By 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.
Tag Archives: critical care
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
Breaking with tradition in paediatric RSI
‘Traditional’ rapid sequence induction of anaesthesia is often described with inclusion of cricoid pressure and the strict omission of any artifical ventilation between paralytic drug administration and insertion of the tracheal tube. These measures are aimed at preventing pulmonary aspiration of gastric contents although there is no convincing evidence base to support that. However it is known that cricoid pressure can worsen laryngoscopic view and can occlude the paediatric airway. We also know that children desaturate quickly after the onset of apnoea, and although apnoeic diffusion oxygenation via nasal cannula can prevent or delay that, in some cases it may be preferable to bag-mask ventilate the patient while awaiting full muscle relaxation for laryngoscopy.
A Swiss study looked at 1001 children undergoing RSI for non-cardiac surgery. They used a ‘controlled rapid sequence induction and intubation (cRSII)’ approach for children assumed to have full stomachs. This procedure resembled RSI the way it is currently done in many modern critical care settings, including the retrieval service I work for:
- No cricoid pressure
- Ketamine for induction if haemodynamically unstable
- A non-depolarising neuromuscular blocker rather than succinylcholine
- No cricoid pressure
- Gentle facemask ventilation to maintain oxygenation until intubation conditions achieved
- Intubation with a cuffed tracheal tube
- Still no cricoid pressure
The authors comment:
The main finding was that cRSII demonstrated a considerably lower incidence of oxygen desaturation and consecutive hemodynamic adverse events during anesthesia induction than shown by a previous study on classic RSII in children. Furthermore, there was no incidence of pulmonary aspiration during induction, laryngoscopy, and further course of anesthesia.
Looks like more dogma has been lysed, and this study supports the current trajectory away from traditional teaching towards an approach more suitable for critically ill patients.
Controlled rapid sequence induction and intubation – an analysis of 1001 children
Paediatr Anaesth. 2013 Aug;23(8):734-40
[EXPAND Abstract]
BACKGROUND: Classic rapid sequence induction puts pediatric patients at risk of cardiorespiratory deterioration and traumatic intubation due to their reduced apnea tolerance and related shortened intubation time. A ‘controlled’ rapid sequence induction and intubation technique (cRSII) with gentle facemask ventilation prior to intubation may be a safer and more appropriate approach in pediatric patients. The aim of this study was to analyze the benefits and complications of cRSII in a large cohort.
METHODS: Retrospective cohort analysis of all patients undergoing cRSII according to a standardized institutional protocol between 2007 and 2011 in a tertiary pediatric hospital. By means of an electronic patient data management system, vital sign data were reviewed for cardiorespiratory parameters, intubation conditions, general adverse respiratory events, and general anesthesia parameters.
RESULTS: A total of 1001 patients with cRSII were analyzed. Moderate hypoxemia (SpO2 80-89%) during cRSII occurred in 0.5% (n = 5) and severe hypoxemia (SpO2 <80%) in 0.3% of patients (n = 3). None of these patients developed bradycardia or hypotension. Overall, one single gastric regurgitation was observed (0.1%), but no pulmonary aspiration could be detected. Intubation was documented as ‘difficult’ in two patients with expected (0.2%) and in three patients with unexpected difficult intubation (0.3%). The further course of anesthesia as well as respiratory conditions after extubation did not reveal evidence of ‘silent aspiration’ during cRSII.
CONCLUSION: Controlled RSII with gentle facemask ventilation prior to intubation supports stable cardiorespiratory conditions for securing the airway in children with an expected or suspected full stomach. Pulmonary aspiration does not seem to be significantly increased.
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Atropine for Paediatric RSI?
In some areas it has been traditional to pre-medicate or co-medicate with atropine when intubating infants and children, despite a lack of any evidence showing benefit. It is apparently still in the American Pediatric Advanced Life Support (PALS) Provider Manual when age is less than 1 year or age is 1–5 years and receiving succinylcholine. However it is not recommended with rapid sequence intubation in the British and Australasian Advanced Paediatric Life Support manual and course.
A French non-randomised observational study compares intubations with and without atropine in the neonatal and paediatric critical care setting. Atropine use was associated with significant acceleration of heart rate, and no atropine use was associated with a higher incidence of new dysrhythmia, the most common being junctional rhythm, but with none appearing to be clinically significant.
The incidence of the most important peri-intubation cause of bradycardia – hypoxia – is not reported. It is also not clear how many intubation attempts were required. The authors admit:
“it is not possible using our methodology to deduce whether bradycardia was due to hypoxia, laryngoscopy, or sedation drugs.”
Actual rapid sequence was rarely employed – their use of muscle relaxants was low – making this difficult to extrapolate to modern emergency medicine / critical care practice.
My take home message here is that this study provides no argument whatsoever for the addition of atropine in routine RSI in the critically ill child. Why complicate a procedure with an unnecessary tachycardia-causing drug when the focus should be on no desat / no hypotension / first look laryngoscopy?
The Effect of Atropine on Rhythm and Conduction Disturbances During 322 Critical Care Intubations
Pediatr Crit Care Med. 2013 Jul;14(6):e289-97
[EXPAND Abstract]
OBJECTIVES: Our objectives were to describe the prevalence of arrhythmia and conduction abnormalities before critical care intubation and to test the hypothesis that atropine had no effect on their prevalence during intubation.
DESIGN: Prospective, observational study.
SETTING: PICU and pediatric/neonatal intensive care transport.
SUBJECTS: All children of age less than 8 years intubated September 2007-2009. Subgroups of intubations with and without atropine were analyzed.
INTERVENTION: None.
MEASUREMENT AND MAIN RESULTS: A total of 414 intubations were performed in the study period of which 327 were available for analysis (79%). Five children (1.5%) had arrhythmias prior to intubation and were excluded from the atropine analysis. Atropine was used in 47% (152/322) of intubations and resulted in significant acceleration of heart rate without provoking ventricular arrhythmias. New arrhythmias during intubation were related to bradycardia and were less common with atropine use (odds ratio, 0.14 [95% CI, 0.06-0.35], p < 0.001). The most common new arrhythmia was junctional rhythm. Acute bundle branch block was observed during three intubations; one Mobitz type 2 rhythm and five ventricular escape rhythms occurred in the no-atropine group (n = 170). Only one ventricular escape rhythm occurred in the atropine group (n = 152) in a child with an abnormal heart. One child died during intubation who had not received atropine.
CONCLUSIONS: Atropine significantly reduced the prevalence of new arrhythmias during intubation particularly for children over 1 month of age, did not convert sinus tachycardia to ventricular tachycardia or fibrillation, and may contribute to the safety of intubation.
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Blood pressure target in septic shock
A study comparing mean arterial pressure (MAP) targets of 80 to 85 mm Hg (high-target group) with 65 to 70 mm Hg (low-target group) n 776 septic shock patients – the SEPSISPAM study – did not show a difference in the primary endpoint of 28 day mortality. Among patients with chronic hypertension, those in the high-target group required less renal-replacement therapy than did those in the low-target group. In my view this supports an approach that targets MAP based on the individual patient’s history rather than a blanket one-number-fits-all approach. The MAPs actually achieved in the low-target group were between 70-75 mm of Hg.
For a more thorough review check out the great PulmCCM blog.
High versus Low Blood-Pressure Target in Patients with Septic Shock.
N Engl J Med. 2014 Mar 18. [Epub ahead of print] Free Full Text
[EXPAND Abstract]
Background: The Surviving Sepsis Campaign recommends targeting a mean arterial pressure of at least 65 mm Hg during initial resuscitation of patients with septic shock. However, whether this blood-pressure target is more or less effective than a higher target is unknown.
Methods: In 31 emergency departments in the United States, we randomly assigned patients with septic shock to one of three groups for 6 hours of resuscitation: protocol-based EGDT; protocol-based standard therapy that did not require the placement of a central venous catheter, administration of inotropes, or blood transfusions; or usual care. The primary end point was 60-day in-hospital mortality. We tested sequentially whether protocol-based care (EGDT and standard-therapy groups combined) was superior to usual care and whether protocol-based EGDT was superior to protocol-based standard therapy. Secondary outcomes included longer-term mortality and the need for organ support.
Results: At 28 days, there was no significant between-group difference in mortality, with deaths reported in 142 of 388 patients in the high-target group (36.6%) and 132 of 388 patients in the low-target group (34.0%) (hazard ratio in the high-target group, 1.07; 95% confidence interval [CI], 0.84 to 1.38; P=0.57). There was also no significant difference in mortality at 90 days, with 170 deaths (43.8%) and 164 deaths (42.3%), respectively (hazard ratio, 1.04; 95% CI, 0.83 to 1.30; P=0.74). The occurrence of serious adverse events did not differ significantly between the two groups (74 events [19.1%] and 69 events [17.8%], respectively; P=0.64). However, the incidence of newly diagnosed atrial fibrillation was higher in the high-target group than in the low-target group. Among patients with chronic hypertension, those in the high-target group required less renal-replacement therapy than did those in the low-target group, but such therapy was not associated with a difference in mortality.
Conclusions: Targeting a mean arterial pressure of 80 to 85 mm Hg, as compared with 65 to 70 mm Hg, in patients with septic shock undergoing resuscitation did not result in significant differences in mortality at either 28 or 90 days.
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No Benefit From Early Goal Directed Therapy
The first of three major trials assessing early goal directed therapy (EGDT) in sepsis – the American ProCESS Trial – has been published.
It showed what many of us thought – that the specific monitoring via a central line of central venous oxygen saturation – was not necessary for improved survival.
However the trial randomised 1341 patients to one of three arms:
(1) protocolised EGDT
(2) protocol-based standard therapy that did not require the placement of a central venous catheter, administration of inotropes, or blood transfusions
(3) ‘usual care’ which was not standardised.
There were no differences in any of the primary or secondary outcomes between the groups.
Interestingly, in the six hours of early care that the trial dictated, the volume of intravenous fluids administered differed significantly among the groups (2.8 litres in the protocol-based EGDT group, 3.3 litres in the protocol-based standard-therapy group, and 2.3 litres in the usual-care group).
There was also a difference in the amount of vasopressor given, with more patients in the two protocol-based groups receiving vasopressors (54.9% in the protocol-based EGDT group, 52.2% in the protocol-based standard-therapy group, 44.1% in the usual-care group).
The use of intravenous fluids, vasopressors, dobutamine, and blood transfusions between 6 and 72 hours did not differ significantly among the groups.
Overall 60 day mortality was in the region of 20% for all groups.
What are the take home points here? Firstly, overall sepsis outcomes have improved over recent years, and early recognition and antibiotic administration may be the most important components of care. In the early emergency department phase of care, protocolised fluid and vasopressor therapy may not be as important as we thought. Good clinical assessment and regular review seem to be as effective and perhaps more important than any specific monitoring modality or oxygen delivery-targeted drug and blood therapy.
We all await the ARISE and ProMISE studies which may shed more light on the most important components of early sepsis care.
A Randomized Trial of Protocol-Based Care for Early Septic Shock
NEJM Mar 18 2014 (Full Text Link)
[EXPAND Abstract]
Background: In a single-center study published more than a decade ago involving patients presenting to the emergency department with severe sepsis and septic shock, mortality was markedly lower among those who were treated according to a 6-hour protocol of early goal-directed therapy (EGDT), in which intravenous fluids, vasopressors, inotropes, and blood transfusions were adjusted to reach central hemodynamic targets, than among those receiving usual care. We conducted a trial to determine whether these findings were generalizable and whether all aspects of the protocol were necessary.
Methods: In 31 emergency departments in the United States, we randomly assigned patients with septic shock to one of three groups for 6 hours of resuscitation: protocol-based EGDT; protocol-based standard therapy that did not require the placement of a central venous catheter, administration of inotropes, or blood transfusions; or usual care. The primary end point was 60-day in-hospital mortality. We tested sequentially whether protocol-based care (EGDT and standard-therapy groups combined) was superior to usual care and whether protocol-based EGDT was superior to protocol-based standard therapy. Secondary outcomes included longer-term mortality and the need for organ support.
Results: We enrolled 1341 patients, of whom 439 were randomly assigned to protocol-based EGDT, 446 to protocol-based standard therapy, and 456 to usual care. Resuscitation strategies differed significantly with respect to the monitoring of central venous pressure and oxygen and the use of intravenous fluids, vasopressors, inotropes, and blood transfusions. By 60 days, there were 92 deaths in the protocol-based EGDT group (21.0%), 81 in the protocol-based standard-therapy group (18.2%), and 86 in the usual-care group (18.9%) (relative risk with protocol-based therapy vs. usual care, 1.04; 95% confidence interval [CI], 0.82 to 1.31; P=0.83; relative risk with protocol-based EGDT vs. protocol-based standard therapy, 1.15; 95% CI, 0.88 to 1.51; P=0.31). There were no significant differences in 90-day mortality, 1-year mortality, or the need for organ support.
Conclusions: In a multicenter trial conducted in the tertiary care setting, protocol-based resuscitation of patients in whom septic shock was diagnosed in the emergency department did not improve outcomes
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Therapeutic hypothermia does not improve arrest outcome
A paper published today represents to me what’s great about science.
I am impressed with those investigators who had the wherewithall to subject previous therapeutic hypothermia studies to skeptical scrutiny and then design and conduct a robust multicentre trial to answer the question.
One of the criticisms of the original two studies was that those patients who were not actively cooled did not have their temperature tightly controlled, and therefore some were allowed to become hypERthermic, which is bad for brains.
This latest study showed no difference in survival or neurological outcome after cardiac arrest between target temperatures of 33°C and 36°C.
So controlling the temperature after cardiac arrest is still important, but cooling down to the recommended range of 32-4°C is not.
Cool.
Read the full study at the NEJM site.
Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest
NEJM November 17, 2013 Full text
[EXPAND Abstract]
BACKGROUND Unconscious survivors of out-of-hospital cardiac arrest have a high risk of death or poor neurologic function. Therapeutic hypothermia is recommended by international guidelines, but the supporting evidence is limited, and the target temperature associated with the best outcome is unknown. Our objective was to compare two target temperatures, both intended to prevent fever.
METHODS In an international trial, we randomly assigned 950 unconscious adults after out-of-hospital cardiac arrest of presumed cardiac cause to targeted temperature management at either 33°C or 36°C. The primary outcome was all-cause mortality through the end of the trial. Secondary outcomes included a composite of poor neurologic function or death at 180 days, as evaluated with the Cerebral Performance Category (CPC) scale and the modified Rankin scale.
RESULTS In total, 939 patients were included in the primary analysis. At the end of the trial, 50% of the patients in the 33°C group (235 of 473 patients) had died, as compared with 48% of the patients in the 36°C group (225 of 466 patients) (hazard ratio with a temperature of 33°C, 1.06; 95% confidence interval [CI], 0.89 to 1.28; P=0.51). At the 180-day follow-up, 54% of the patients in the 33°C group had died or had poor neurologic function according to the CPC, as compared with 52% of patients in the 36°C group (risk ratio, 1.02; 95% CI, 0.88 to 1.16; P=0.78). In the analysis using the modified Rankin scale, the comparable rate was 52% in both groups (risk ratio, 1.01; 95% CI, 0.89 to 1.14; P=0.87). The results of analyses adjusted for known prognostic factors were similar.
CONCLUSIONS In unconscious survivors of out-of-hospital cardiac arrest of presumed cardiac cause, hypothermia at a targeted temperature of 33°C did not confer a benefit as compared with a targeted temperature of 36°C.
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Double balloon pump fail
Two recent trials question the ongoing use of intra-aortic balloon pumps: in patients with acute myocardial infarction with cardiogenic shock undergoing revascularisation(1), and patients with poor left ventricular function undergoing coronary artery bypass surgery(2).
Editorialists Krischan D Sjauw and Jan J Piek from the Netherlands make the following commentary(3) in reference to one of the studies:
Although the results of IABP-SHOCK II question the usefulness of IABP therapy in cardiogenic shock, there still might be an indication for initial stabilisation of severely compromised patients, especially in centres without facilities for early revascularisation, as an adjunct to thrombolytic therapy, or to allow transport to specialised tertiary centres.
So retrieval specialists like me may still be up in the night transferring patients with balloon pumps, but these studies suggest this should be restricted to those with cardiogenic shock pending corrective therapy (eg. revascularisation for AMI or surgery for acute mitral valvular dysfunction). Unless the ECMO team gets to them first, of course.
1. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial
The Lancet, Volume 382, Issue 9905, Pages 1638 – 1645
[EXPAND Abstract]
BACKGROUND: In current international guidelines the recommendation for intra-aortic balloon pump (IABP) use has been downgraded in cardiogenic shock complicating acute myocardial infarction on the basis of registry data. In the largest randomised trial (IABP-SHOCK II), IABP support did not reduce 30 day mortality compared with control. However, previous trials in cardiogenic shock showed a mortality benefit only at extended follow-up. The present analysis therefore reports 6 and 12 month results.
METHODS: The IABP-SHOCK II trial was a randomised, open-label, multicentre trial. Patients with cardiogenic shock complicating acute myocardial infarction who were undergoing early revascularisation and optimum medical therapy were randomly assigned (1:1) to IABP versus control via a central web-based system. The primary efficacy endpoint was 30 day all-cause mortality, but 6 and 12 month follow-up was done in addition to quality-of-life assessment for all survivors with the Euroqol-5D questionnaire. A masked central committee adjudicated clinical outcomes. Patients and investigators were not masked to treatment allocation. Analysis was by intention to treat. This trial is registered at ClinicalTrials.gov, NCT00491036.
FINDINGS: Between June 16, 2009, and March 3, 2012, 600 patients were assigned to IABP (n=301) or control (n=299). Of 595 patients completing 12 month follow-up, 155 (52%) of 299 patients in the IABP group and 152 (51%) of 296 patients in the control group had died (relative risk [RR] 1·01, 95% CI 0·86-1·18, p=0·91). There were no significant differences in reinfarction (RR 2·60, 95% CI 0·95-7·10, p=0·05), recurrent revascularisation (0·91, 0·58-1·41, p=0·77), or stroke (1·50, 0·25-8·84, p=1·00). For survivors, quality-of-life measures including mobility, self-care, usual activities, pain or discomfort, and anxiety or depression did not differ significantly between study groups.
INTERPRETATION: In patients undergoing early revascularisation for myocardial infarction complicated by cardiogenic shock, IABP did not reduce 12 month all-cause mortality.
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2. A Randomized Controlled Trial of Preoperative Intra-Aortic Balloon Pump in Coronary Patients With Poor Left Ventricular Function Undergoing Coronary Artery Bypass Surgery
Crit Care Med. 2013 Nov;41(11):2476-83
[EXPAND Abstract]
BACKGROUND: Preoperative intra-aortic balloon pump use in high-risk patients undergoing surgical coronary revascularization is still a matter of debate. The objective of this study is to determine whether the preoperative use of an intra-aortic balloon pump improves the outcome after coronary operations in high-risk patients.
DESIGN: Single-center prospective randomized controlled trial.
SETTING: Tertiary cardiac surgery center, research hospital.
PATIENTS: One hundred ten subjects undergoing coronary operations, with a poor left ventricular ejection fraction (< 35%) and no hemodynamic instability.
INTERVENTIONS:
Patients randomized to receive preincision intra-aortic balloon pump or no intervention.
MEASUREMENTS AND MAIN RESULTS: The primary outcome measurement was postoperative major morbidity rate, defined as one of prolonged mechanical ventilation, stroke, acute kidney injury, surgical revision, mediastinitis, and operative mortality. There was no difference in major morbidity rate (40% in intra-aortic balloon pump group and 31% in control group; odds ratio, 1.49 [95% CI, 0.68-3.33]). No differences were observed for cardiac index before and after the operation; at the arrival in the ICU, patients in the intra-aortic balloon pump group had a significantly (p = 0.01) lower mean systemic arterial pressure (80.1 ± 15.1 mm Hg) versus control group patients (89.2 ± 17.9 mm Hg). Fewer patients in the intra-aortic balloon pump group (24%) than those in the control group (44%) required dopamine infusion (p = 0.043).
CONCLUSIONS: This study demonstrates that in patients undergoing nonemergent coronary operations, with a stable hemodynamic profile and a left ventricular ejection fraction less than 35%, the preincision insertion of intra-aortic balloon pump does not result in a better outcome. Given the possible complications of intra-aortic balloon pump insertion, and the additional cost of the procedure, this approach is not justified.
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3. Is the intra-aortic balloon pump leaking?
Lancet 2013;382:1616-7
Beta blockers potentially beneficial in septic shock
Counterintuitive as it sounds, this is pretty cool. I blogged about these guys before when they published their findings on microcirculatory flow in septic patients given beta blockers.
It’s a small study – 77 patients with septic shock and a heart rate of 95/min or higher requiring high-dose norepinephrine to maintain a mean arterial pressure of at least 65 mm Hg were randomised to receive a continuous infusion of esmolol titrated to maintain heart rate between 80/min and 94/min for their ICU stay. 77 patients received standard treatment. It should be noted the primary outcome (target heart rate) was not a patient-oriented endpoint. Interestingly though, there were no increased adverse events in the beta blocker group, which demonstrated improved left ventricular stroke work, lower lactate levels, decreased noradrenaline and fluid requirements, improved oxygenation, and a lower mortality.
Caution is appropriate here though: this study was a small, single-centre open-label trial. It will be very interesting to see if these effects are reproduced and whether they will ultimately translate to meaningful outcome benefits.
Read more about the study at the PulmCCM site.
There is also a great critical appraisal of the study at Emergency Medicine Literature of Note/a>.
Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock: a randomized clinical trial
JAMA. 2013 Oct 23;310(16):1683-91
[EXPAND Abstract]
IMPORTANCE: β-Blocker therapy may control heart rate and attenuate the deleterious effects of β-adrenergic receptor stimulation in septic shock. However, β-Blockers are not traditionally used for this condition and may worsen cardiovascular decompensation related through negative inotropic and hypotensive effects.
OBJECTIVE: To investigate the effect of the short-acting β-blocker esmolol in patients with severe septic shock.
DESIGN, SETTING, AND PATIENTS: Open-label, randomized phase 2 study, conducted in a university hospital intensive care unit (ICU) between November 2010 and July 2012, involving patients in septic shock with a heart rate of 95/min or higher requiring high-dose norepinephrine to maintain a mean arterial pressure of 65 mm Hg or higher.
INTERVENTIONS: We randomly assigned 77 patients to receive a continuous infusion of esmolol titrated to maintain heart rate between 80/min and 94/min for their ICU stay and 77 patients to standard treatment.
MAIN OUTCOMES AND MEASURES: Our primary outcome was a reduction in heart rate below the predefined threshold of 95/min and to maintain heart rate between 80/min and 94/min by esmolol treatment over a 96-hour period. Secondary outcomes included hemodynamic and organ function measures; norepinephrine dosages at 24, 48, 72, and 96 hours; and adverse events and mortality occurring within 28 days after randomization.
RESULTS: Targeted heart rates were achieved in all patients in the esmolol group compared with those in the control group. The median AUC for heart rate during the first 96 hours was -28/min (IQR, -37 to -21) for the esmolol group vs -6/min (95% CI, -14 to 0) for the control group with a mean reduction of 18/min (P < .001). For stroke volume index, the median AUC for esmolol was 4 mL/m2 (IQR, -1 to 10) vs 1 mL/m2 for the control group (IQR, -3 to 5; P = .02), whereas the left ventricular stroke work index for esmolol was 3 mL/m2 (IQR, 0 to 8) vs 1 mL/m2 for the control group (IQR, -2 to 5; P = .03). For arterial lactatemia, median AUC for esmolol was -0.1 mmol/L (IQR, -0.6 to 0.2) vs 0.1 mmol/L for the control group (IQR, -0.3 for 0.6; P = .007); for norepinephrine, -0.11 μg/kg/min (IQR, -0.46 to 0.02) for the esmolol group vs -0.01 μg/kg/min (IQR, -0.2 to 0.44) for the control group (P = .003). Fluid requirements were reduced in the esmolol group: median AUC was 3975 mL/24 h (IQR, 3663 to 4200) vs 4425 mL/24 h(IQR, 4038 to 4775) for the control group (P < .001). We found no clinically relevant differences between groups in other cardiopulmonary variables nor in rescue therapy requirements. Twenty-eight day mortality was 49.4% in the esmolol group vs 80.5% in the control group (adjusted hazard ratio, 0.39; 95% CI, 0.26 to 0.59; P < .001).
CONCLUSIONS AND RELEVANCE: For patients in septic shock, open-label use of esmolol vs standard care was associated with reductions in heart rates to achieve target levels, without increased adverse events. The observed improvement in mortality and other secondary clinical outcomes warrants further investigation.
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Colloids again: still no benefit.
It’s nice to have big randomised trials to guide critical care practice. The age-old crystalloid/colloid debate (is that still going?) has fueled a multicentre and multinational study in 2857 patients with hypovolaemic shock on intensive care units. Patients were classified as having sepsis, trauma, or other causes of hypovolaemic shock.
In the crystalloids group, allowed treatments included isotonic or hypertonic saline and any buffered solutions. In the colloids group, gelatins, albumin from 4-25%, dextrans, and hydroxyethyl starches were permitted.
The primary outcome of 28 day mortality was no different between groups. The study had an open-label design and recruitment took place over nine years.
This finding – no clinical benefit from colloids in critically ill patients – is in keeping with other major ICU trials of colloid therapy: Saline versus Albumin Fluid Evaluation (SAFE), Efficacy of Volume Substitution and Insulin Therapy in Severe Sepsis (VISEP), Scandinavian Starch for Severe Sepsis/Septic Shock (6S), and the Crystalloid versus Hydroxyethyl Starch Trial (CHEST).
Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: the CRISTAL randomized trial
JAMA. 2013 Nov 6;310(17):1809-17
[EXPAND Abstract]
IMPORTANCE: Evidence supporting the choice of intravenous colloid vs crystalloid solutions for management of hypovolemic shock remains unclear.
OBJECTIVE: To test whether use of colloids compared with crystalloids for fluid resuscitation alters mortality in patients admitted to the intensive care unit (ICU) with hypovolemic shock.
DESIGN, SETTING, AND PARTICIPANTS: A multicenter, randomized clinical trial stratified by case mix (sepsis, trauma, or hypovolemic shock without sepsis or trauma). Therapy in the Colloids Versus Crystalloids for the Resuscitation of the Critically Ill (CRISTAL) trial was open label but outcome assessment was blinded to treatment assignment. Recruitment began in February 2003 and ended in August 2012 of 2857 sequential ICU patients treated at 57 ICUs in France, Belgium, North Africa, and Canada; follow-up ended in November 2012.
INTERVENTIONS: Colloids (n = 1414; gelatins, dextrans, hydroxyethyl starches, or 4% or 20% of albumin) or crystalloids (n = 1443; isotonic or hypertonic saline or Ringer lactate solution) for all fluid interventions other than fluid maintenance throughout the ICU stay.
MAIN OUTCOMES AND MEASURES: The primary outcome was death within 28 days. Secondary outcomes included 90-day mortality; and days alive and not receiving renal replacement therapy, mechanical ventilation, or vasopressor therapy.
RESULTS: Within 28 days, there were 359 deaths (25.4%) in colloids group vs 390 deaths (27.0%) in crystalloids group (relative risk [RR], 0.96 [95% CI, 0.88 to 1.04]; P = .26). Within 90 days, there were 434 deaths (30.7%) in colloids group vs 493 deaths (34.2%) in crystalloids group (RR, 0.92 [95% CI, 0.86 to 0.99]; P = .03). Renal replacement therapy was used in 156 (11.0%) in colloids group vs 181 (12.5%) in crystalloids group (RR, 0.93 [95% CI, 0.83 to 1.03]; P = .19). There were more days alive without mechanical ventilation in the colloids group vs the crystalloids group by 7 days (mean: 2.1 vs 1.8 days, respectively; mean difference, 0.30 [95% CI, 0.09 to 0.48] days; P = .01) and by 28 days (mean: 14.6 vs 13.5 days; mean difference, 1.10 [95% CI, 0.14 to 2.06] days; P = .01) and alive without vasopressor therapy by 7 days (mean: 5.0 vs 4.7 days; mean difference, 0.30 [95% CI, -0.03 to 0.50] days; P = .04) and by 28 days (mean: 16.2 vs 15.2 days; mean difference, 1.04 [95% CI, -0.04 to 2.10] days; P = .03).
CONCLUSIONS AND RELEVANCE: Among ICU patients with hypovolemia, the use of colloids vs crystalloids did not result in a significant difference in 28-day mortality. Although 90-day mortality was lower among patients receiving colloids, this finding should be considered exploratory and requires further study before reaching conclusions about efficacy.
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