Category Archives: Acute Med

Acute care of the medically sick adult

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.

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


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:


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, 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

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]

Esmolol for refractory VF

Already well publicised on social media, the team at Hennepin County published a retrospective comparison between patients with refractory VF who received esmolol with those who did not(1). The results are impressive and I look forward to further studies on this.

I work in an ED in a hospital with no cath lab and no access to extracorporeal life support, limiting our options for patients who remain in shockable rhythms despite ACLS interventions. We now have esmolol available in our resus room. You might want to keep it in your list of options for ACLS-refractory VF, which might also include double sequential external defibrillation(2) and even stellate ganglion block.

The dose of esmolol used was: loading dose 500 mcg/kg, followed by infusions of 0, 50, or 100 mcg/kg/min

An important point to note in the esmolol study is that almost all patients received high-quality mechanical CPR with the combined use of an impedence threshold device to augment venous return and cardiac output. The authors “speculate that this additional hemodynamic support may be essential given the hypotensive effects of esmolol.”

1. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation
Resuscitation. 2014 Oct;85(10):1337-41

INTRODUCTION: We compare the outcomes for patients who received esmolol to those who did not receive esmolol during refractory ventricular fibrillation (RVF) in the emergency department (ED).

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

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

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

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

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

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

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

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

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

Open cardiac massage in asthmatic arrests?

This idea was provoked by a colleague some years ago who could not achieve a palpable pulse during CPR of an arrested asthmatic child. He wondered whether the severe hyperinflation was rendering external cardiac compressions ineffective and whether he should have done a (prehospital) thoracotomy.

The literature is not strong. The 2010 AHA Guidelines rightly focus on reducing hyperinflation by disconnecting the tracheal tube from the ventilator circuit, and they mention ECMO for refractory cases, but there is no mention of open chest CPR.

I can only find two papers discussing it, both pretty old. A case series in the British Medical Journal from 1968 describes three patients with asthma who had asystolic arrests but did not achieve femoral pulses with external compressions(1). In two, open cardiac massage was performed resulting in restoration of sinus rhythm and cardiac output, and one appeared to make a neurological recovery.

A case report in 1987 describes a 32 year old man in asystolic cardiac arrest due to asthma(2):

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

He achieved ROSC and became haemodynamically stable but failed to wake up and treatment was withdrawn some days later.

Neither reports include mention of disconnection strategies to reduce hyperinflation. The lack of neurological recovery is not surprising given the apparent prolonged state of arrest the patients were resuscitated from. However there does appear to be a survivor who may not have made it had standard resuscitation (at the time) been continued.

Does this mean I would open the chest in an arrested asthma patient?
Not straight away, no. I would treat dynamic hyperinflation with tube disconnection and external compressions. I would correct absolute and relative hypovolaemia with crystalloid. I would treat bronchospasm (and possible anaphylaxis) with intravenous adrenaline/epinephrine. And I would exclude pneumothorax, possibly with ultrasound or more likely with bilateral open thoracostomies. If however these measures resulted in no detectable carotid flow with external cardiac compressions, ECMO was not available, and the arrest was not prolonged, I would definitely consider doing internal cardiac massage via thoracotomy.

What about you?

1. Grant IW, Kennedy WP, Malone DN
Deaths from asthma
Br Med J. 1968 May 18;2(5602):429–30

2. Diament RH, Sloan JP
Failed resuscitation in acute severe asthma: a medical indication for emergency thoracotomy?
Arch Emerg Med. 1987 Dec;4(4):233–5

London Cardiac Arrest Symposium 2014

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

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

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

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

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

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


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


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


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


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

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

Happy Holidays & Keep Well

Louisa Chan