Category Archives: Acute Med

Acute care of the medically sick adult

Analysing Difficult Resuscitation Cases – 2

Towards Excellence in Resuscitation – Analysing Difficult Resuscitation Cases #2

Occasionally we step out of the resuscitation room feeling like a case should have gone better, but it can be hard to put our finger on just where it went wrong. In my last post I discussed the STEPS approach to analysing resuscitation cases: Self, Team, Environment, Patient and System.

Occasionally you can get a case where the STEPS seem to be aligned but things still feel bad. In which the outcome was unsatisfactory because the plan was wrong, or the team wasn’t able to execute the plan. Consider the following case.

1. A patient with a past history of DVT no longer on anticoagulants presents with chest pain and syncope. She is severely hypotensive with a raised jugular venous pressure and a clear chest x-ray. A working diagnosis of pulmomary embolism is made. Discussions ensue regarding empirical fibrinolysis and a respiratory physician is consulted, who over the phone cautions against treating without a CT pulmonary angiogram. The patient is given heparin and transferred to the CT scanner where she arrests. Intravenous rtPA is given during CPR but no return of spontaneous circulation is achieved and she is pronounced dead after 30 minutes of resuscitation.

 

On this occasion the team worked efficiently and communicated well under clear leadership. Everyone knew the plan and shared the mental model. The environment was well controlled and the patient had been swiftly moved to CT within 20 minutes of arrival. Thanks to simulation training the well rehearsed cardiac arrest resuscitation was conducted with precision and the team was able to rapidly access the thrombolytic and knew the correct dose.

By a quick STEPS analysis, this case appears to have gone as well as could be expected. Perhaps there is nothing to learn. Some you win, some you lose, no?

No. Autopsy revealed type A aortic dissection with pericardial tamponade.

The management may have been efficient but it failed to be effective. In other words, things were done right, but the wrong things were done.

This might be an example where STEPS is inadequate, and instead we should evaluate the clinical trajectory. The cognitive bias that led to a lack of consideration of alternative diagnoses might be classifiable under ‘self’ or ‘team’ but I find it more helpful to consider it under a failure of strategy. What is strategy? Strategy in my mind is another word for plan. The plan is based on a particular resuscitation goal, and will consist of the procedures & skills required to action the plan. We can thus break down an attempted clinical trajectory into:

Goal (what are we trying to achieve)
Strategy, or Plan (what’s our plan to get there?)
Tactics, or Actions (what procedures will be required to execute the plan)
And, at more granular level: If we’re failing at the procedural level, the components of procedures, namely Skills & Microskills.

So, as we zoom in from macro to micro in setting the clinical trajectory, we can look at Goals, Plan, Actions, and Skills:

In the above case it appears the following was applied, in terms of Goal-Plan-Actions-Skills:
G – resuscitate hypotensive patient
P – give fibrinolysis for likely PE
A – consult respiratory physician, get CTPA
S – request scan, give heparin, transport to CT

The goal was appropriate, but the plan was ineffective.

The following approach would have been more effective.

G – resuscitate hypotensive patient
P – identify cause of undifferentiated hypotension and initiate treatment in the resus room 
A – thorough bedside assessment in patient too sick to move: history, physical, CXR, ECG, labs, POCUS
S – Basic cardiac ultrasound

By planning to identify and treat the cause of hypotension in the resus room, the more appropriate investigation would have been selected (cardiac ultrasound) and the correct diagnosis is much more likely to have been made.

Let’s look at some other cases:

2. An 88-year-old male presents by ambulance to the ED with dizziness. He is hypotensive, pyrexial, hypoxic and confused. His chest x-ray shows likely bronchopneumonia. He has appropriate initial resuscitation and ICU is consulted. Soon he is intubated and on high dose vasoactive medication with escalating doses despite ongoing hypotension, anuria, and a lactate of 11 mmol/l, increased from 8 on arrival. As he is being wheeled off down the corridor towards ICU his distraught and frail wife arrives. She is taken to the quiet room where she explains that her husband would never want to be ‘on a life support machine’ and asks ‘can’t you just keep him comfortable’?

 

G – the goal – to provide maximally aggressive resuscitation – was not in keeping with the patient’s wishes. If the goal had been to provide care in accordance with his wishes, the plan could have included attempts to ascertain these sooner while providing initial treatment. Upon gaining sufficient information, a new goal can be established: maximising the patient’s comfort and dignity.

3. An obese 30-year-old female presents with syncope. At triage she is pale, tachycardic & hypotensive. Clinical and sonographic assessment, including free intraperitoneal fluid and a positive urine HCG, is suggestive of ruptured ectopic pregnancy. The gynaecologist and anaesthetist ask the ED team to bring the patient straight to the operating room. The ED team spends 20 minutes struggling to obtain intravenous access, eventually placing a 22G intravenous catheter in the patient’s hand and a humeral intraosseous needle. Her shock is considerably worse on arrival in theatre, despite attempts to transfuse O negative blood en route.

 

Goal – get her safely to the operating room
Plan – vascular access, cross match blood, start haemostatic resuscitation, go to OR as soon as possible
Actions – peripheral and/or intraosseous cannulation attempts
Skills – vascular access skills

Here the failure was at the actions and skills level. Better vascular access could have been attained using ultrasound guided peripheral cannulation, or central vascular access, or earlier intraosseous insertion.

4. A 120kg 32-year-old male with a history of deliberate self harm presents on the night shift with coma due to mixed benzodiazepine and venlafaxine overdose. The decision is made to intubate for airway protection. After rapid sequence induction direct laryngoscopy is attempted by the emergency registrar who obtains a grade 4 view. Cricoid pressure is removed resulting in a grade 3 view. The registrar asks for a bougie which she passes and then railroads the tracheal tube over it. The cuff is inflated, capnography is connected, and the self-inflating bag is connected and squeezed while the chest is auscultated. The abdomen distends, the capnograph remains flat, and gastric contents are seen to pass upward through the tube into the self-inflating bag. The tube is immediately removed and bag-mask ventilation is attempted. The oxygen saturation is now 78% and the airway is soiled. The airway is suctioned and repeat attempts to bag-mask ventilate fail. A successful cricothyroidotomy is performed and the patient subsequent has full neurological recovery.

 

Goal – Provide supportive care and minimise complications from overdose
Plan – Airway protection and admit to ICU for monitoring
Actions – Rapid sequence intubation, ICU referral
Skills – Pre-, peri- and post-intubation oxygenation techniques; patient positioning; rapid sequence induction of anaesthesia; direct laryngoscopy; bougie handling techniques; external laryngeal manipulation

In this case the patient was not placed in the ramped position and no nasal cannulae were applied for apnoeic oxygenation. A tube was railroaded over an oesophageal bougie, which arguably should not occur if ‘hold up’ is sought when the bougie is placed. Although the goal, plan and actions were appropriate, the team did not demonstrate adequate skill in this procedure. Likely due to a failure of training, standardised procedures, and checklists (or their application), this could also be identified as a ‘system’ problem in STEPS. It is also possible that the intubator forgot her training under stress – a problem classifiable under ‘self’. Alternatively other members of the team may have had knowledge but didn’t speak up or cross-check their colleague, which would be a ‘team’ issue.

Limitations of this approach

This sort of analysis is retrospective and subjective and at risk of hindsight bias (e.g. distortion due to projection, denial, or selective recall). However, these limitations do not negate the value of the learning exercise, particularly if we are aware of them and strive to minimise their impact (e.g. write down the details of a cases as soon as possible afterward). It at least provides a structure for individuals and teams to begin the conversation about where and how things may have been suboptimal.

Goals may be multiple and may change according to incoming information, and for each goal there may be several viable alternative plans. STEPS and GPAS may overlap, eg. team failures may result in inappropriate goals and strategies, or in failed procedures.

Summary

These models may prove helpful as a means of dissecting a case in a structured way. Put simply, STEPS offers a structure for identifying efficiency improvements (“doing things right”) and GPAS  can help us assess effectiveness (“doing the right things”).  Another way of looking at it is that STEPS provides the components of a resus at any point in time, and GPAS defines the trajectory: where the resus is going and how to get there.

I use this structure to analyse cases in my own clinical practice and in my teaching. I would be interested to hear from others’ experience. Do you find this approach useful in identifying areas for improvement in those cases that you feel should have gone better?

Thanks to Chris Nickson for his comments and improvements to this post

Analysing Difficult Resuscitation Cases

Towards Excellence in Resuscitation – Analysing Difficult Resuscitation Cases #1

A resuscitationist agonises. These words, expressed by Scott Weingart during a podcast we did together, ring true to all of us who strive to improve our practice. Driven by the passionate conviction that we should never lose a salvageable patient through imperfect care, we relive cases and re-run them through our mental simulators to identify areas for improvement.

In the search for actionable items though, we occasionally exit this process empty-handed. Something about a case felt wrong although ostensibly all the clinical interventions may have been appropriate. It is in these cases that it can be helpful to have a structure to aid analysis.

I, along with an international, interdisciplinary faculty of resuscitationists, have previously proposed an easily remembered system for optimising the clinical and non-technical components of resuscitation immediately before and during a patient encounter, dubbed the ‘Zero Point Survey’ (ZPS)(1), so called because first contact with a patient is rarely ‘Time Zero’ for a prehospital mission or hospital resuscitation case; there is invariably time for preparation of oneself, one’s team, and the environment (including equipment) prior to the primary survey and commencement of resuscitation. Following the assessment and management of STEP (self, team, environment & patient), the team should be regularly Updated on patient status and informed of the Priorities

.

But ‘self, team, environment and patient’ isn’t just a useful system for case preparation. It can also be used for case analysis. I have found by discussing many ‘unsatisfactory’ cases over the years with participants in human factors workshops that STEP can help us identify where the issues lie. Accompanying all these factors is another ’S’: the system in which they interplay – the organisational rules, processes, policies, resources and deficiencies that may facilitate or obstruct an effective resuscitation(2).

Using STEPS to analyse cases

The following (genuinely) hypothetical resus cases demonstrate how the application of this framework – Self, Team, Environment, Patient, System – might help identify correctible factors for future resuscitations:

1. Cardiac arrest in the bathroom on the orthopaedic ward – “it was chaos, there were too many people, and the resus trolley wasn’t properly stocked”.

STEPS analysis:
Team – Leader needed to assign roles and allocate tasks
Environment – Crowd control needed, lack of equipment
System – Adequate checks for resus trolley not in place

2. 19-year-old male stabbed in the chest and arrested on arrival in hospital. CPR provided but went from PEA to asystole. Team leader discontinued resus after 20 minutes. Resident: “I thought he needed a resuscitative thoracotomy but no-one was willing to do it. No-one even mentioned it”.

STEPS analysis:
Self – Lacked confidence to speak up, doubted own knowledge or influence
Team – Lack of team situational awareness or knowledge or skill regarding required intervention
System – Insufficient training and preparation for penetrating traumatic cardiac arrest scenario

3. 30-year-old mother with abdominal wound and her 2-year-old daughter with massive open head injury, both due to gunshot wounds, having been shot by husband/father who killed himself on scene. Child arrests in the ED, without ROSC, witnessed by mother before mother is taken to operating theatre.

STEPS analysis:
Patient(s) – tragic case with upsetting circumstances and compounded psychological distress for patient and staff. The best resuscitation team in the world is not going to feel good about this one.

4. 46-year-old previously healthy male with VF arrest achieved ROSC after prehospital defibrillation and brought to the ED of a non-cardiac centre comatose and intubated. Further refractory VF in ED. Received multiple shocks, antiarrhythmics, double sequential external defibrillation. No on-site access to mechanical CPR, cardiac catheterisation, or ECMO. Patient declared dead in ED.

STEPS analysis:
System – Prehospital team gave excellent care but brought the patient to a hospital ill-equipped to manage his ongoing needs, due to lack of ambulance service policy regarding appropriate destination hospital for cardiac arrest cases.

Summary

You can see from the above cases how STEPS may be applied to make some sense of where a resus has gone wrong. Note that I am not recommending this as a way of structuring a team debrief or formal incident investigation – many institutions already have processes for conducting these and various rules and sensitivities have to be accommodated. Rather, this is a format I’ve found helpful in applying during informal discussions that aim to get the nub of where things could or should have gone better.

Occasionally, you can get a case where the STEPS seem to be aligned but things still feel bad – in which the outcome was unsatisfactory because the plan was wrong, or the team wasn’t able to execute the plan. In my next post I’ll discuss another way of analysing cases that can accompany STEPS.

1. Reid C, Brindley P, Hicks CM, Carley S, Richmond C, Lauria MJ, Weingart S.  Zero point survey: a multidisciplinary idea to STEP UP resuscitation effectiveness. Clin Exp Emerg Med. 2018 – In Press

2. Hicks C, Petrosoniak A. The Human Factor. Emergency Medicine Clinics of North America. 2018 Feb;36(1):1–17. 

Understanding Elevated Lactate

I find clinicians are quick to consider sepsis and hypoperfusion/ischaemia as causes of a raised lactate, but slow to include other causes in their differential.

Although an elevated lactate has been shown to be associated with worse outcomes in numerous studies, not all causes of a raised lactate are sinister. It’s therefore important to diagnose the cause both to allow the right treatment and to avoid assuming an inappropriately poor prognosis.

This 12 minute video offers an approach to diagnosing the cause of elevated lactate based on an understanding of lactate physiology using a simple visual aid – a ‘lactate map’ and a memorable acronym.

Reference
1. Reid C, Rees V, Collyer-Merritt H. Non-septic hyperlactataemia in the emergency department. Emerg Med J. 2010 May;27(5):411–2

Spot the WOBBLER in syncope!

Syncope is a common ED presentation. An ECG is a critical investigation in syncope to identify the cause, including rare conditions associated with risk of sudden cardiac death.

So we should be really grateful when we are invited to interpret an ECG while we’re in the middle of six other tasks.

The problem with syncope is that some of the important life-threatening causes have fairly obscure ECG features that might be hard to remember. Some of these disorders and their ECG features are not entirely familiar to the clinicians who first screen the ECG.

When you’re busy and cognitively stretched you can save time and reduce the risk of missing important findings by having a structured, memorable checklist. I use the acronym WOBBLER, because I don’t want these people to wobble and kiss the dirt again.

The nice thing about WOBBLER is that it uses the sequence that you follow when you look at an ECG, ie from left to right, or from P wave to T wave.

The key is that this is for ECGs without obvious ischaemia or dysrhythmia. If you see something like this (STEMI):

or this (VT):

you don’t need WOBBLER, you need to be treating that patient. So here goes:

W is Wolff-Parkinson-White syndrome – look for a short PR interval or delta wave:

O is obstructed AV pathway – look for 2nd or 3rd degree block:

or axis deviation:

…which is the first step in looking for B bifascicular block, or the combination of axis deviation and right bundle branch block:

the second B is Brugada, looking for characteristic morphology of the ST segment, so called coved ST elevation:

Now syncope, especially exertional syncope, can be caused by left ventricular outflow tract obstruction. Two conditions not to be missed associated with this (and exertional syncope) are hypertrophic cardiomyopathy and aortic stenosis. These both characteristically cause L– left ventricular hypertrophy:

E– stands for epsilon wave, a feature of arrythmogenic right ventricular cardiomyopathy, a rare disorder associated with sudden cardiac death. The epsilon wave looks a bit like the J wave of hypothermia and may be associated with other T wave abnormalities in V1-V3:

Finally, R stands for Repolarisation abnormality, particularly delayed Repolarisation as found in long QT syndrome:

but remember there is also a short QT syndrome too:

 

So WOBBLER may help you find the important and rare abnormalities not to be missed in the syncope patient, going from left to right from P wave through to T wave, in the patient that does not have obvious dysrhythmia or ischaemia. Try it and let me know if it helps!

 

All ECGs reproduced with kind permission of Life in the Fast Lane

It’s Tamponade – Now What?

You ultrasound the chest of your shocked patient in resus with fluid refractory hypotension. You see fluid around the heart. The right ventricle keeps bowing inwards, which you recall being described as ‘a little invisible man jumping up and down using the RV as a trampoline’, and you know this is in fact a sign of right ventricular diastolic collapse.
 

image courtesy of thebluntdissection.org

The collapse of the right side of the heart during diastole is the mechanism for shock and cardiac arrest due to tamponade, because the high pericardial pressures prevent the right heart from filling in diastole. This patient therefore has ‘tamponade physiology’ on ultrasound. A quick scan of the IVC shows it is dilated and does not collapse with respiration. This confirms a high central venous pressure (as do the patient’s distended neck veins), also consistent with tamponade physiology.
 
A formal echo done in resus confirms your suspicion of a dliated aortic root and visible dissection flap, so the diagnosis is now clear. This is type A aortic dissection with tamponade. The patient remains hypotensive and mottled with increasing drowsiness. Cardiothoracic surgery is based at another hospital site 30 minutes away by ambulance.
 
As the critical care clinician responsible for, or assisting with this patient’s care (emergency physician, intensivist, anaesthetist, rural GP, physician’s assistant, etc.), how do we get this patient to definitive care and mitigate the risk of deterioration en route? Let’s discuss the options using real life case examples, and consider the physiology, the evidence, and the dogma.
 
Here are four key questions to consider:
1. To drain or not to drain the pericardium?
2. To intubate or not to intubate?
3. If they arrest – CPR or no CPR?
4. How to transfer – physician escort or just send in an ambulance on lights and sirens?
 
Here are three scenarios that follow the intial assessment of the above patient. They are based on similar cases shared with me by participants on the Critical Care in the Emergency Department course.
 

Case 1

The patient is obtunded with profound shock and too unstable for transfer. The resus team undertakes pericardiocentesis and aspirates 30 ml of blood. The patient becomes conscious and cooperative and the systolic blood pressure (SBP) is 95 mmHg. The patient is transferred by paramedic ambulance to the cardothoracic centre where he is successfully operated on, resulting in a full recovery.
 

Case 2

As the patient is unconscious and requires interhospital transfer, the decision is made to intubate him for airway protection. He undergoes rapid sequence induction with ketamine, fentanyl, and rocuronium in the resus room. After capnographic confirmation of tracheal intubation he is manually ventilated via a self-inflating bag. The ED nurse reports a loss of palpable pulse and CPR is started. A team member suggests pericardiocentesis but a senior critical care physician says there is no point because ‘it won’t fix the underlying problem of aortic dissection’ and ’the blood will be clotted anyway’. After a brief attempt at standard ACLS, resuscitation efforts are discontinued and the patient is declared dead.
 

Case 3

The patient is hypotensive with a SBP of 90mmHg and drowsy but cooperative. The receiving centre has accepted the referral and an ambulance has been requested. The critical care physician responsible for patient transfers is requested to accompany the patient but declines, on the basis that ‘these cases are just like abdominal aortic aneurysms – they just need to get there asap. If they deteriorate en route we’re not going to do anything.’
The patient is transferred but 15 minutes into the journey he becomes unresponsive and loses his cardiac output. The transporting paramedics provide chest compressions and adrenaline/epinephrine but are unable to resuscitate him.
 
These cases illustrate some of the pitfalls and fallacies associated with tamponade due to type A dissection.
 

Pericardiocentesis

Pericardiocentesis can definitely be life-saving, restoring vital organ perfusion and buying time to get the patient to definitive surgery. Numerous case reports and case series provide evidence of its utility, even in patients in PEA cardiac arrest(1). The authors of the two largest cases series both used 8F pigtail drainage catheters(1,2).
Reports of pericardiocentesis in tamponade due to aortic dissection. From Cruz et al (1)
Reports of pericardiocentesis in tamponade due to aortic dissection. From Cruz et al (1)
One key component of procedural success was controlled pericardial drainage, removing small volumes and reassessing the blood pressure, aiming for a SBP of 90 mmHg. The danger is overshooting, resulting in hypertension and extending the underlying aortic dissection which can be fatal (3).
 
Those still unconvinced by the evidence may be swayed by guidelines. The 2015 European Society of Cardiology Guidelines for the diagnosis and management of pericardial diseases (4) state:
 
“In the setting of aortic dissection with haemopericardium and suspicion of cardiac tamponade, emergency transthoracic echocardiography or a CT scan should be performed to confirm the diagnosis. In such a scenario, controlled pericardial drainage of very small amounts of the haemopericardium can be attempted to temporarily stabilize the patient in order to maintain blood pressure at 90 mmHg. (Class IIa, Level C)”
 

Intubation

Deterioration of tamponade patients following intubation is well described in the literature and the risk is well appreciated by cardiothoracic anaesthetists(5). Once positive pressure ventilation is started, positive pleural pressure is transmitted to the pericardium, where pressures can exceed right ventricular diastolic pressure and prevent cardiac filling. The result is a fall in and possible loss of cardiac output. This is further exacerbated by the addition of PEEP(6). One suggested approach if the patient must be intubated for airway protection but is not yet in the operating room with a surgeon ready to cut, is to consider intubation under local anaesthesia and allow the patient to breathe spontaneously (maintaining negative pleural pressure) through the tube until the surgeon is ready to open the chest(5). Alternatively preload with fluid, use cautious doses of induction agent, and ventilate with low tidal volumes and zero PEEP. However the patient can still crash, so remember that these effects of ventilation on cardiac output in tamponade can be mitigated by the removal of a relatively small volume of pericardial fluid(6).
 

Cardiac Arrest

In cardiac arrest, external chest compressions are unlikely to be of benefit. In a study on baboons subjected to cardiac tamponade, closed chest massage resulted in an increase in intrapericardial pressure. There was an increase in systolic pressure, but a marked decrease in diastolic pressure, with an overall decrease in mean arterial pressure(7).
Pressure changes from CPR during tamponade in baboons. From Möller et al (6)
Pressure changes from CPR during tamponade in baboons. From Möller et al (6)
This would lead to impaired coronary perfusion and would be very unlikely to result in return of spontaneous circulation (ROSC). In the clinical situation described above, it is only relief of tamponade that is going to provide an arrested patient with a chance of recovery.
 

Transport

For patients with cardiac tamponade requiring interhospital (or intrahospital) transfer, it would seem vital therefore that the patient is accompanied by a clinician willing and capable to perform pericardiocentesis in the event of severe deterioriation or arrest en route. This simple life-saving intervention to deliver the patient alive to the operating room should be made available should the need arise.
 
 

Summary

  • Patients presenting in shock from cardiac tamponade often have treatable underlying causes and represent a situation where the planning and actions of the resuscitationist can be truly life-saving.
  • Pericardiocentesis is recommended in profound shock to buy time for definitive intervention. Controlled pericardiocentesis should be performed paying strict attention to SBP to avoid ‘overshooting’ to a hypertensive state in type A aortic dissection. In cardiac arrest, chest compressions are likely to be ineffective and pericardiocentesis is mandatory for ROSC.
  • The institution of positive pressure ventilation often results in worsened shock or cardiac arrest, and this is exacerbated by PEEP. Where possible, avoid intubation until the patient is in the operating room, or use low tidal volumes and no PEEP. Even then pericardiocentesis may be necessary to maintain or restore cardiac output.
  • Patients requiring transport who have tamponade should be accompanied by a clinician able to perform pericardiocentesis in the event of en route deterioration.

References

  1. Cruz I, Stuart B, Caldeira D, Morgado G, Gomes AC, Almeida AR, et al. Controlled pericardiocentesis in patients with cardiac tamponade complicating aortic dissection: Experience of a centre without cardiothoracic surgery. European Heart Journal: Acute Cardiovascular Care. 2015 Mar 19;4(2):124–8.
  2. Hayashi T, Tsukube T, Yamashita T, Haraguchi T, Matsukawa R, Kozawa S, et al. Impact of Controlled Pericardial Drainage on Critical Cardiac Tamponade With Acute Type A Aortic Dissection. Circulation. 2012 Sep 10;126(11_suppl_1):S97–S101.
  3. Isselbacher EM, Cigarroa JE, Eagle KA. Cardiac tamponade complicating proximal aortic dissection. Is pericardiocentesis harmful? Circulation. 1994 Nov 1;90(5):2375–8.
  4. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. European Heart Journal. 2015 Nov 7;36(42):2921–64.
  5. Ho AMH, Graham CA, Ng CSH, Yeung JHH, Dion PW, Critchley LAH, et al. Timing of tracheal intubation in traumatic cardiac tamponade: A word of caution. Resuscitation. 2009 Feb;80(2):272–4.
  6. Möller CT, Schoonbee CG, Rosendorff C. Haemodynamics of cardiac tamponade during various modes of ventilation. Br J Anaesth. 1979 May;51(5):409–15.
  7. Luna GK, Pavlin EG, Kirkman T, Copass MK, Rice CL. Hemodynamic effects of external cardiac massage in trauma shock. The Journal of Trauma: Injury, Infection, and Critical Care. 1989 Oct;29(10):1430–3.

Advice To A Young Resuscitationist

Advice-to-Young-Resuscitationist

This talk was the opening plenary given at smacc Chicago. The title they gave me was ‘Advice To A Young Resuscitationist. It’s Up To Us To Save The World‘ but I ditched the last half because, as I point out later in the talk, I don’t think it is up to us to save the whole World. Some AV muppetry at the conference centre prevented the smacc team from being able to include the slides, so I’ll post those too at some point. You can hear the talk as a podcast at the ICN or on iTunes

The references for the talk are here

 

Louisa in London – Prehospital Lessons from LTC2015

The London Trauma Conference remains up there on my list of ‘must go’ conferences to attend. It marks the end of the year, fills me with hope and inspires me for the future. Unfortunately this year I was torn between the conference and the demands of clinical directorship so I could only get to the “Air Ambulance & Prehospital Care Day”. At least this way I’m saved from the dilemma of which sessions to attend!
So what were the highlights of the Prehospital Day? For me, they were Prehospital ECMO,’Picking Up the Pieces’, and the REBOA update.

Prehospital ECMO
Professor Pierre Carli gave us an update on prehospital ECMO. Professor Carli (not to be confused with the equally awesome Professor Carley) is the medical director of Service d’Aide Médicale Urgente (SAMU) in Paris. They’ve been doing prehospital ECMO in Paris since 2011 and the data analysed over three years reveals a 10% survival to hospital discharge rate. We know from the work in Asia that successful outcome following traditional cardiac arrest management and ECPR is related to the speed of the intervention. Transposing the time to intervention from his 2011 – 2013 data onto the survival curve that Chen et al produced explains why the success rate is limited:

LTC2015

The revised 2015 process aims to reduce the duration of CPR, reduce time to ECMO and therefore improve survival to discharge rates. They are doing this by dispatching the ECMO team earlier.

The eligibility criteria for ECPR is also changing; patients >18 and <75years, refractory cardiac arrest (defined as failure of ROSC after 20min of CPR), no flow for < 5 minutes with shockable rhythm or signs of life or hypothermia or intoxication, EtCO2 > 10mmHg at time of inclusion and no major comorbidity.

Already there appears to be an improvement with 16 patients treated using the revised protocol with 5 survivors (31%) – although we must be wary of the small numbers.
A concern that was expressed by the French Department of Health was the fear of a reduction in organ donation with the introduction of ECPR – it turns out that rates have remained stable. In fact the condition of non heart beating donated organs is better when ECMO has been instigated; the long term effects on organ donation are being assessed.

I’m without doubt that prehospital ECMO/ED ECMO is the future although currently in the UK our hospital systems aren’t ready for this. If you want to learn more then look at the ED ECMO site or book on one of the many emerging courses on ED ECMO including the one that is run by Dr Simon Finney at the London Trauma Conference, or if you want to go further afield you could try San Diego (although places are fully booked on the next course).

Picking Up the Pieces
The Keynote speaker was Professor Sir Simon Wessely. He is a psychiatrist with a specialist interest in military psychology and his brief was to describe to us the public response to traumatic incidents. He has worked with the military and in civilian situations. After the 7/7 London bombings the population of London was surveyed: those most likely to be affected were of lower social class, of Muslim faith, those that had a relative that was injured, those unsure of the safety of others, those with no previous experience of terrorism and those experiencing difficulty in contacting others by mobile phone. Obviously there are many factors that we cannot influence however on the basis of the last risk factor our response to incidents has changed – the active discouragement to make phone calls has been changed to a recommendation of making short calls to friends and relatives.
The previous practice of offering immediate psychological debriefing to those involved in incidents was discounted by Prof Wessely – his research demonstrated that this intervention was not only not required but could actually result in harm: only a minority have ongoing psychological distress that can benefit from formal psychological input, which should occur later.
The approach that should be taken is to allow that individual to utilise their own social networks (family, friends, and colleagues) and to accept that in some cases the individual may not want or need to talk. This has led to the development of the Trauma Risk Management (TRIM) system which provides individuals within organisations that are exposed to traumatic events the skills required to identify those at risk of developing psychological problems and to recognise the signs and symptoms of those in difficulty. To a certain extent we naturally do this for our peers – I have spent many a night sitting in the ‘Good Samaritan’ pub with colleagues from the Royal London Hospital and London’s Air Ambulance – but having a more formal system is probably of benefit to enable those who have ongoing difficulties to access additional support.

REBOA update
Finally, the REBOA update – Resuscitative Endovascular Balloon Occlusion of the Aorta. One year on, Dr Sammy Sadek informed us that there are now more courses teaching the REBOA technique than there are (prehospital) patients that have received it. Over the last year only seven patients have qualified for this intervention in London, far fewer than they had anticipated. Another three patients died before REBOA could be instigated. All patients had a positive cardiovascular response. Four of the seven died from causes other than exsanguination. Is it worth all the effort and resource to deliver this intervention when such a select group will benefit?

Obviously there was much more covered in the day, this is just a taste. If you’ve never been to the London Trauma Conference then I definitely would recommend it and even if you have been before there are so many breakout sessions now there is always something for everyone.

More on the London Trauma Conference:

Merry Christmas and see you next year!

Louisa Chan

Dabigatran Reversal Agent – Idarucizumab

Thanks to Rob MacSweeney‘s fantastic Critical Care Reviews I learned of Idarucizumab, a monoclonal antibody fragment that binds the (pesky) anticoagulant dabigatran. Two industry-supported studies this week show rapid, complete reversal of anticoagulation in healthy volunteers(1) and patients who were either bleeding or undergoing procedures(2). The dose given to patients was 5g intravenously.

An accompanying editorial(3) highlights that the clinical study did not have a control group, and these patients had a high mortality. Further controlled studies examining patient-orientated outcomes will be helpful.

Of interest, another editorialist(4) lists other potential antidotes for Non-vitamin-K antagonist oral anticoagulants (NOACs) that have been or are being tested: an antidote against all oral direct factor Xa inhibitors called andexanet alpha (a recombinant activated factor X that binds direct factor Xa inhibitors), and a modified thrombin has been shown to be effective in vitro and in animals for reversal of dabigatran and potentially also other direct thrombin inhibitors.

1. Safety, tolerability, and efficacy of idarucizumab for the reversal of the anticoagulant effect of dabigatran in healthy male volunteers: a randomised, placebo-controlled, double-blind phase 1 trial
The Lancet Volume 386, No. 9994, p680–690, 15 August 2015


BACKGROUND: Idarucizumab is a monoclonal antibody fragment that binds dabigatran with high affinity in a 1:1 molar ratio. We investigated the safety, tolerability, and efficacy of increasing doses of idarucizumab for the reversal of anticoagulant effects of dabigatran in a two-part phase 1 study (rising-dose assessment and dose-finding, proof-of-concept investigation). Here we present the results of the proof-of-concept part of the study.

METHODS: In this randomised, placebo-controlled, double-blind, proof-of-concept phase 1 study, we enrolled healthy volunteers (aged 18-45 years) with a body-mass index of 18·5-29·9 kg/m2 into one of four dose groups at SGS Life Sciences Clinical Research Services, Belgium. Participants were randomly assigned within groups in a 3:1 ratio to idarucizumab or placebo using a pseudorandom number generator and a supplied seed number. Participants and care providers were masked to treatment assignment. All participants received oral dabigatran etexilate 220 mg twice daily for 3 days and a final dose on day 4. Idarucizumab (1 g, 2 g, or 4 g 5-min infusion, or 5 g plus 2·5 g in two 5-min infusions given 1 h apart) was administered about 2 h after the final dabigatran etexilate dose. The primary endpoint was incidence of drug-related adverse events, analysed in all randomly assigned participants who received at least one dose of dabigatran etexilate. Reversal of diluted thrombin time (dTT), ecarin clotting time (ECT), activated partial thromboplastin time (aPTT), and thrombin time (TT) were secondary endpoints assessed by measuring the area under the effect curve from 2 h to 12 h (AUEC2-12) after dabigatran etexilate ingestion on days 3 and 4. This trial is registered with ClinicalTrials.gov, number NCT01688830.

FINDINGS: Between Feb 23, and Nov 29, 2013, 47 men completed this part of the study. 12 were enrolled into each of the 1 g, 2 g, or 5 g plus 2·5 g idarucizumab groups (nine to idarucizumab and three to placebo in each group), and 11 were enrolled into the 4 g idarucizumab group (eight to idarucizumab and three to placebo). Drug-related adverse events were all of mild intensity and reported in seven participants: one in the 1 g idarucizumab group (infusion site erythema and hot flushes), one in the 5 g plus 2·5 g idarucizumab group (epistaxis); one receiving placebo (infusion site haematoma), and four during dabigatran etexilate pretreatment (three haematuria and one epistaxis). Idarucizumab immediately and completely reversed dabigatran-induced anticoagulation in a dose-dependent manner; the mean ratio of day 4 AUEC2-12 to day 3 AUEC2-12 for dTT was 1·01 with placebo, 0·26 with 1 g idarucizumab (74% reduction), 0·06 with 2 g idarucizumab (94% reduction), 0·02 with 4 g idarucizumab (98% reduction), and 0·01 with 5 g plus 2·5 g idarucizumab (99% reduction). No serious or severe adverse events were reported, no adverse event led to discontinuation of treatment, and no clinically relevant difference in incidence of adverse events was noted between treatment groups.

INTERPRETATION: These phase 1 results show that idarucizumab was associated with immediate, complete, and sustained reversal of dabigatran-induced anticoagulation in healthy men, and was well tolerated with no unexpected or clinically relevant safety concerns, supporting further testing. Further clinical studies are in progress.

2. Idarucizumab for Dabigatran Reversal
N Engl J Med. 2015 Aug 6;373(6):511-20


BACKGROUND: Specific reversal agents for non-vitamin K antagonist oral anticoagulants are lacking. Idarucizumab, an antibody fragment, was developed to reverse the anticoagulant effects of dabigatran.

METHODS: We undertook this prospective cohort study to determine the safety of 5 g of intravenous idarucizumab and its capacity to reverse the anticoagulant effects of dabigatran in patients who had serious bleeding (group A) or required an urgent procedure (group B). The primary end point was the maximum percentage reversal of the anticoagulant effect of dabigatran within 4 hours after the administration of idarucizumab, on the basis of the determination at a central laboratory of the dilute thrombin time or ecarin clotting time. A key secondary end point was the restoration of hemostasis.

RESULTS: This interim analysis included 90 patients who received idarucizumab (51 patients in group A and 39 in group B). Among 68 patients with an elevated dilute thrombin time and 81 with an elevated ecarin clotting time at baseline, the median maximum percentage reversal was 100% (95% confidence interval, 100 to 100). Idarucizumab normalized the test results in 88 to 98% of the patients, an effect that was evident within minutes. Concentrations of unbound dabigatran remained below 20 ng per milliliter at 24 hours in 79% of the patients. Among 35 patients in group A who could be assessed, hemostasis, as determined by local investigators, was restored at a median of 11.4 hours. Among 36 patients in group B who underwent a procedure, normal intraoperative hemostasis was reported in 33, and mildly or moderately abnormal hemostasis was reported in 2 patients and 1 patient, respectively. One thrombotic event occurred within 72 hours after idarucizumab administration in a patient in whom anticoagulants had not been reinitiated.

CONCLUSIONS: Idarucizumab completely reversed the anticoagulant effect of dabigatran within minutes. (Funded by Boehringer Ingelheim; RE-VERSE AD ClinicalTrials.gov number, NCT02104947.).

3. Targeted Anti-Anticoagulants
N Engl J Med. 2015 Aug 6;373(6):569-71

4. Antidotes for anticoagulants: a long way to go
The Lancet Volume 386, No. 9994, p634–636, 15 August 2015

Inhaled nitric oxide: a tool for all resuscitationists?

NOsmThe use of inhaled nitric oxide is established in certain groups of patients: it improves oxygenation (but not survival) in patients with acute respiratory distress syndrome(1), and it is used in neonatology for management of persistent pulmonary hypertension of the newborn(2). But it can be applied in other resuscitation settings: in arrested or peri-arrest patients with pulmonary hypertension.

Read this (modified) description of a case managed by one of my resuscitationist friends from an overseas location:

A young lady suffered a placental abruption requiring emergency hysterectomy. She arrested twice in the operating room after suspected amniotic fluid embolism. She had fixed dilated pupils.

She developed extreme pulmonary hypertension with suprasystemic pulmonary artery pressures, and she went down the pulmonary HT spiral as I stood there. On ultrasound her distended RV was making her LV totally collapse. She arrested. Futile CPR was started.

I have never had an extreme pulmonary HT survive an arrest. I grabbed a bag and rapidly set up a manual inhaled Nitric Oxide system and bagged and begged…

She achieved ROSC after some minutes. A repeat ultrasound showed a well functioning LV and less dilated RV.

Today, after 12 hours she is opening her eyes and obeying commands. Still a long way to go, but alive.

 

It sounds impressive. I don’t have more case details, and don’t know how confident they could be about the diagnosis of amniotic fluid embolism but the presentation certainly fits with acute pulmonary hypertension with RV failure. The use of inhaled nitric oxide has certainly been described for similar scenarios before(3). But it raises bigger questions: is this something we should all be capable of? Are there cardiac arrests involving or caused by pulmonary hypertension that will not respond to resuscitation without nitric oxide?

Nitric oxide
Inhaled nitric oxide is a pulmonary vasodilator. It decreases right-ventricular afterload and improves cardiac index by selectively decreasing pulmonary vascular resistance without causing systemic hypotension(4).

RV failure and pulmonary hypertension
Patients may become shocked or suffer cardiac arrest due to acute right ventricular dysfunction. This may be due to a primary cardiac cause such as right ventricular infarction (always consider this in a hypotensive patient with inferior STEMI, and confirm with a right ventricular ECG and/or echo). Alternatively it could be due to a pulmonary or systemic cause resulting in severe pulmonary hypertension, causing secondary right ventricular dysfunction. The commonest causes of acute pulmonary hypertension are massive PE, sepsis, and ARDS(5).

The haemodynamic consequences of RV failure are reduced pulmonary blood flow and inadequate left ventricular filling, leading to decreased cardiac output, shock, and arrest. In severe acute pulmonary hypertension the RV distends, resulting in a shift of the interventricular septum which compresses the LV and further inhibits LV filling (the concept of ventricular interdependence).

What’s wrong with standard ACLS?
In some patients with PHT who arrest, CPR may be ineffective due to a failure to achieve adequate pulmonary blood flow and ventricular filling. In one study of patients with known chronic PHT who arrested in the ICU, survival rates even for ventricular fibrillation were extremely poor and when measured end tidal carbon dioxide levels were very low. In the same study it was noted that some of the survivors had received an intravenous bolus administration of iloprost, a prostacyclin analogue (and pulmonary vasodilator) during CPR(6).

CPR may therefore be ineffective. Intubation and positive pressure ventilation may also be associated with haemodynamic deterioration in PHT patients(7), and intravenous epinephrine (adrenaline) has variable effects on the pulmonary circulation which could be deleterious(8).

If inhaled nitric oxide (iNO) can improve pulmonary blood flow and reduce right ventricular afterload, it could theoretically be of value in cases of shock or arrest with RV failure, especially in cases of pulmonary hypertension; these are patients who otherwise have poor outcomes and may not benefit from CPR.

Is the use of iNO described in shock or arrest?
Numerous case reports and series demonstrate recovery from shock or arrest following nitric oxide use in various situations of decompensated right ventricular failure from pulmonary hypertension secondary to pulmonary fibrotic disease(9), pneumonectomy surgery(10), and pulmonary embolism(11) including post-embolectomy(12).

Acute hemodynamic improvement was demonstrated following iNO therapy in a series of right ventricular myocardial infarction patients with cardiogenic shock(13).

A recent systematic review of inhaled nitric oxide in acute pulmonary embolism documented improvements in oxygenation and hemodynamic variables, “often within minutes of administration of iNO”. The authors state that these case reports underscore the need for randomised controlled trials to establish the safety and efficacy of iNO in the treatment of massive acute PE(14).

Why aren’t they telling us to use it?
If iNO may be helpful in certain cardiac arrest patients, why isn’t ILCOR recommending it? Actually it is mentioned – in the context of paediatric life support. The European Resuscitation Council states:

ERC Guideline: (Paediatric) Pulmonary hypertension

There is an increased risk of cardiac arrest in children with pulmonary hypertension.

Follow routine resuscitation protocols in these patients with emphasis on high FiO2 and alkalosis/hyperventilation because this may be as effective as inhaled nitric oxide in reducing pulmonary vascular resistance.

Resuscitation is most likely to be successful in patients with a reversible cause who are treated with intravenous epoprostenol or inhaled nitric oxide.

If routine medications that reduce pulmonary artery pressure have been stopped, they should be restarted and the use of aerosolised epoprostenol or inhaled nitric oxide considered.

Right ventricular support devices may improve survival

 
Should we use it?
So if acute (or acute on chronic) pulmonary hypertension can be suspected or demonstrated based on history, examination, and echo findings, and the patient is in extremis, it might be anticipated that standard ACLS approaches are likely to be futile (as they often are if the underlying cause is not addressed). One might consider attempts to induce pulmonary vasodilation to improve pulmonary blood flow and LV filling, improving oxygenation, and reducing RV afterload as means of reversing acute cor pulmonale.

Are there other pulmonary vasodilators we can use?
iNO is not the only means of inducing pulmonary vasodilation. Oxygen, hypocarbia (through hyperventilation)(15), and alkalosis are all known pulmonary vasodilators, the latter providing an argument for intravenous bicarbonate therapy from some quarters(16). Prostacyclin is a cheaper alternative to iNO(17) and can be given by inhalation or intravenously, although is more likely to cause systemic hypotension than iNO. Some inotropic agents such as milrinone and levosimendan can lower pulmonary vascular resistance(18).

What’s the take home message?
The take home message for me is that acute pulmonary hypertension provides yet another example of a condition that requires the resuscitationist to think beyond basic ACLS algorithms and aggressively pursue and manage the underlying cause(s) of shock or arrest. Inhaled pulmonary vasodilators may or may not be available but, as always, whatever resources and drugs are used, they need to be planned for well in advance. What’s your plan?

 
References
1. Adhikari NKJ, Dellinger RP, Lundin S, Payen D, Vallet B, Gerlach H, et al.
Inhaled Nitric Oxide Does Not Reduce Mortality in Patients With Acute Respiratory Distress Syndrome Regardless of Severity.
Critical Care Medicine. 2014 Feb;42(2):404–12

2. Steinhorn RH.
Neonatal pulmonary hypertension.
Pediatric Critical Care Medicine. 2010 Mar;11:S79–S84 Full text

3. McDonnell NJ, Chan BO, Frengley RW.
Rapid reversal of critical haemodynamic compromise with nitric oxide in a parturient with amniotic fluid embolism.
International Journal of Obstetric Anesthesia. 2007 Jul;16(3):269–73

4. Creagh-Brown BC, Griffiths MJ, Evans TW.
Bench-to-bedside review: Inhaled nitric oxide therapy in adults.
Critical Care. 2009;13(3):221 Full text

5. Tsapenko MV, Tsapenko AV, Comfere TB, Mour GK, Mankad SV, Gajic O.
Arterial pulmonary hypertension in noncardiac intensive care unit.
Vasc Health Risk Manag. 2008;4(5):1043–60 Full text

6. Hoeper MM, Galié N, Murali S, Olschewski H, Rubenfire M, Robbins IM, et al.
Outcome after cardiopulmonary resuscitation in patients with pulmonary arterial hypertension.
American Journal of Respiratory and Critical Care Medicine. 2002 Feb 1;165(3):341–4.
Full text

7. Höhn L, Schweizer A, Morel DR, Spiliopoulos A, Licker M.
Circulatory failure after anesthesia induction in a patient with severe primary pulmonary hypertension.
Anesthesiology. 1999 Dec;91(6):1943–5 Full text

8. Witham AC, Fleming JW.
The effect of epinephrine on the pulmonary circulation in man.
J Clin Invest. 1951 Jul;30(7):707–17 Full text

9. King R, Esmail M, Mahon S, Dingley J, Dwyer S.
Use of nitric oxide for decompensated right ventricular failure and circulatory shock after cardiac arrest.
Br J Anaesth. 2000 Oct;85(4):628–31. Full text

10. Fernández-Pérez ER, Keegan MT, Harrison BA.
Inhaled nitric oxide for acute right-ventricular dysfunction after extrapleural pneumonectomy.
Respir Care. 2006 Oct;51(10):1172–6 Full text

11. Summerfield DT, Desai H, Levitov A, Grooms DA, Marik PE.
Inhaled Nitric Oxide as Salvage Therapy in Massive Pulmonary Embolism: A Case Series.
Respir Care. 2012 Mar 1;57(3):444–8 Full text

12. Schenk P, Pernerstorfer T, Mittermayer C, Kranz A, Frömmel M, Birsan T, et al.
Inhalation of nitric oxide as a life-saving therapy in a patient after pulmonary embolectomy.
Br J Anaesth. 1999 Mar;82(3):444–7 Full text

13. Inglessis I, Shin JT, Lepore JJ, Palacios IF, Zapol WM, Bloch KD, et al.
Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock.
Journal of the American College of Cardiology. 2004 Aug;44(4):793–8 Full text

14. Bhat T, Neuman A, Tantary M, Bhat H, Glass D, Mannino W, Akhtar M, Bhat A, Teli S, Lafferty J.
Inhaled nitric oxide in acute pulmonary embolism: a systematic review.
Rev Cardiovasc Med 2015;16(1):1–8.

15. Mahdi M, Joseph NJ, Hernandez DP, Crystal GJ, Baraka A, Salem MR.
Induced hypocapnia is effective in treating pulmonary hypertension following mitral valve replacement.
Middle East J Anaesthesiol. 2011 Jun;21(2):259-67

16. Evans S, Brown B, Mathieson M, Tay S.
Survival after an amniotic fluid embolism following the use of sodium bicarbonate.
BMJ Case Rep. 2014;2014

17. Fuller BM, Mohr NM, Skrupky L, Fowler S, Kollef MH, Carpenter CR.
The Use of Inhaled Prostaglandins in Patients With ARDS: A Systematic Review and Meta-analysis.
Chest. 2015 Jun;147(6):1510–22 Full text

18. LITFL: Right Ventricular Failure

Further reading
Life In The Fast Lane iNO info

LITFL on Pulmonary Hypertension

CPR in Pectus Excavatum

nussSome pectus excavatum patients have a metal ‘Nuss bar’ inserted below the sternum which can make chest compressions more difficult. In those without one, standard compression depths compress the left ventricle more than in non-pectus subjects, and might lead to myocardial injury.

This has led to a recommendation in the journal Resuscitation:

Until further studies are available, we recommend strong chest compressions, according to the current guidelines, in PE patients with a sternal Nuss bar and, to minimize the risk of myocardial injury, we suggest a reduced chest compression depth (approximately 3–4 cm) at the level of lower half of the sternum in PE patients who have not had corrective surgery.

 

Cardiopulmonary resuscitation in pectus excavatum patients: Is it time to say more?
Resuscitation. 2014 Dec 10.[Epub ahead of print]