Category Archives: ICU

Stuff relevant to patients on ICU

Head Rotation for Mask Ventilation

This is a guest post from Dr Per Bredmose, anaesthetist and retrieval medicine physician in Norway, also known as Viking One

I struggle to ventilate the patient in the resus room, airway pressures are high, the bag doesn’t empty properly. In my mind I plan ahead for the next step. Through my mind goes the thought – is this the one, the one that I cannot ventilate? Statistically it is not likely to be, but I am prepared to add two-person technique, airway adjuncts like nasopharyngeal or oropharyngeal, or supraglottic devices that I use frequently in theatre. I feel confident in the use of these methods, and (in the worst case) in cricothyroidotomy. I have practiced that numerous times on our live-tissue course on anaesthetised pigs. However – before I start any of these actions.. I routinely, almost as a reflex from theatre turn the patient’s head 45 degrees to the left, and then the bag suddenly empties easily – and I can ventilate the patient.

Some people think that time with TIVA in theatre has little value for emergency medicine and advanced prehospital care. I strongly disagree. This is some of the most relevant and valuable time I have for keeping and optimising my practical skills. Bag-valve-mask (BVM) ventilation is an essential core skill for any prehospital provider. In theatre this manoeuvre is well known and frequently practiced. It is my impression that this head rotation is less used, and even maybe less well known outside theatre, and especially in the prehospital field. Therefore this is a reminder of an old technique.

When to do it: When encountering difficulties in conventional BVM ventilation, either when you cannot ventilate or when it’s just difficult to ventilate.

How to do it: Keep a firm one hand grip and gently rotate the head 45 degrees towards the side of the hand with the jaw grip. At the same time, one can try to optimise the one-hand-jaw thrust that goes along with BVM ventilation. Occasionally one needs to extend (dorsiflex) the neck a bit further to fully open the airway. The technique can also be used as a two-person technique, although this is rarely needed.

Opposition: Frequently I hear that I cannot transfer practice from theatre to the prehospital field. Well, this seems to work well in theatre, in ICU and in the field – airways are airways!!

Recently an article in European Journal of Anaesthesiology by Itagaki et al(1) with a cross over design showed an increase in tidal volume when the patients were ventilated in a head rotated position compared to neutral position with the same airway pressure. Their conclusion was as follows: Head rotation of 45° in anaesthetised apnoeic adults significantly increases the efficiency of mask ventilation compared with the neutral head position. Head rotation is an effective alternative to improve mask ventilation if airway obstruction is encountered. Therefore – this is a useful tool that one always should have in the “practical toolbox”. It is not always the solution, but occasionally it saves you (and the patient) a lot of trouble.

Thoughts from Dr Cliff Reid
I haven’t used this approach and wasn’t aware of previous research showing an increase in the retroglossal (but not retropalatine) spaces in (awake) patients with head rotation(2).

The mechanism is thought to be gravitational. It is also possible that neck rotation increases upper airway wall tension that reduces collapsibility of the lumen.

In this elegantly designed new study, a two handed BMV technique was used, similar to that advocated in my prehospital & emergency medicine environments. The rotation was always to the right, although the authors comment that they would expect the same results on the left. The increased tidal volume effect with head rotation occurred mostly in younger patients and patients with Mallampati classification I. Such patients are unlikely to be difficult to mask-ventilate, limiting the applicability of these findings to patients who are difficult to ventilate. However having one more option to employ to improve BMV efficacy (after two person technique, optimising ear-to-sternal-notch positioning, and inserting oro- and/or nasopharyngeal airways) may be useful, and the experience and perspective of my anaesthetic colleague Viking One is definitely food for thought. Obviously one should avoid this if there is potential neck injury so I won’t be trying it my trauma patients.


1. Itagaki T, Oto J, Burns SM, Jiang Y, Kacmarek RM, Mountjoy JR. The effect of head rotation on efficiency of face mask ventilation in anaesthetised apnoeic adults. Eur J Anaesthesiol. 2017 Jul;34(7):432–40.

2. Ono T, Otsuka R, Kuroda T, Honda E, Sasaki T. Effects of head and body position on two- and three-dimensional configurations of the upper airway. J Dent Res. 2000 Nov;79(11):1879–84.

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

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 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)”


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.


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.


  • 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.


  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.

Difficult Airway? What Kind Exactly?

Mention the term ‘difficult airway’ and many of us will conjure mental images of some kind of distorted anatomy. However, airway management may be ‘difficult’ for a number of reasons, and no internationally agreed definition of the term exists. Given the wrong staff and circumstances, an ‘easy’ airway in your or my hands may indeed become very difficult. In their editorial “The myth of the difficult airway: airway management revisited” (1) Huitink & Bouwman state:

“In our opinion, the ‘difficult airway’ does not exist. It is a complex situational interplay of patient, practitioner, equipment, expertise and circumstances.”

Airways that are anatomically difficult (eg. limited mouth opening, short thyromental distance, large tongue, neck immobility, etc.) and physiologically difficult (hypoxaemia, hypotension, acidosis) are well described among FOAM resources (2-4). In addition to these, a third category of difficulty is well worth considering.

At the smaccDUB conference, intensivist and human factors legend Peter Brindley described three types of difficult airway:

  1. Anatomically difficult
  2. Physiologically difficult
  3. Situationally difficult
    Brindley = Legend

This last category probably surfaces more commonly than realised, particularly outside the operating room.

Imagine attending a cardiac arrest call on a medical ward. The patient is a 70 year old 120 kg male. The nurses have flattened the bed and discarded the pillow to optimise supine position for CPR. Gobs of vomitus splash from the patient’s pharynx with each compression. The wall suction system is disconnected. There is no bougie in the crash cart’s airway drawer. The nearest capnograph is on another floor of the hospital. In this scenario, no matter how excellent the critical care practitioner’s airway skills, this is a damned difficult airway.

I think Brindley’s third category is a term that should catch on, as a way of helping analyse cases that progress suboptimally and to identify factors during pre-intubation checks that can be addressed. It is terminology that I have added to my own Resuscitese Lexicon, particularly for case discussions during morbidity & mortality and airway audit meetings.

I would like to hear the ‘Situationally Difficult Airway‘ become more widely used, as it fills a gap in how we describe this important area of resuscitation practice.



1. Huitink JM, Bouwman RA. The myth of the difficult airway: airway management revisited. Anaesthesia. 2015 Mar;70(3):244–9. (Full text)

2. LITFL: Airway Assessment

3. EMCrit: HOP Killers

4. PulmCCM: The Physiologically Difficult Airway

Convergent Evolution in the Jungles of Critical Care

boss-of-the-mob-1400090-1279x1923By Stuart Duffin
Expat Brit, intensive care physician and anaesthetist at Karolinska University Hospital in Stockholm, Sweden. Stuart trained in the UK, and spent some time working Australian emergency departments.

One of the most striking things for me about our new/old pan-specialty of critical care, brought into focus by the world-shrinking effects of FOAM and twitter, is just how differently it falls into the domains of the established specialities in different parts of the world. This leads inevitably to comments like, “emergency physicians shouldn’t intubate”, “anaesthetists cant do sick”, “nurses cant be doing such and such”, and so on. All of these statements are clearly equally rubbish because obviously, in certain parts of the world, they do. And they do it really well. Sure there are differences between countries and continents, populations and environments, but when it comes down to it, it doesn’t matter where you are, people still get sick, infected, pregnant, run over, stabbed or hit around the head with heavy things.

All over the world, in our previously quite isolated environments, these same ‘selection pressures’ have forced healthcare providers to evolve by the process of convergent evolution. Although obviously not strictly darwinian, the undeniable effects of simultaneous evolution by survival of the fittest-to-practice can be seen.

Convergent evolution is the process by which, in different parts of the world, completely different species have evolved in parallel to fill similar roles and have similar features. It didn’t matter whether it was a deer, a wildebeest or a kangaroo, there was a vacancy for a fairly big animal who liked eating grass and moved in big groups, and someone stepped up.

Unsurprisingly, critical care resuscitationists are also a little different from country to country and from continent to continent. They have different titles and work in slightly different ways. But when you really look at a critical care doc in action, or talk to one, or follow one on Twitter, we are all cut from the same cloth. I would argue that FOAM has created a critical care zoo in which the kangaroos and antelopes, lemurs and monkeys, aardvarks and echidnas and anaesthetists and emergency physicians are all chucked into the same cage. They’re all looking at each other thinking, “you look like me, but somehow not. We seem to do the same stuff, but we’re not identical – it cant be right!”.

In The United States, the idea of an anaesthetist doing a clamshell thoracotomy would be a little strange. In Scandinavia, an emergency physician doing central lines and fiberoptic intubation in resus would be just as eyebrow raising. A Swedish intensivist and anaesthetist spent some time working in Australia as an ICU senior reg. When attending a patient in resus the emergency physician there announced “we need an airway guy”. My colleague answered “I’m the airway guy”. “No an anaesthetist” replied the emergency physican. “I am an anaesthetist!” “No an….” and so it went on.

The effects of this process are of course by no means limited to doctors. Nurses, paramedics and physiotherapists are all part of this still changing ecosystem. A colleague of mine was showing a visiting Australian emergency physician our trauma bay and describing how major trauma is managed here without the involvement of emergency physicians at all. “When it’s really urgent, it’s anaesthesia and surgery” he explained. I wonder how that went down? There is an element of truth to the statement but the words are wrong. It should have been “When it’s really urgent, it’s airway, access, transfusion, invasive procedures and resuscitation thinking”.

The job title of the person who actually holds the knife/laryngoscope/needle and has what it takes to get it done isn’t important. When the push comes to shove and the bad stuff bounces off the fan, it’s more about skillset and mindset, and less about the collection of letters under your name on your badge, or after your name on your CV.

Advice To A 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


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, 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 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?

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

Be Like That Guy – Dr John Hinds



The critical care and #FOAMed community lost our friend Dr John Hinds a few days ago.

We’re in the business of sudden death. As prehospital, emergency, acute medicine and intensive care clinicians, facing the reality of the tragic loss of a living person, loved by their friends and family, is our day job. This makes me think we shouldn’t really have any reason to be ‘shocked’ or ‘surprised’. But we have every right to be sad.

The news came in the same week as the tragic Flight for Life Helicopter Crash in Colorado, bringing us another unwelcome reminder of the dangers of prehospital work. My HEMS colleagues and I are always mindful of the possibility that every time we get in the helicopter it could be our last, and I’ve no doubt John appreciated this reality when responding on his motorcycle.

I admired John as he was the quintessential resuscitationist. He was not bound by specialty or location in his passion for excellence in life-saving medicine. He was a master (and innovator) of advanced prehospital emergency medicine in a region where it still barely exists. He was supportive of emergency physicians providing emergency anaesthesia. He performed the first thoracotomy for more than a decade in one hospital, prompting a review of systems, equipment and training and bringing specialties together to embrace multidisciplinary trauma management. He inspired our friends across the world with his approach to intensive care patients.

Two weeks ago John and I gave two of the opening talks at the SMACC conference in Chicago. My talk went first – entitled ‘Advice to a Young Resuscitationist’. I attempted to list a number of tips that could help a resuscitationist become more effective at saving lives while surviving and thriving in our often traumatic milieu. The talk will be uploaded soon, and I’ve listed the pieces of advice below. What strikes me now like a slap across the face with a large wet fish is the realisation that John exemplified every one of these characteristics and habits:

1. Carve your own path that takes you on a richer path than that worn by trainees in a single specialty
John was an anaesthetist, an intensivist, and prehospital doctor.

2. Never waste an opportunity to learn from other clinicians – leave your ego at the door. See any feedback as an opportunity to learn and to improve, no matter how painful it is to receive.
Despite being among the best in his field, John would on occasion discuss challenging cases and ask if we could think of anything else that should have been done (our answer being, without exception, “no”).

3. Have the confidence and self-belief to perform actions you are competent to perform when needed, to avoid the tragedy of acts of omission.
John’s amazing talk on “crack the chest – get crucified” (when no-one else would) shows how he embraced this mindset: do what needs to be done – with honourable intentions – and manage the consequences later.

4. You can’t save every one, but you can make each case count. When a case goes wrong you need to change something – yourself, your colleagues or the system.
John was a super-agent of change wherever he operated. One beautiful example is how in one hospital the thoracotomy tray ended up being named after him!


5. Caring is so critical to what we do, and is one of the most important things to patients and their families.
As Greg Henry taught me (quoting Theodore Roosevelt) : ‘Nobody cares how much you know until they know how much you care’

John was gentle, kind, and humble. So many of his tributes remark on his compassion and dedication to patients.

6. Choose your colleagues & your environment well. Greater team cohesiveness is protective against burnout and compassion fatigue.
John was proud of the teamwork he enjoyed with his ICU colleagues, and worked with forward thinking colleagues who contribute significantly to #FOAMed.

7. Strive for balance in your life and your work. Consider part time working or mixing your critical care with a non-clinical or non-critical care interest.
John was revered and loved within the world of motorcycle racing, a passion he managed to combine with his flair for critical care.

8. Train your brain to be aware of and to utilise strategies that protect it against cognitive traps and avoidable performance limitations under stress – learn the hacks for your MINDWARE.
Many of us now introduce stressors into our simulation training to help us learn to deal with the adrenal load of a difficult resuscitation. But I doubt many of us can hope to achieve the intense focus and concentration under pressure that is required of motorcycle racers. John sent me a link to this video of racer Michael Dunlop a few weeks ago with the comment ‘How about this for a scare!’

9. Maintain perspective. It’s not all about you or your resus room.The most effective resuscitationists save lives when they’re not there. They work on the systems – the processes, the training, the governance, the audit, the research.
John was a brilliant educator and systems thinker. The care given at the roadside, in the ED, the ICU and the operating room at many sites is better because of the teaching he gave and the approaches he developed.

10. Understand that everything you say and do in a resuscitation casts memorable impressions in trainees’ minds like the tossing of pebbles into a pond, whose ripples reach out and out to affect so many future lives and deaths in other resuscitation rooms.
You can imagine the obstacles and personalities John faced when trying to improve care in the environments in which he worked. But through it all he remained a gentleman. Always constructive, always collaborative, always supportive. I’ve never heard him say a bad word about any named individual or criticise another specialty. He truly embodied the non-tribal spirit of SMACC, which sets an example for us all to aspire to, and will influence future resuscitation room behaviour in far-reaching locations.

11. Behave as you would want to be remembered, and be mindful of the extent of the ripples in the pond. But don’t let that put you off throwing the pebbles – embrace the challenge of the highs and lows and above all enjoy the ride, for it is awesome.
In just 35 years of life John saved the lives of many and changed the lives of many more. He knew how to throw pebbles and wasn’t afraid to point out the lack of emperor’s clothes around many traditional aspects of medical practice. And that smile seen in all the pictures of him shows there’s no doubt John enjoyed the ride, and it was awesome. Thanks to his wit, intelligence, teaching, charm, and resuscitation brilliance, he helped us enjoy it all the more too.

I spent a lot of time preparing my talk ‘Advice to a Young Resuscitationist’. It’s clear to me now that I needn’t have bothered. Sharing the stage with John, I could have saved everyone’s time by simply saying: ‘Try to be like THIS guy’.

I am extremely privileged to know him, to have learned from him, and to have shared some moments from his days at smaccUS.

We will mourn, we will remember, and we will honour him by being the best resuscitationists we can.

You can also honour him by signing the Northern Ireland Air Ambulance petition


Currently the RAGE Podcast site is recovering from a cold, so here are the show notes for the pre-SMACC mini RAGE episode released June 2015.

Here is the podcast

And here are the references:

SMACC Conference

It’s a knockout

GoodSAM App

Oxygen therapy

AVOID: Air Versus Oxygen in ST-Segment Elevation Myocardial Infarction.

HOT or NOT trial: HyperOxic Therapy OR NormOxic Therapy after out-of-hospital cardiac arrest (HOT OR NOT): a randomised controlled feasibility trial.

Helicopter Emergency Medical Services
Survival benefit of a physician-staffed HEMS assistance for severely injured patients

Willingness to pay for lives saved by HEMS

Intraosseous access
Intraosseous infusion rates under high pressure: a cadaveric comparison of anatomic sites.

Intraosseous hypertonic saline: myonecrosis in swine

Intraosseous hypertonic saline: safe in swine

Discussion post about intraosseous hypertonic saline at Sydney HEMS

Handstands: a treatment for supraventricular tachycardia?

Impact of a modified Valsalva manoeuvre in the termination of paroxysmal supraventricular tachycardia

Handstands keep you awake


The next RAGE Podcast will air late August / early September