was initiated and an Impella LV assist device was placed. This restored cardiac output which was followed by episodes of venticular fibrillation and then ROSC. His initial low ejection fraction of 15% recovered after targeted temperature management on ICU to 50% and he fully recovered neurologically.
This patient already had femoral arterial access for introduction of the Impella, since he was in a cath lab. He also had immediate CPR on arresting, and was an abnormally fit 72 year old. It remains to be seen whether this procedure can be applied to other patients in cardiac arrest. The authors state:

“..until ECLS is readily available, poor survival and neurological outcome after cardiac arrest might be avoided in many patients by the use of pLVAD to offload the LV and enhance perfusion. Furthermore, there may be a subset of patients, in whom the support that pLVAD offers is sufficient to optimize hemodynamic parameters and bridge to ROSC, thus reducing the need for ECLS.”

This video by Dr. I-Wen Wang from the Barnes-Jewish Hospital explains how the Impella is inserted and how it works.
 

 
Full Neurologic Recovery and Return of Spontaneous Circulation Following Prolonged Cardiac Arrest Facilitated by Percutaneous Left Ventricular Assist Device
Ther Hypothermia Temp Manag. 2014 Sep 3. [Epub ahead of print]
[EXPAND Abstract]

Sudden cardiac arrest is associated with high early mortality, which is largely related to postcardiac arrest syndrome characterized by an acute but often transient decrease in left ventricular (LV) function. The stunned LV provides poor cardiac output, which compounds the initial global insult from hypoperfusion. If employed early, an LV assist device (LVAD) may improve survival and neurologic outcome; however, traditional methods of augmenting LV function have significant drawbacks, limiting their usefulness in the periarrest period. Full cardiac support with cardiopulmonary bypass is not always readily available but is increasingly being studied as a tool to intensify resuscitation. There have been no controlled trials studying the early use of percutaneous LVADs (pLVADs) in pericardiac arrest patients or intra-arrest as a bridge to return of spontaneous circulation. This article presents a case study and discussion of a patient who arrested while undergoing an elective coronary angioplasty and suffered prolonged cardiopulmonary resuscitation. During resuscitation, treatment included placement of a pLVAD and initiation of therapeutic hypothermia. The patient made a rapid and full recovery.

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Image is of M. Joshua Morris, a happy LVAD recipient (not the patient in the described study) who kindly alerted me to this article. Used with permission.
Acute Med, All Updates, Guidelines, ICU, Resus

ARISE study: EGDT no better than standard care

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periph-vasoactive-iconThe second of three major trials assessing early goal directed therapy (EGDT) in sepsis – the Australasian ARISE Trial – has been published.
ARISE tested the hypothesis that EGDT, as compared with usual care, would decrease 90-day all-cause mortality among patients presenting to the emergency department with early septic shock in diverse health care settings.
There was no difference in all-cause mortality at 90 days between EGDT and standard care, in keeping with the results from ProCESS.
Why are the results so different from Rivers’ original EGDT study? The authors explain:


“although our results differ from those in the original trial, they are consistent with previous studies showing that bias in small, single-center trials may lead to inflated effect sizes”

This cautions us all against making major practice changes based on one single centre study. In critical care we’ve learned this before with subjects like tight glycaemic control and Activated Protein C. However I do believe that the things we know to be of benefit – early recognition, source control, antibiotics, and fluids – are effective in making ‘standard’ care “as good as” EGDT because of heightened awareness of the condition and its treatment, and Rivers’ initial study and the subsequent Surviving Sepsis Campaign Guidelines have played a major role in raising that awareness.
The ARISE study is appraised by Wessex’s The Bottom Line and discussed on the one and only EMCrit podcast.
The ARISE Investigators and the ANZICS Clinical Trials Group.
Goal-Directed Resuscitation for Patients with Early Septic Shock
N Engl J Med. 2014 Oct;:141001063014008.Full Text
[EXPAND Abstract]


Background
Early goal-directed therapy (EGDT) has been endorsed in the guidelines of the Surviving Sepsis Campaign as a key strategy to decrease mortality among patients presenting to the emergency department with septic shock. However, its effectiveness is uncertain.

Methods In this trial conducted at 51 centers (mostly in Australia or New Zealand), we randomly assigned patients presenting to the emergency department with early septic shock to receive either EGDT or usual care. The primary outcome was all-cause mortality within 90 days after randomization.

Results Of the 1600 enrolled patients, 796 were assigned to the EGDT group and 804 to the usual-care group. Primary outcome data were available for more than 99% of the patients. Patients in the EGDT group received a larger mean (±SD) volume of intravenous fluids in the first 6 hours after randomization than did those in the usual-care group (1964±1415 ml vs. 1713±1401 ml) and were more likely to receive vasopressor infusions (66.6% vs. 57.8%), red-cell transfusions (13.6% vs. 7.0%), and dobutamine (15.4% vs. 2.6%) (P<0.001 for all comparisons). At 90 days after randomization, 147 deaths had occurred in the EGDT group and 150 had occurred in the usual-care group, for rates of death of 18.6% and 18.8%, respectively (absolute risk difference with EGDT vs. usual care, -0.3 percentage points; 95% confidence interval, -4.1 to 3.6; P=0.90). There was no significant difference in survival time, in-hospital mortality, duration of organ support, or length of hospital stay.

Conclusions In critically ill patients presenting to the emergency department with early septic shock, EGDT did not reduce all-cause mortality at 90 days.

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

Non-ST-Elevation Acute Coronary Syndromes

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The latest AHA/ACC guidelines on NSTEACS have been published ahead of print in Circulation.
Full text is available, and the Executive Summary is available here
Amsterdam EA, Wenger NK, Brindis RG, Casey DE, Ganiats TG, Holmes DR, et al.
2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.
Circulation. 2014 Sep 23. [Epub ahead of print]

Acute Med, All Updates, ICU, Kids, Resus

Profound hypothermia and no ECMO?

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CPRsnow2sm
Patients in cardiac arrest due to severe hypothermia benefit from extracorporeal rewarming, and it is often recommended that they are treated at centres capable of providing cardiopulmonary bypass or extracorporeal membrane oxygenation (ECMO).
But what if they’re brought to a centre that doesn’t have those facilities?
If you work in such a centre do you have a plan, and are you familiar with what equipment you could use?
One option if you have an ICU is to provide extracorporeal warming using a haemofiltration machine used for renal replacement therapy(1). A double lumen haemofiltration catheter is inserted into a central vein and an ICU nurse can often do the rest, although some variables have to be set by the intensivist, often aided by a standard renal replacement therapy prescription chart. The machines are mobile and can be wheeled into the resus room (I have practiced this set up in resus). It might be worth discussing and practicing this option with your ICU.
Another extracorporeal option is to rig up a rapid infusion device such as a ‘Level 1’ to connect to arterial and venous catheters so that blood from the patient flows through and is warmed by the machine before being returned to the patient(2). Rapid rewarming has been achieved by this method but it requires some modification to the usual set up and so is much less likely to be a realistic option for most teams doing this on very rare occasions.
Less technical options are the traditionally taught warm saline lavage of body cavities such as the thorax and the peritoneal cavity. These can be achieved with readily available catheters and of course should be combined with ventilation with warmed gas and administration of warm intravenous fluid.
Thoracic lavage can be achieved with open thoracotomy or tube thoracostomy. One or two chest tubes can be placed on each side. One technique was described as:


Two 36 French chest tubes were placed in each hemithorax. One tube was placed in the fourth intercostal space in the mid-clavicular line. Another tube was placed into the sixth intercostal space in the mid-axillary line. Sterile saline at 39.0◦C was infused by gravity into each superior chest tube and allowed to drain passively through each inferior tube.(3)

Rapid rewarming at a rate of 6.8◦C per hour was achieved in an arrested hypothermic man using peritoneal lavage. It was done in the operating room with peritoneal lavage (saline 40◦C) with a rapid infusion system (Level 1) through two laparoscopic access sites. It was combined with external forced air rewarming and warm intravenous infusions(4).
Finally some devices manufactured for inducing hypothermia in post-cardiac arrest patients can also be used to rewarm patients, which might be endovascular devices, such as the Cool Line® catheter(5), or external, such as the Arctic Sun® Temperature Management System(6). It’s definitely worth finding out what your critical care services have as far as this equipment goes.
In summary, although the ‘exam answer’ for cardiac arrest due to profound hypothermia is often ECMO/cardiopulmonary bypass, in most centres that’s not an option. It’s helpful to remind ourselves that (1) other extracorporeal rewarming options exist and (2) non-extracorporeal techniques can provide rapid rewarming.
 
1. Spooner K, Hassani A. Extracorporeal rewarming in a severely hypothermic patient using venovenous haemofiltration in the accident and emergency department. J Accid Emerg Med. 2000 Nov;17(6):422–4. Full text
2. Gentilello LM, Cobean RA, Offner PJ, Soderberg RW, Jurkovich GJ. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. The Journal of Trauma: Injury, Infection, and Critical Care. 1992 Mar;32(3):316–25 PubMed
3. Plaisier BR. Thoracic lavage in accidental hypothermia with cardiac arrest — report of a case and review of the literature. Resuscitation. 2005 Jul;66(1):99–104. PubMed
4. Gruber E, Beikircher W, Pizzinini R, Marsoner H, Pörnbacher M, Brugger H, et al. Non-extracorporeal rewarming at a rate of 6.8°C per hour in a deeply hypothermic arrested patient. Resuscitation. 2014 Aug;85(8):e119–20. PubMed
5. Kiridume K, Hifumi T, Kawakita K, Okazaki T, Hamaya H, Shinohara N, et al. Clinical experience with an active intravascular rewarming technique for near-severe hypothermia associated with traumatic injury. Journal of Intensive Care. BioMed Central Ltd; 2014;2(1):11. link to abstract
6. Cocchi MN, Giberson B, Donnino MW. Rapid rewarming of hypothermic patient using arctic sun device. Journal of Intensive Care Medicine. 2012 Mar;27(2):128–30. PubMed

Acute Med, All Updates, PHARM, Resus

Down with "down" time!

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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.