Difficult intubation on ICU
May 12, 2013 by Cliff
Filed under All Updates, ICU
A 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
May 8, 2013 by Cliff
Filed under Acute Med, All Updates, ICU, Resus, Ultrasound
One 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.
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
April 19, 2013 by Cliff
Filed under All Updates, ICU, Resus
A new breed, and new terminology
Scott 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:
Potential benefits of ED-intensivists – and associated adequately staffed areas within ED that facilitate ongoing critical care delivery – include:
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
As 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
When 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
Another 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:
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
Is 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):
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
April 5, 2013 by Cliff
Filed under Acute Med, All Updates, ICU, Resus
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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.
Beherrsche die Reanimation
April 2, 2013 by Cliff
Filed under All Updates, Inspiration, Resus
The whole purpose behind my career and this blog is to save life. Like most emergency physicians I don’t see a huge number of resuscitation patients myself in a given week, so my best hope in making a difference is to develop my teaching skills so that I can motivate and inspire others to improve their ability to manage resuscitation.
The highlight of my week therefore has been the receipt of some email feedback from a colleague in Germany. An intensivist, internist, and prehospital doctor (I like him already) who tells me he found my ‘Own the Resus‘ talk helpful:
Dear Dr. Reid,
Few days ago, too tired too sleep after a long shift on my ICU (18 beds internal medicine ICU, I am specialist in internal medicine specialized in intensive care and prehospital emergency medicine in a major German city) I watched your talk via emcrit podcast. I was immediately caught, I soaked in every word, I was fascinated, watched it twice in the middle of the night and next afternoon I listened to it in my car driving to work.
At this very day I did some overdue crap beyond the end of my shift when I heard the ominous shuffling of feet and rolling of the emergency cart from the other end of the ward… “I think we need your help….”
There it was, difficult airway situation. Patient crashing.
Then what followed was a kind of “out of body experience”. I did what was necessary, made things happen like calling anesthesia difficult airway code, calling the surgeons, organizing fiber optics and meanwhile trying to secure that airway myself until i could dispatch anesthesia to the head and surgeons to the neck. Within few minutes there were 6 doctors and 5 nurses shuffling on 9 square meters…
I found myself 1 meter behind the foot end of the pts bed and with your talk in my head I found me consciously controlling the crowd. There was suddenly the messages of your talk and there was me. I don’t know how to put it into words, I wouldn’t have done something else in medical terms but thanks to your talk I had the vocabulary, the tools to reflect myself as the leader to be in charge of the situation somehow with more distance, and after a successful resus the 10 people involved in this code went off with a good feeling that everybody contributed in what they could and all for the pts benefit.
Your talk was a kind of transition to the next level for me: from the colleague who asks how to get out of trouble in many situations because he was often deeply in trouble, to the one who leads out of trouble.
With your talk many things suddenly became clear and I am looking forward to be able to work harder on this role of leading.
Thank you very much.
D
High flow nasal cannula oxygen
Where I work high flow humidified nasal cannula oxygen (HFNC) is used for infants with bronchiolitis and our ICU also employs it for selected adult patients. This is a relatively recent addition to our choice of oxygen delivery systems, and many emergency physicians may still be unfamiliar with it.
A recent review outlines the (scant) evidence for its use in neonates, infants, and adults, and proposes some mechanisms for its effect.
It’s a bit like the traditional delivery of oxygen via nasal cannulae. However, it is recommended that flow rates above 6 l/min are heated and humidified, so the review referred to heated, humidified, high flow nasal cannulae (HFNC).
Neonates
HFNC began as an alternative to nasal CPAP for premature infants. There are as yet no definitive studies showing its superiority over CPAP.
Infants
HFNC may decrease the need for intubation when compared to standard nasal cannula in infants with bronchiolitis.
Adults
No hard outcome data yet exist. It has mainly been used for hypoxemic respiratory failure rather than patients with hypercarbia such as COPD patients.
How it works
The following are proposed mechanisms for improvements in gas exchange / oxygenation:
1. A high FiO2 is maintained because flow rates are higher than spontaneous inspiratory demand, compared with standard facemasks and low flow nasal cannulae which entrain a significant amount of room air.
2. Nasopharyngeal dead space ‘washout’. The additional gas flow within the nasopharyngeal space may reduce dead space: tidal volume ratio. There are some animal neonatal data to show improved CO2 clearance with flows up to 8 l/min.
3. Stenting of the upper airway by positive pressure may decrease upper airways resistance and reduce work of breathing.
4. Some positive pressure (akin to CPAP) may be generated, which can help recruit lung and decrease ventilation–perfusion mismatch; however this is not consistently present in all studies, and high flows are needed to generate even modest pressures. For example, in a study on postoperative cardiac surgery patients, HFNC at 35 l/min generated a nasopharyngeal pressure of only 2.7 ± 1 cmH2O.
Drawbacks and things to know
Studies suggest that if benefit is going to be seen in adult or paediatric patients, this should be evident in the first 30-60 minutes.
Any modest positive pressure generated will be reduced by an open mouth or when there is a significant leak between the cannulae and the nares.
HFNC maintain a fixed flow and generate variable pressures, and the pressures may be more inconsistent in patients with respiratory distress with high respiratory rates and mouth breathing. Compare this with non-invasive ventilation (CPAP and or BiPAP) in which variable flow is used to generate a fixed pressure.
The authors’ summary is helpful:
We postulate that the predominant benefit of HFNC is the ability to match the inspiratory demands of the distressed patient while washing out the nasopharyngeal dead space. Generation of positive airway pressure is dependent on the absence of significant leak around the nares and mouth and seems less likely to be a predominant factor in relieving respiratory distress for most patients.
NIV such as CPAP and bilevel positive airway pressure should still be considered first line therapy in moderately distressed patients in whom supplementation oxygen is insufficient and when a consistent positive pressure is indicated.
There are numerous ongoing trials which should hopefully clarify indications for HFNC and the mechanisms by which it may be beneficial.
An earlier summary of the evidence was written by my Scandinavian chums. And Reuben Strayer uses it to optimise oxygenation during RSI as a modification of the NODESAT technique.
Use of high flow nasal cannula in critically ill infants, children, and adults: a critical review of the literature
Intensive Care Med. 2013 Feb;39(2):247-57
BACKGROUND: High flow nasal cannula (HFNC) systems utilize higher gas flow rates than standard nasal cannulae. The use of HFNC as a respiratory support modality is increasing in the infant, pediatric, and adult populations as an alternative to non-invasive positive pressure ventilation.OBJECTIVES: This critical review aims to: (1) appraise available evidence with regard to the utility of HFNC in neonatal, pediatric, and adult patients; (2) review the physiology of HFNC; (3) describe available HFNC systems (online supplement); and (4) review ongoing and planned trials studying the utility of HFNC in various clinical settings.
RESULTS: Clinical neonatal studies are limited to premature infants. Only a few pediatric studies have examined the use of HFNC, with most focusing on this modality for viral bronchiolitis. In critically ill adults, most studies have focused on acute respiratory parameters and short-term physiologic outcomes with limited investigations focusing on clinical outcomes such as duration of therapy and need for escalation of ventilatory support. Current evidence demonstrates that HFNC generates positive airway pressure in most circumstances; however, the predominant mechanism of action in relieving respiratory distress is not well established.
CONCLUSION: Current evidence suggests that HFNC is well tolerated and may be feasible in a subset of patients who require ventilatory support with non-invasive ventilation. However, HFNC has not been demonstrated to be equivalent or superior to non-invasive positive pressure ventilation, and further studies are needed to identify clinical indications for HFNC in patients with moderate to severe respiratory distress.
Save a life by watching telly?
March 20, 2013 by Cliff
Filed under Acute Med, All Updates, EMS, ICU, Inspiration, Kids, Resus, Trauma
If you’re in the United Kingdom on Thursday 21st March please consider watching BBC’s Horizon program at 9pm on BBC2.
I’m in Australia so I’ll miss it, but I’m moved by the whole background to this endeavour and really want you to help me spread the word.
Many of you will be familiar with the tragic case of Mrs Elaine Bromiley, who died from hypoxic brain injury after clinicians lost control of her airway during an anaesthetic for elective surgery. Her husband Martin has heroically campaigned for a greater awareness of the need to understand human factors in healthcare so such disasters can be prevented in the future.
Mr Bromiley describes the program, which is hosted by intensivist and space medicine expert Dr Kevin Fong:
Kevin and the Horizon team have produced something inspirational yet scientific, and – just as importantly – it’s by a clinician, for clinicians. It’s written in a way that will appeal to both those in healthcare and the public. It uses a tragic death to highlight human factors that all of us are prone to, and looks at how we can learn from others both in and outside healthcare to make a real difference in the future.
The lessons of this programme are for everyone in healthcare.
It would be wonderful if you could pass on details of the programme to anyone you know who works in healthcare. My goal is that by the end of this week, every one of the 1 million or so people who work in healthcare in the UK will be able to watch it (whether on Thursday or on iPlayer).
From the Health Foundation blog
Please help us reach this 1000 000 viewer target by watching on Thursday or later on iPlayer. Tweet about it or forward this message to as many healthcare providers you know. Help Martin help the rest of us avoid the kind of tragedy that he and his children have so bravely endured.
For more information on Mrs Bromiley’s case, watch ‘Just a Routine Operation’:
Cliff
Ketamine & cardiovascular stability
I ‘jumped ship’ from etomidate to ketamine for rapid sequence intubation (RSI) in sick patients about seven years ago. Good thing too, since I later moved to Australia where we don’t have etomidate. I’ve been one of the aggressive influences behind my prehospital service’s switch to ketamine as the standard induction agent for prehospital RSI. It’s no secret that I think propofol has no place in RSI in the critically ill.
I love ketamine for its haemodynamic stability compared with other induction agents. In fact, I very rarely see a drop in blood pressure when I use it for RSI even in significantly shocked patients. One should however try to remain open to evidence that disconfirms ones biases, lest we allow science to be replaced by religion. I therefore was interested to read a report of two cases of cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI)(1).
The first case was a 25 year old with septic shock due to an intestinal perforation, with a respiratory rate of 30 ‘labored’ breaths per minute and hypoxaemia prior to intubation with 2mg/kg ketamine who became bradycardic and then had a 10-15 minute PEA arrest after ketamine administration (but prior to intubation). Pre-arrest oxygen saturation and pre-induction blood gases are not reported.
The second case was an 11 year old with septic shock and pneumonia, hypoxaemia, and a severe metabolic acidosis. She arrest with bradycardia then a brief period of asystole one minute after receiving 2.4 mg/kg ketamine with rocuronium for intubation.
Was the ketamine responsible for the arrests? Ketamine usually exhibits a stimulatory effect on the cardiovascular system, through effects which are incompletely understood but include a centrally mediated sympathetic response and probable inhibition of norepinephrine (noradrenaline) reuptake. However ketamine can have a direct depressant effect on cardiac output which is usually overridden by the sympathetic stimulation. In critically ill severely stressed patients the depressant effect may predominate. In a study on 12 critically ill surgical patients, haemodynamic indices were measured using pulmonary artery catheters within 5 minutes of ketamine administration (at a mean of 70 mg)(2). Six patients demonstrated decreases in ventricular contractility, and four had decreases in cardiac output. Mean arterial blood pressure decreased in four patients. The authors commented:
The patients..were septic, hypovolemic, or cirrhotic, and had severe stress preoperatively. It is possible that in these ill patients adrenocortical and catechol stores had been depleted prior to ketamine administration. Alternatively, in the setting of prolonged preoperative stress, there may be resistance to further sympathetic and/or adrenocotical stimulation by ketamine. In either case, preoperative stress may blunt the usual physiologic responses to ketamine, setting the stage for possible adverse effects.
The negative cardiovascular effects of ketamine may also be precipitated by larger doses or repeated doses of ketamine(3).
While this small case series of cardiac arrest following ketamine administration is interesting, we should bear in mind the other possible precipitants of arrest in these patients, which are not all discussed by the authors:
i) Both patients were hypoxaemic prior to induction and their peri-intubation oxygen saturations are not reported. Arrests following bradycardia at the time of induction in the critically ill are frequently related to hypoxaemia.
ii) The second patient had a severe metabolic acidosis and the first – an abdominal sepsis patient with a labored respiratory rate of 30 – very probably did too. A failure to match a patient’s compensatory respiratory alkalosis with hyperventilation after anaesthesia is known to precipitate arrest in acidaemic patients.
iii) Finally, if the ketamine was responsible for the arrests, one should consider that the doses given to these shocked and highly unstable patients were well in excess of what many of us would recommend, and doses in the range of 0.5-1 mg/kg might not have been associated with adverse effects.
The takehome points for me are that this report is a helpful reminder that the cardiovascular stimulation-inhibition balance of ketamine may be altered by severe critical illness, and that doses of any induction agent should be significantly reduced in the critically ill patient. In no way does this convince me that I should discard ketamine as my preferred choice for RSI in such patients.
1. Cardiac Arrest Following Ketamine Administration for Rapid Sequence Intubation
J Intensive Care Med. 2012 May 29. [Epub ahead of print]
Given their relative hemodynamic stability, ketamine and etomidate are commonly chosen anesthetic agents for sedation during the endotracheal intubation of critically ill patients. As the use of etomidate has come into question particularly in patients with sepsis, due to its effect of adrenal suppression, there has been a shift in practice with more reliance on ketamine. However, as ketamine relies on a secondary sympathomimetic effect for its cardiovascular stability, cardiovascular and hemodynamic compromise may occur in patients who are catecholamine depleted. We present 2 critically ill patients who experienced cardiac arrest following the administration of ketamine for rapid sequence intubation (RSI). The literature regarding the use of etomidate and ketamine for RSI in critically ill patients is reviewed and options for sedation during endotracheal intubation in this population are discussed.
2. Cardiovascular effects of anesthetic induction with ketamine
Anesth Analg. 1980 May;59(5):355-8
Anesthetic induction with ketamine has been reported to maintain or improve cardiovascular performance in severely ill patients. Using invasive cardiovascular monitoring, we studied physiologic responses to a single dose of ketamine in 12 critically ill patients. Six patient demonstrated decreases in ventricular contractility, and four had decreases in cardiac output. Mean arterial blood pressure decreased in four patients. Pulmonary venous admixture increased in four of six patients, while oxygen consumption decreased in eight of 11 patients. Thus, a single dose of ketamine produced decreases in cardiac and pulmonary performance and in peripheral oxygen transport in this group of patients. It is proposed that in severely ill patients, preoperative stress may alter the usual physiologic responses to ketamine administration, and adverse effects may predominate. Ketamine, therefore, should be used with caution for induction of anesthesia in critically ill and in acutely traumatized patients until additional studies and further information on cardiovascular responses to ketamine are available.
3. A comparison of some cardiorespiratory effects of althesin and ketamine when used for induction of anaesthesia in patients with cardiac disease
Br J Anaesth. 1976 Nov;48(11):1071-81
Cardiorespiratory effects of ketamine and Althesin were measured in two groups of premedicated patients with cardiac disease. The drugs were given in clinically equivalent doses with a second dose administered about 10 min after induction. The first dose of ketamine caused a marked increase in systemic and pulmonary arterial pressure, heart rate, and central venous and wedge pressures and cardiac index. The first dose of Althesin caused a decrease in systemic arterial pressure, central venous pressure, cardiac index and heart work, but little change in heart rate. The second dose of induction agent was administered before the cardiorespiratory effects of the initial dose had resolved. The second dose of Althesin caused changes similar to those following the first dose, but less marked. The changes following the second dose of ketamine were opposite to those following the first dose.
High Frequency Oscillation Trial Results
January 24, 2013 by Cliff
Filed under Acute Med, All Updates, ICU
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Here’s a heads up on a major evidence-based medicine event in critical care: the results of two long awaited randomised controlled trials assessing high-frequency oscillation (HFOV) in Acute Respiratory Distress Syndrome (ARDS) have both been published, and the full text is available from the New England Journal of Medicine at the links below.
In summary, the Oscillation for Acute Respiratory Distress Syndrome Treated Early (OSCILLATE)(1) and the Oscillation in ARDS (OSCAR)(2) trials showed no improvement in in-hospital death or 30 day mortality, respectively. OSCILLATE was terminated early on the basis of a strong signal for increased mortality with HFOV.
An editorial discusses some of the reasons why these outcomes were seen, which include among other factors the possibility that they were related to increased requirements for sedation, paralysis, and vasoactive drugs in the HFOV patients that were not offset by improvements in oxygenation and lung recruitment.
1. High-Frequency Oscillation in Early Acute Respiratory Distress Syndrome
NEJM 22 Jan 2013
BACKGROUND Previous trials suggesting that high-frequency oscillatory ventilation (HFOV) reduced mortality among adults with the acute respiratory distress syndrome (ARDS) were limited by the use of outdated comparator ventilation strategies and small sample sizes
METHODS In a multicenter, randomized, controlled trial conducted at 39 intensive care units in five countries, we randomly assigned adults with new-onset, moderate-to-severe ARDS to HFOV targeting lung recruitment or to a control ventilation strategy targeting lung recruitment with the use of low tidal volumes and high positive end-expiratory pressure. The primary outcome was the rate of in-hospital death from any cause.
RESULTS On the recommendation of the data monitoring committee, we stopped the trial after 548 of a planned 1200 patients had undergone randomization. The two study groups were well matched at baseline. The HFOV group underwent HFOV for a median of 3 days (interquartile range, 2 to 8); in addition, 34 of 273 patients (12%) in the control group received HFOV for refractory hypoxemia. In-hospital mortality was 47% in the HFOV group, as compared with 35% in the control group (relative risk of death with HFOV, 1.33; 95% confidence interval, 1.09 to 1.64; P=0.005). This finding was independent of baseline abnormalities in oxygenation or respiratory compliance. Patients in the HFOV group received higher doses of midazolam than did patients in the control group (199 mg per day [interquartile range, 100 to 382] vs. 141 mg per day [interquartile range, 68 to 240], P<0.001), and more patients in the HFOV group than in the control group received neuromuscular blockers (83% vs. 68%, P<0.001). In addition, more patients in the HFOV group received vasoactive drugs (91% vs. 84%, P=0.01) and received them for a longer period than did patients in the control group (5 days vs. 3 days, P=0.01).
CONCLUSIONS In adults with moderate-to-severe ARDS, early application of HFOV, as compared with a ventilation strategy of low tidal volume and high positive end-expiratory pressure, does not reduce, and may increase, in-hospital mortality. (Funded by the Canadian Institutes of Health Research; Current Controlled Trials numbers, ISRCTN42992782 and ISRCTN87124254, and ClinicalTrials.gov numbers, NCT00474656 and NCT01506401.)
2. High-Frequency Oscillation for Acute Respiratory Distress Syndrome
NEJM 22 Jan 2013
BACKGROUND Patients with the acute respiratory distress syndrome (ARDS) require mechanical ventilation to maintain arterial oxygenation, but this treatment may produce secondary lung injury. High-frequency oscillatory ventilation (HFOV) may reduce this secondary damage.
METHODS In a multicenter study, we randomly assigned adults requiring mechanical ventilation for ARDS to undergo either HFOV with a Novalung R100 ventilator (Metran) or usual ventilatory care. All the patients had a ratio of the partial pressure of arterial oxygen (PaO2) to the fraction of inspired oxygen (FiO2) of 200 mm Hg (26.7 kPa) or less and an expected duration of ventilation of at least 2 days. The primary outcome was all-cause mortality 30 days after randomization
RESULTS There was no significant between-group difference in the primary outcome, which occurred in 166 of 398 patients (41.7%) in the HFOV group and 163 of 397 patients (41.1%) in the conventional-ventilation group (P=0.85 by the chi-square test). After adjustment for study center, sex, score on the Acute Physiology and Chronic Health Evaluation (APACHE) II, and the initial PaO2:FiO2 ratio, the odds ratio for survival in the conventional-ventilation group was 1.03 (95% confidence interval, 0.75 to 1.40; P=0.87 by logistic regression).
CONCLUSIONS The use of HFOV had no significant effect on 30-day mortality in patients undergoing mechanical ventilation for ARDS. (Funded by the National Institute for Health Research Health Technology Assessment Programme; OSCAR Current Controlled Trials number, ISRCTN10416500.
New Sepsis Guidelines
January 21, 2013 by Cliff
Filed under Acute Med, All Updates, EMS, Guidelines, ICU, Kids, Resus
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The latest update of the Surviving Sepsis Campaign Guidelines has been released.
There’s too much interesting stuff to easily summarise, but luckily the full text article is available at the link below.
Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
Crit Care Med 2013 Feb;41(2):580-637 FREE FULL TEXT
