Tag Archives: critical care

Avoiding intubation in ARDS with awake ECMO

ECMOillusiconA letter in Intensive Care Medicine by Hoeper and colleagues from Hannover describes a small case series of six ARDS patients with severe hypoxaemia who went straight from non-invasive ventilation to awake veno-venous ECMO. All had single organ failure and four were immunocompromised, the latter factor influencing the decision to try to avoid invasive mechanical ventilation. Four of the six patients survived to hospital discharge. A larger multicentre study is being planned.

Clinical illustration courtesy of Dr Brian Burns

Extracorporeal membrane oxygenation instead of invasive mechanical ventilation in patients with acute respiratory distress syndrome
Intensive Care Med. 2013 Nov;39(11):2056-2057 (no abstract)

GOLDen Educational Opportunity!



SMACC was my all-time favourite conference ever. Its sequel, smaccGOLD, promises to be even better, as you’ll see from the program

The smaccGOLD online registration goes live this Monday 16th September at 8am in Sydney

This will be 11pm Sunday 15th in London, and 6pm Sunday 15th in New York

Make sure you don’t miss your chance to register for the best critical care conference ever!

Also check out the preconference workshops – a jawdropping line-up of medical masters covering everything you’d want to learn. The only difficult part is deciding what you won’t go to! Places are limited and expected will sell out quickly. Registration is on a first come basis.

Hopefully we’ll see you there.

smaccGOLD is a not-for-profit venture and I receive no payment for any participation in the conference or its promotion

Xenon – no bull?

Xenon, an inert ‘noble’ gas with proven anaesthetic properties, has possible neuroprotective properties and appears to be also cardioprotective in this small study of post-cardiac arrest patients. Its high viscosity affects airway resistance, resulting in higher peak pressures and the need for a strategy to avoid gas trapping (ie. longer expiratory times as with asthma). Apparently it’s expensive, but these results suggest further study is warranted.

Feasibility and Cardiac Safety of Inhaled Xenon in Combination With Therapeutic Hypothermia Following Out-of-Hospital Cardiac Arrest
Crit Care Med. 2013 Sep;41(9):2116-24

OBJECTIVES: Preclinical studies reveal the neuroprotective properties of xenon, especially when combined with hypothermia. The purpose of this study was to investigate the feasibility and cardiac safety of inhaled xenon treatment combined with therapeutic hypothermia in out-of-hospital cardiac arrest patients.

DESIGN: An open controlled and randomized single-centre clinical drug trial (clinicaltrials.gov NCT00879892).

SETTING: A multipurpose ICU in university hospital.

PATIENTS: Thirty-six adult out-of-hospital cardiac arrest patients (18-80 years old) with ventricular fibrillation or pulseless ventricular tachycardia as initial cardiac rhythm.

INTERVENTIONS: Patients were randomly assigned to receive either mild therapeutic hypothermia treatment with target temperature of 33°C (mild therapeutic hypothermia group, n = 18) alone or in combination with xenon by inhalation, to achieve a target concentration of at least 40% (Xenon + mild therapeutic hypothermia group, n = 18) for 24 hours. Thirty-three patients were evaluable (mild therapeutic hypothermia group, n = 17; Xenon + mild therapeutic hypothermia group, n = 16).

MEASUREMENTS AND MAIN RESULTS: Patients were treated and monitored according to the Utstein protocol. The release of troponin-T was determined at arrival to hospital and at 24, 48, and 72 hours after out-of-hospital cardiac arrest. The median end-tidal xenon concentration was 47% and duration of the xenon inhalation was 25.5 hours. The frequency of serious adverse events, including inhospital mortality, status epilepticus, and acute kidney injury, was similar in both groups and there were no unexpected serious adverse reactions to xenon during hospital stay. In addition, xenon did not induce significant conduction, repolarization, or rhythm abnormalities. Median dose of norepinephrine during hypothermia was lower in xenon-treated patients (mild therapeutic hypothermia group = 5.30 mg vs Xenon + mild therapeutic hypothermia group = 2.95 mg, p = 0.06). Heart rate was significantly lower in Xenon + mild therapeutic hypothermia patients during hypothermia (p = 0.04). Postarrival incremental change in troponin-T at 72 hours was significantly less in the Xenon + mild therapeutic hypothermia group (p = 0.04).

CONCLUSIONS: Xenon treatment in combination with hypothermia is feasible and has favorable cardiac features in survivors of out-of-hospital cardiac arrest.

TracMan results

The TracMan trial – a multicentre randomised trial of early vs late tracheostomy in ICU patients – has been published, showing no difference in the primary outcome of mortality.

A review of the trial is posted on the excellent PulmCCM blog:

There was no proven difference between groups in 30-day mortality (30.8% early vs. 31.5% late, primary outcome), nor in any other outcome including 2-year mortality.

Patients getting early tracheostomies required fewer days of sedation, and there was a suggestion of a reduction of -1.7 ventilator days with early trach (mean 13.6 days vs 15.2 days, p=0.06). However, ICU stays were exactly equal at a median 13 days.

Also, 7% of patients had significant bleeding attributed to their tracheostomies (defined as needing IV fluids or another intervention); this amounted to 11 patients in the early group and 8 in the late group.

PulmCCM is an excellent free resource that will deliver critical care updates to your inbox. It has a number of other useful features, like free board review questions – highly recommended!

Effect of early vs late tracheostomy placement on survival in patients receiving mechanical ventilation: the TracMan randomized trial
JAMA. 2013 May 22;309(20):2121-9

IMPORTANCE: Tracheostomy is a widely used intervention in adult critical care units. There is little evidence to guide clinicians regarding the optimal timing for this procedure.

OBJECTIVE: To test whether early vs late tracheostomy would be associated with lower mortality in adult patients requiring mechanical ventilation in critical care units.

DESIGN AND SETTING: An open multicentered randomized clinical trial conducted between 2004 and 2011 involving 70 adult general and 2 cardiothoracic critical care units in 13 university and 59 nonuniversity hospitals in the United Kingdom.

PARTICIPANTS: Of 1032 eligible patients, 909 adult patients breathing with the aid of mechanical ventilation for less than 4 days and identified by the treating physician as likely to require at least 7 more days of mechanical ventilation.

INTERVENTIONS: Patients were randomized 1:1 to early tracheostomy (within 4 days) or late tracheostomy (after 10 days if still indicated).

MAIN OUTCOMES AND MEASURES: The primary outcome measure was 30-day mortality and the analysis was by intention to treat.

RESULTS: Of the 455 patients assigned to early tracheostomy, 91.9% (95% CI, 89.0%-94.1%) received a tracheostomy and of 454 assigned to late tracheostomy, 44.9% (95% CI, 40.4%-49.5%) received a tracheostomy. All-cause mortality 30 days after randomization was 30.8% (95% CI, 26.7%-35.2%) in the early and 31.5% (95% CI, 27.3%-35.9%) in the late group (absolute risk reduction for early vs late, 0.7%; 95% CI, -5.4% to 6.7%). Two-year mortality was 51.0% (95% CI, 46.4%-55.6%) in the early and 53.7% (95% CI, 49.1%-58.3%) in the late group (P = .74). Median critical care unit length of stay in survivors was 13.0 days in the early and 13.1 days in the late group (P = .74). Tracheostomy-related complications were reported for 6.3% (95% CI, 4.6%-8.5%) of patients (5.5% in the early group, 7.8% in the late group).

CONCLUSIONS AND RELEVANCE: For patients breathing with the aid of mechanical ventilation treated in adult critical care units in the United Kingdom, tracheostomy within 4 days of critical care admission was not associated with an improvement in 30-day mortality or other important secondary outcomes. The ability of clinicians to predict which patients required extended ventilatory support was limited.

The non-intubation checklist



A 79 year old previously well female presents with loss of consciousness, having been found unresponsive by her daughter who saw her well one hour previously.

Examination reveals a GCS of E1V2M3 = 6 and reactive pupils with no lateralising signs. She is hypertensive. A VBG reveals a normal glucose and sodium and a pCO2 of 60 mmHg (7.9 kPa).

The emergency physician’s plan is to intubate and get a CT scan of her brain. This is explained to the daughter.

A no-brainer? You’d think so.

A consistent issue that recurs during discussions with UK emergency medicine colleagues is that of having to rely on anaesthesia and/or ICU colleagues for intubation of their patients in the ED. The pain comes not from disagreeing about who does the procedure or what drugs to use, but rather on the decision to intubate.

The refusal to intubate can stall or halt a resuscitation plan, delay care, result in risky transfers to the imaging suite, and even deny potential outcome-improving therapy (for example post-ROSC cooling). It can undermine team leadership and disrupt the team dynamic.

There are often different ways to ‘skin a cat’ and it is frequently helpful to invite the opinion of other critical care specialists. However, it is clear from multiple discussions with frustrated EM colleagues that the decision not to intubate is often influenced by non-clinical factors, most often ICU bed availability. Other times, it appears to be that the ‘gatekeeper’ to airway care (and to ICU beds) does not share the same appreciation of the clinical issues at stake. Examples here include the self-fulfilling pessimism post-ROSC based on inappropriate assignment of predictive value to neurological signs, and the assumption of non-treatable pathology in elderly patients presenting with coma.

The obvious solution to this is that the responsibility for managing the ‘A’ of ABC should not be delegated to non-emergency medicine personnel. Sadly, this is not achievable 24/7 in all UK departments right now for a number of awkward reasons.

So what’s a team leader to do when faced with a colleague’s refusal to intubate? The best approach would be to gently and politely persuade them to change their mind by stating some clinical facts that enable a shared mental model and agreed management plan, and to ensure the most senior available physicians are participating in the discussion.

Sometimes that fails. What next? Here’s a suggestion. This is slightly tongue-in-cheek but take away from it what you will.

It is imperative that the individual declining intubation appreciates the gravity of his or her decision. They must not be under the impression that they’ve done you (and the patient) a favour by giving their opinion after an ‘airway consult’. They have declined a resuscitative intervention requested by the emergency medicine team leader and should appreciate the consequences of this decision and the need to document it as such.

Perhaps say something along the lines of:

I see we haven’t managed to agree on this. We’ll just need you to complete the non-intubation form please for our quality improvement process. This will also help prevent your point being forgotten or misunderstood if we’re unlucky enough to face any complaints or litigation. I can fill it in on your behalf but I suspect you’d want to represent yourself as accurately as possible when documenting such a bold decision

And here’s the form. It is provocative, cheeky, and in no way should really be used in its current form:


Difficult intubation on ICU

icu-intub-iconA score to predict difficulty of intubation in ICU patients underwent derivation and validation in French ICUs. The main predictors included Mallampati score III or IV, obstructive sleep apnoea syndrome, reduced mobility of cervical spine, limited mouth opening, severe hypoxia, coma, and where the operator was a nonanesthesiologist.

The striking thing is the overall rate of difficult intubations, defined as three or more laryngoscopy attempts or taking over 10 minutes using conventional laryngoscopy(!) and the high rate of severe complications.

The incidence of difficult intubation was 11.3% (113 of 1,000 intubation procedures) in the original cohort and 8% (32 of 400 intubation procedures) in the validation cohort.

In the development cohort, overall complications occurred in 437 of 1,000 intubation procedures (43.7%), with 381 (38.1%) severe complications (26 cardiac arrests, 2.6%; five deaths, 0.5%; 274 severe collapses, 27.4%; 155 severe hypoxemia, 15.5%) and 112 (11.2%) moderate complications (15 agitations, 1.5%; 32 cardiac arrhythmias, 3.2%; 23 aspirations, 2.3%; 48 esophageal intubations, 4.8%; six dental injuries, 0.6%).

There is no comment on incidence of propofol use for induction; I was tempted to speculate whether it was implicated in any of the cardiac arrests – something we observe time and again in the critically ill – but the authors state: “The drugs used for intubation, in particular neuromuscular blockers, did not differ between groups… However, midazolam use was more frequent in case of difficult intubation.

Capnography was used only in 46% of intubations, and there was no mention of checklist use. It is fascinating how some aspects of airway management that might be considered minimum and basic safety standards in some practice settings are not yet routine in other specialties or locations.

An interesting study, from which one of the take home messages for me has to be a resounding ‘Yikes!’.

Early Identification of Patients at Risk for Difficult Intubation in the Intensive Care Unit
Am J Respir Crit Care Med. 2013 Apr 15;187(8):832-9

Rationale: Difficult intubation in the intensive care unit (ICU) is a challenging issue.

Objectives: To develop and validate a simplified score for identifying patients with difficult intubation in the ICU and to report related complications.

Methods: Data collected in a prospective multicenter study from 1,000 consecutive intubations from 42 ICUs were used to develop a simplified score of difficult intubation, which was then validated externally in 400 consecutive intubation procedures from 18 other ICUs and internally by bootstrap on 1,000 iterations.

Measurements and Main Results: In multivariate analysis, the main predictors of difficult intubation (incidence = 11.3%) were related to patient (Mallampati score III or IV, obstructive sleep apnea syndrome, reduced mobility of cervical spine, limited mouth opening); pathology (severe hypoxia, coma); and operator (nonanesthesiologist). From the β parameter, a seven-item simplified score (MACOCHA score) was built, with an area under the curve (AUC) of 0.89 (95% confidence interval [CI], 0.85-0.94). In the validation cohort (prevalence of difficult intubation = 8%), the AUC was 0.86 (95% CI, 0.76-0.96), with a sensitivity of 73%, a specificity of 89%, a negative predictive value of 98%, and a positive predictive value of 36%. After internal validation by bootstrap, the AUC was 0.89 (95% CI, 0.86-0.93). Severe life-threatening events (severe hypoxia, collapse, cardiac arrest, or death) occurred in 38% of the 1,000 cases. Patients with difficult intubation (n = 113) had significantly higher severe life-threatening complications than those who had a nondifficult intubation (51% vs. 36%; P < 0.0001).

Conclusions: Difficult intubation in the ICU is strongly associated with severe life-threatening complications. A simple score including seven clinical items discriminates difficult and nondifficult intubation in the ICU.

Predicting volume responsiveness

IVCiconOne of the current Holy Grails of ED critical care is to find a reliable measure of fluid responsiveness in those patients with impaired organ perfusion, such as those with severe sepsis. This would enable us to identify those patients whose cardiac output would be improved by fluid therapy, and avoid subjecting ‘non-responders’ to the risks associated with fluid overload. Thanks to the uptake of early goal-directed therapy in sepsis, under-resuscitation is now much less common in the ED. However a growing evidence base reveals the dangers of over-resuscitation. We have a responsibility to optimise fluid therapy as best we can with the equipment we have, according to the latest evidence.

Inferior Vena Cava Ultrasound
Some tests of fluid responsiveness rely on the effect of respiration-induced changes in pleural pressure on the circulation. Inferior vena cava (IVC) size and degree of inspiratory collapse correlate with central venous pressure (CVP), but CVP is not a reliable predictor of volume status or responsiveness. Skinny, collapsing IVCs detected on ultrasound suggest volume responsiveness, but the lack of this finding does not exclude fluid responsiveness. IVC size and measurement can be affected by patient position, probe position, and a variety of health states from athleticism to increased abdominal pressure.

Pulse Pressure Variation
Respiratory pulse pressure variation derived from an arterial line trace in mechanically ventilated patients who are adequately sedated and receiving large tidal volumes can predict fluid responsiveness too. Variability in tidal volume, the presence of spontaneous breathing activity in a ventilated patient, and cardiac dysrhythmia can all confound the usefulness of this method.

End expiratory occlusion
Another test in mechanically ventilated patients is the end expiratory occlusion test. A positive pressure inspiratory breath cyclically decreases the left cardiac preload. Occluding the circuit at end-expiration prevents this cyclic impediment in left cardiac preload and acts like a fluid challenge. A 15 second expiratory occlusion is performed and an increase in pulse pressure or (if you can measure it) cardiac index predicts fluid responsiveness with a high degree of accuracy. The patient must be able to tolerate the 15 second interruption to ventilation without initiating a spontaneous breath.

Passive Leg Raise
Passive leg raising (PLR) involves measuring cardiac output (or its surrogate, velocity-time integral, or VTI) before and after tilting the semirecumbent patient supine and raising the legs to 45 degrees. This ‘autotransfuses’ blood from the lower limbs to the core and acts as a reversible fluid challenge. An increase in VTI identifies fluid responders. It would be nice if a PLR-induced increase in blood pressure revealed the answer, but BP does not reliably inform us of changes in cardiac output.

All these tests have limitations. Pulse pressure variation fails in patients with low respiratory system compliance, such as is found in ARDS(1). End-expiratory occlusion and PLR work in low respiratory system compliance, but the former still requires mechanical ventilation, and the latter requires a means of estimating cardiac output or a surrogate – oesophageal Doppler, the velocity-time integral measured by transthoracic echocardiography, and femoral artery flow (measured by arterial Doppler) have all been used. Non-invasive cardiac output monitors that are not operator dependent exist, such as the NICOM(TM) bioreactance device. Bioreactance cardiac output measurement is based on an analysis of relative phase shifts of an oscillating current that occurs when this current traverses the thoracic cavity. Its advantages are that it is noninvasive, it does not require endotracheal intubation or an arterial line, and it provides a good estimate of stroke volume in patients with atrial fibrillation.

A recent study evaluating the combination of PLR with NICOM(TM) bioreactance monitoring revealed that another tool could indicate volume responsiveness: an increase in carotid blood flow after PLR, as measured by carotid Doppler flow imaging(2). A threshold increase in carotid Doppler flow imaging of 20% for predicting volume responsiveness had a sensitivity and specificity of 94% and 86%, respectively. This was studied in a heterogenous group of hemodynamically unstable patients, suggesting applicability to the kind of patients who present to the ED, although numbers were small so more validation is required.

End-tidal carbon dioxide
End-tidal carbon dioxide (ETCO2) levels depend on cardiac output. Increasing cardiac output with a fluid challenge or PLR increases ETCO2,as long as ventilatory and metabolic conditions remain stable. In a recent small study, a PLR-induced increase in ETCO2 ≥ 5 % predicted a fluid-induced increase in cardiac index ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %(3). The maximal effects of PLR on CI and ETCO2 were observed within 1 min.

So what can I use?
In summary, differentiating fluid responders from non-responders in the ED remains a challenge. The method used depends on available equipment and expertise, and whether the patient is spontaneously breathing or mechanically ventilated. The NICOM(TM) shows great promise but until your department can afford one, ultrasound is the way to go; small collapsing IVCs suggest fluid responders. Learning to measure a VTI on transthoracic echo or carotid Doppler flow will help you assess the response to a PLR in spontaneously ventilating patients. If they’re mechanically ventilated, then looking for an ETCO2 rise after PLR could be a simpler alternative.

Fluid responsiveness assessment – options in the Emergency Department

Inferior Vena Cava Ultrasound
Helpful if skinny / large degree of respirophasic collapse – suggests fluid responsive – ventilated or spontaneous breathing

Passive Leg Raise
Good in ventilated or spontaneous breathing patients; need to measure cardiac output or a surrogate, such as VTI (echo), NICOM(TM), carotid Doppler flow, or ETCO2 (if ventilation and metabolic status constant)

Pulse Pressure Variation
Requires full mechanical ventilation; no good if low respiratory compliance / disturbed heart-lung interaction

End expiratory occlusion
Requires mechanical ventilation and patient tolerance of 15 seconds of apnoea. Acts like a passive leg raise so need a measure of cardiac output or surrogate

I look forward to more studies on these modalities, and to trying some of them in the resus room at every available opportunity.


1. Passive leg-raising and end-expiratory occlusion tests perform better than pulse pressure variation in patients with low respiratory system compliance
Crit Care Med. 2012 Jan;40(1):152-7

OBJECTIVES: We tested whether the poor ability of pulse pressure variation to predict fluid responsiveness in cases of acute respiratory distress syndrome was related to low lung compliance. We also tested whether the changes in cardiac index induced by passive leg-raising and by an end-expiratory occlusion test were better than pulse pressure variation at predicting fluid responsiveness in acute respiratory distress syndrome patients.

DESIGN: Prospective study.

SETTING: Medical intensive care unit.

PATIENTS: We included 54 patients with circulatory shock (63 ± 13 yrs; Simplified Acute Physiology Score II, 63 ± 24). Twenty-seven patients had acute respiratory distress syndrome (compliance of the respiratory system, 22 ± 3 mL/cm H2O). In nonacute respiratory distress syndrome patients, the compliance of the respiratory system was 45 ± 9 mL/cm H2O.

MEASUREMENTS AND MAIN RESULTS: We measured the response of cardiac index (transpulmonary thermodilution) to fluid administration (500 mL saline). Before fluid administration, we recorded pulse pressure variation and the changes in pulse contour analysis-derived cardiac index induced by passive leg-raising and end-expiratory occlusion. Fluid increased cardiac index ≥ 15% (44% ± 39%) in 30 “responders.” Pulse pressure variation was significantly correlated with compliance of the respiratory system (r = .58), but not with tidal volume. The higher the compliance of the respiratory system, the better the prediction of fluid responsiveness by pulse pressure variation. A compliance of the respiratory system of 30 mL/cm H2O was the best cut-off for discriminating patients regarding the ability of pulse pressure variation to predict fluid responsiveness. If compliance of the respiratory system was >30 mL/cm H2O, then the area under the receiver-operating characteristics curve for predicting fluid responsiveness was not different for pulse pressure variation and the passive leg-raising and end-expiratory occlusion tests (0.98 ± 0.03, 0.91 ± 0.06, and 0.97 ± 0.03, respectively). By contrast, if compliance of the respiratory system was ≤ 30 mL/cm H2O, then the area under the receiver-operating characteristics curve was significantly lower for pulse pressure variation than for the passive leg-raising and end-expiratory occlusion tests (0.69 ± 0.10, 0.94 ± 0.05, and 0.93 ± 0.05, respectively).

CONCLUSIONS: The ability of pulse pressure variation to predict fluid responsiveness was inversely related to compliance of the respiratory system. If compliance of the respiratory system was ≤ 30 mL/cm H2O, then pulse pressure variation became less accurate for predicting fluid responsiveness. However, the passive leg-raising and end-expiratory occlusion tests remained valuable in such cases.

2. The use of bioreactance and carotid doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients
Chest. 2013 Feb 1;143(2):364-70

BACKGROUND: The clinical assessment of intravascular volume status and volume responsiveness is one of the most difficult tasks in critical care medicine. Furthermore, accumulating evidence suggests that both inadequate and overzealous fluid resuscitation are associated with poor outcomes. The objective of this study was to determine the predictive value of passive leg raising (PLR)- induced changes in stroke volume index (SVI) as assessed by bioreactance in predicting volume responsiveness in a heterogenous group of patients in the ICU. A secondary end point was to evaluate the change in carotid Doppler fl ow following the PLR maneuver.

METHODS: During an 8-month period, we collected clinical, hemodynamic, and carotid Doppler data on hemodynamically unstable patients in the ICU who underwent a PLR maneuver as part of our resuscitation protocol. A patient whose SVI increased by . 10% following a fluid challenge was considered a fluid responder.

RESULTS: A complete data set was available for 34 patients. Twenty-two patients (65%) had severe sepsis/septic shock, whereas 21 (62%) required vasopressor support and 19 (56%) required mechanical ventilation. Eighteen patients (53%) were volume responders. The PLR maneuver had a sensitivity of 94% and a specificity of 100% for predicting volume responsiveness (one false negative result). In the 19 patients undergoing mechanical ventilation, the stroke volume variation was 18.0% 5.1% in the responders and 14.8% 3.4% in the nonresponders ( P 5 .15). Carotid blood fl ow increased by 79% 32% after the PLR in the responders compared with 0.1% 14% in the nonresponders ( P , .0001). There was a strong correlation between the percent change in SVI by PLR and the concomitant percent change in carotid blood fl ow ( r 5 0.59, P 5 .0003). Using a threshold increase in carotid Doppler fl ow imaging of 20% for predicting volume responsiveness, there were two false positive results and one false negative result, giving a sensitivity and specificity of 94% and 86%, respectively. We noted a significant increase in the diameter of the common carotid artery in the fluid responders.

CONCLUSIONS: Monitoring the hemodynamic response to a PLR maneuver using bioreactance provides an accurate method of assessing volume responsiveness in critically ill patients. In addition, the study suggests that changes in carotid blood fl ow following a PLR maneuver may be a useful adjunctive method for determining fluid responsiveness in hemodynamically unstable patients.

3. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test
Intensive Care Med. 2013 Jan;39(1):93-100

PURPOSE: In stable ventilatory and metabolic conditions, changes in end-tidal carbon dioxide (EtCO(2)) might reflect changes in cardiac index (CI). We tested whether EtCO(2) detects changes in CI induced by volume expansion and whether changes in EtCO(2) during passive leg raising (PLR) predict fluid responsiveness. We compared EtCO(2) and arterial pulse pressure for this purpose.

METHODS: We included 65 patients [Simplified Acute Physiology Score (SAPS) II = 57 ± 19, 37 males, under mechanical ventilation without spontaneous breathing, 15 % with chronic obstructive pulmonary disease, baseline CI = 2.9 ± 1.1 L/min/m(2)] in whom a fluid challenge was decided due to circulatory failure and who were monitored by an expiratory-CO(2) sensor and a PiCCO2 device. In all patients, we measured arterial pressure, EtCO(2), and CI before and after a fluid challenge. In 40 patients, PLR was performed before fluid administration. The PLR-induced changes in arterial pressure, EtCO(2), and CI were recorded.

RESULTS: Considering the whole population, the fluid-induced changes in EtCO(2) and CI were correlated (r (2) = 0.45, p = 0.0001). Considering the 40 patients in whom PLR was performed, volume expansion increased CI ≥ 15 % in 21 “volume responders.” A PLR-induced increase in EtCO(2) ≥ 5 % predicted a fluid-induced increase in CI ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %. The prediction ability of the PLR-induced changes in CI was not different. The area under the receiver-operating characteristic (ROC) curve for the PLR-induced changes in pulse pressure was not significantly different from 0.5.

CONCLUSION: The changes in EtCO(2) induced by a PLR test predicted fluid responsiveness with reliability, while the changes in arterial pulse pressure did not.

Upstairs vs Downstairs: an EPIC Conundrum

A new breed, and new terminology

USAflagb&WResusScott Weingart MD and colleagues have published a discussion paper [1] outlining the role of emergency physicians who have completed additional critical care training – ED intensivists – and the potential benefits these individuals might bring to patients, emergency departments, and their emergency physician colleagues.

The paper also introduces a glossary of new terms which might help clarify future discussion of this practice area:

Emergency medicine critical care a subspecialty of emergency medicine dealing with the care of the critically ill both in the ED and in the rest of the hospital
EP intensivist a physician who has completed a residency in emergency medicine and a fellowship in critical care
ED critical care emergency medicine critical care practiced specifically in the ED
ED intensivist (EDI) EPIs who practice ED critical care as a portion of their clinical time
Resuscitationists EPs who have additional knowledge, training, and interest in the care of the critically ill patient
EDICU a unit within an ED with the same or similar staffing, monitoring, and capability for therapies as an ICU
RED-ICU a hybrid resuscitation area and EDICU allowing a department to adopt the ED intensive care model with minimal cost and no changes to the physical plant

Potential benefits of ED-intensivists – and associated adequately staffed areas within ED that facilitate ongoing critical care delivery – include:

Full intensive care provided to patients unable to be moved to ICU (usually due to bed unavailability)
Development of protocols and care pathways that allow other EPs to deliver enhanced critical care
Gaining of advanced skills for ED nurses
Removal of need for ICU bed for conditions that can be improved in a few hours (eg. some overdoses, DKA, acute pulmonary oedema)
Cost saving due to decreased ICU stay (if the above ‘short term critical care’ patients are admitted to ICU, ward bed unavailability can make it difficult to discharge them from ICU)
Additional airway skills in ED (and training around that)
Improved invasive and non-invasive ventilatory management (and training) in ED
Gaining of ED experience in ventilator weaning and extubation
Gaining of ED experience in haemodynamic monitoring, vasoactive support, and even mechanical circulatory support (balloon pumps and ECMO)
Improved sepsis care
Improved post-cardiac arrest care
Improved trauma management
Greater exposure to invasive procedures
Improved end of life care
Better critical care exposure for trainees

Improved ED-ICU communication and shared protocols

Scott’s whole mission is about bringing ‘upstairs care downstairs’, and educating others to do that, at which he is a true master. No doubt he will singlehandedly have inspired a large cohort of emergency physicians to train in critical care. Examples of ED intensivists and their roles are listed here on the EMCrit site.

Emergency physician intensivists in the Old Country

epic__logoUKflagAs an ‘ED-intensivist’ myself, I do believe many of those advantages can be realised. In the UK when I originally trained in both EM and ICM there was a small number of similarly trained individuals and we collectively called ourselves ‘EPIC’ – ‘Emergency Physicians in Intensive Care’.

Our shared energy and enthusiasm led to a dedicated conference in 2011 and it’s possible that our proselytizing combined with publications like Terry Brown’s ‘Emergency physicians in critical care: a consultant’s experience‘[2] may have made some small contribution to the subsequent explosion in interest in dual accreditation in EM & ICM in the UK.

Disappearing upstairs

AusflagWhen I moved to Australia in 2008 I was excited to hear that emergency docs now made up the largest proportion of dual trained new intensivists. When I asked a leading member of this group whether he saw any role for an ‘EPIC’ community in Australia I was surprised and disappointed with the response:

‘Nice idea but I don’t see the point. I can’t think of anyone who dual trained who’s still working in emergency medicine’

So it seems those who were in the best position to bring upstairs care downstairs had all disappeared upstairs. Many will admit it’s not just because they find critical care more interesting than emergency medicine; the combination of a significantly higher income (through private practice) with better working conditions plays a significant role.

There are other opportunities in Australia for emergency physicians to practice critical care. Prehospital & retrieval medicine services undertake interhospital critical care transport of patients from small and often remote facilities where all of the first few hours of intensive care must be delivered by retrieval teams in often challenging environments with limited personnel and equipment. In some cases it’s these retrieval physicians who are able to fulfil the role of ED-intensivist in their own EDs.

Integrated critical care models and SuperDoctors

ChrisTIconAnother Australian example is the ‘integrated critical care’ model pioneered in some regional centres in rural New South Wales where emergency physicians with critical care training aim to provide seamless care to patients in the prehospital, ED, ICU and ward environments. I was lucky enough to do some locum shifts in one of these centres – Tamworth – where the service is delivered by some of the most highly skilled and dedicated physicians I’ve ever met. Check out their registrar job ad for a flavour of their work. This model was described in a 2003 publication[3] by my Sydney HEMS colleague Craig Hore which lists its features as follows:

Features of integrated critical care
Multiskilled critical-care specialists trained and experienced in the various aspects of critical care in rural hospitals.

Multidisciplinary critical-care teams that provide:

A more seamless interface between the various phases of critical care and between its respective disciplines;

A rapid response to, and a continuum of care for, critically ill and injured patients;

Clinical leadership in evaluating and managing critically ill and injured patients, both in the hospital (including the emergency department, critical-care unit and hospital wards) and in the community (including retrievals, and support for ambulance crews, peripheral hospitals and general practitioners); and

Training of medical students, medical staff, nursing staff and allied health professionals to recognise and provide a systematic approach to critical illness and injury.

Team members who are empowered to work beyond perceived traditional boundaries, but within the realms of their clinical expertise and credentials, to enable the best use of available resources.

So it appears the benefits to patients, hospitals, and team skills of ED-intensivists have been espoused for some years in the Anglo-Australian setting, and different practice models evolve to best serve local need.

Resuscitating the resuscitationists

UKflagIs it time to revive EPIC? I chased up my UK buddies who co-founded it, and here are extracts from their replies (note ‘CCT’ refers to certificate of completion of training – the UK equivalent of specialist accreditation or board certification):

“Interesting to hear that most Aussies leave EM, my experience of [our regional] trainees is the opposite; of 4 EM / ITU dual CCT over last 5 years, I’m the only one still doing a little bit of CCM, the rest have all ended up in full time EM posts, despite all doing periods of locum consultant work in CCM. (Although, after last 4 winter months of UK EM, I’m beginning to appreciate that I backed the wrong horse! (In the wrong country!!))”
“Having recently dropped ICU/ED 40/60 mix for full time ED i think those gravitating to ICU have a point – an error on my part. The ED represents much more intense work with fewer staff and a work load that far far exceeds resources. As such time to deliver care falls and skills with it. I have just spend 5 weeks [overseas]. I spent time with several directors who pointed out they no longer look to the UK for high quality ED docs as they manage depts as opposed to caring for patients, lack critical care skills and lack the experience to review and manage patients as they improve or deteriorate – a sad state of affairs indeed.”
“I would like to see EPIC back in force and do see an increasing role. around 1 in 4 of our trainees here are looking to joint qualify and we have 3 in their last 2 years. two are currently looking for posts but struggling to find any with a 50-50 mix and are been told to choose one or the other both by prospective ED and ICU employers.”
“I am concerned that dual trained folk here will, like in Australia gravitate to ICU. Whether that is a reflection of where EM is currently in the UK or a personal reflection I’m not sure. Where as I still have days in the ED where I come home and think ‘best job in the world’ these are overshadowed by the stresses of trying to deliver quality care in a failing system. My impression is that urgent care in the UK may well implode soon as ever decreasing workforce meets an over increasing work load. Inevitable closures of units will speed up this process. I currently have a 50/50 ICM/ED job split but that might change to become more ICU.”
“The ED/ICU community in the UK is growing and it wlll be interesting to see the effect of the ICM CCT has on this. There is sadly still a paucity of ED/ICU jobs in the UK and we probably missed a trick with the trauma centres.”
“It would be great to re-create EPIC to make it a real player for the future.”

So it appears emergency physician intensivists are growing in number, but employment prospects in both specialties are not guaranteed. If we are to recruit them to work as ED intensivists (ie. providing critical care in the ED) we have a challenge in making such posts attractive and sustainable. Emergency medicine in the UK is suffering at the moment, and we’ll have to work hard to stop those who are dual trained from disappearing upstairs.

Your comments on this are invited. Should there be more critical care- trained EPs? Shouldn’t ALL EPs have the right critical care skills to manage the first few hours of critical care? Can you call yourself an emergency physician and not be a ‘resuscitationist’? Where do retrievalists fit into this spectrum? How do we help motivate those who are dual trained to stay in the ED for some of their time? Is there a need for a body like EPIC to guide those who are considering dual training, and to provide recommendations to employers and physicians on models of care and job planning? I would love to get more of an international perspective on this issue.

1. ED intensivists and ED intensive care units
Am J Emerg Med. 2013 Mar;31(3):617-20
Full text link available from here

2. Emergency physicians in critical care: a consultant’s experience
Emerg Med J. 2004 Mar;21(2):145-8
Full text link available from here

There is a growing interest in the interface between emergency medicine and critical care medicine. Previous articles in this journal have looked at the opportunities and advantages of training in critical care medicine for emergency medicine trainees. In the UK there are a small number of emergency physicians who also have a commitment to critical care medicine. This article describes a personal experience of such a job, looking at the advantages and disadvantages. Depending upon future developments in the role of emergency medicine in the UK, together with the proposed expansion in critical care medicine, such posts may become more common.

3. Integrated critical care: an approach to specialist cover for critical care in the rural setting
Med J Aust. 2003 Jul 21;179(2):95-7

Critical care encompasses elements of emergency medicine, anaesthesia, intensive care, acute internal medicine, postsurgical care, trauma management, and retrieval. In metropolitan teaching hospitals these elements are often distinct, with individual specialists providing discrete services. This may not be possible in rural centres, where specialist numbers are smaller and recruitment and retention more difficult. Multidisciplinary integrated critical care, using existing resources, has developed in some rural centres as a more relevant approach in this setting. The concept of developing a specialty of integrated critical-care medicine is worthy of further exploration.

Hypothermia as an inotrope

This small study supports the hypothesis that therapeutic hypothermia can have positive inotropic effects in patients with cardiogenic shock of ischaemic or non-ischaemic origin.

Cooling resulted in a temperature-dependent decrease in heart rate and temperature-dependent increases in stroke volume index, cardiac index, mean arterial pressure, and cardiac power output. These changes reversed when the patients were rewarmed.

The authors summarise as follows:

In summary, our studies demonstrate that moderate hypothermia is feasible and safe also for patients in cardiogenic shock.

Improved cardiac performance may contribute to the considerable decrease of mortality for survivors of cardiac arrest, and the use of hypothermia can be recommended for patients with a clear indication for cooling and poor cardiac performance.

Moreover, hypothermia might be considered as a positive inotropic intervention during cardiogenic shock.

Moderate hypothermia for severe cardiogenic shock (COOL Shock Study I & II)
Resuscitation. 2013 Mar;84(3):319-25.

AIM OF THE STUDY: Hypothermia exerts profound protection from neurological damage and death after resuscitation from circulatory arrest. Its application during concomitant cardiogenic shock has been discussed controversially, and still hypothermia is used with reserve when haemodynamic parameters are impaired. On the other hand hypothermia improves force development in isolated human myocardium. Thus, we hypothesized that hypothermia could beneficially affect cardiac function in patients during cardiogenic shock.

METHODS: 14 Patients, admitted to Intensive Care Unit for cardiogenic shock under inotropic support, were enrolled and moderate hypothermia (33°C) was induced for either one (n=5, short-term) or twenty-four (n=9, mid-term) hours.

RESULTS: 12 patients suffered from ischaemic cardiomyopathy, 2 were female, and 6 were included after cardiac arrest and resuscitation. Body temperature was controlled by an intravascular cooling device. Short-term hypothermia consistently decreased heart rate, and increased stroke volume, cardiac index and cardiac power output. Metabolic and electrocardiographic parameters remained constant during cooling. Improved cardiac function persisted during mid-term hypothermia, but was reversed during re-warming. No severe or persistent adverse effects of hypothermia were observed.

CONCLUSION: Moderate Hypothermia is safe and feasable in patients during cardiogenic shock. Moreover, hypothermia improved parameters of cardiac function, suggesting that hypothermia might be considered as a positive inotropic intervention rather than a risk for patients during cardiogenic shock.