Important RCT's form ESICM Vienna 10-2017

Early application of airway pressure release ventilation may reduce the duration of mechanical ventilation in acute respiratory distress syndrome Compared with conventional LTV, the early application of APRV in patients with ARDS was associated with better oxygenation and respiratory system compliance, lower plateau airway pressure, less sedation requirement, more ventilator-free days at day 28, and a shorter dura-tion of ICU stay Early goal-directed nutrition versus standard of care in adult intensivecare patients: the single-centre, randomised,outcome assessor-blinded EAT-ICU trial A single-centre, randomised, stratifed,parallel-grouped, outcome assessor-blinded clinical trial including 203 acutely admitted, adult ICU patients who were mechanically ventilated, to test the efects of a combined and individualised energy–protein nutrition guided by indirect calorimetry and 24-h urinary urea excretion (nitrogen balance), i.e. EGDN. The EGDNgroup received more energy and protein and had lower nutritional defcits in the ICU as compared to the standard of care group, but we observed no diference betweenthe two groups in physical quality of life at 6 months orin mortality, rates of organ failures, serious adverse reactions or nosocomial infections in the ICU, length of ICU or hospital stay, or days alive without life support at 90 days.

Antithrombotic Reversal

More Evidence That Contrast-Induced Nephropathy Is Not Clinically Important

More Evidence That Contrast-Induced Nephropathy Is Not Clinically Important

The paradox of reduced myocardial shortening in the presence of preserved EF

The paradox of reduced myocardial shortening in the presence of preserved EF is explained mathematically through geometric factors, where EF can be constant for a large variation in shortening if other geometric factors are altered to compensate. Increased wall thickness and/or reduced ED volume augment EF, and therefore can maintain a normal EF despite reduced shortening. EF is quadratically dependent on circumferential shortening and only linearly dependent on longitudinal shortening; hence, EF is less sensitive to a reduction in longitudinal shortening. Our findings suggest that strain measurements reflect systolic function better than EF in patients with preserved EF.



Comparison Between Ejection Fraction and Strain


Editorial Comment V. Fuster MP4

Oliguria is a poor marker for perfusion

Oliguria is an overused parameter to guide resuscitation  and  must  always  be  interpreted  within  the  clinical  context

The 2016 version of  the “Surviving Sepsis Campaign” no longer mentions a UO of  ≥0.5 mL/
 kg/h as a goal of resuscitation. Isolated oliguria with-out  signs  of  vasoplegia,  hypovolemia,  or  low  cardiac output  is  unlikely  to  be  explained  by  a  systemic  hemo-dynamic  cause  and  must  not  evoke  the  administration of additional fluids or vasopressors.

Oliguria should also not  trigger  further  hemodynamic  interventions  in  the clinical  setting  of  established  AKI.

 Oliguria resulting from vasodilatory hypotension  should  preferably  be  treated  with  a vasopressor.  However, a MAP of 80–85 mmHg as target does not seem to be  a  beneficial  strategy,  except  in  patients  with  chronic hypertension.

Reference articles:

Does this critically ill patient with oliguria need more fuids, a vasopressor, or neither?


The Ten Principles behind Arterial Pressure

Flow

New Guidelines to Estimate LAP with ECHO

Check out @HeartToProve's Tweet: https://twitter.com/HeartToProve/status/878607784467628032?s=09

Tricuspid valve and device complications

The following are key points to remember about this review of tricuspid valve dysfunction following pacemaker (PPM) or implantable cardioverter-defibrillator (ICD) placement:

1. Endocardial leads are associated with a number of adverse consequences to tricuspid valve (TV) structure and function. Damage to TV leaflets or subvalvular structures may occur during lead implantation, and it may not be apparent with routine follow-up imaging studies. Avulsion may occur during lead extraction. Chronic interaction between endocardial leads and leaflet and/or chordal structures can result in a foreign body inflammatory and fibrotic response leading to the entrapment of the lead.
2. The prospective incidence of TV damage during lead placement is not known. Retrospective case reports are limited by lack of baseline tricuspid regurgitation (TR) assessment. Most studies suggest that there is a higher incidence of worsening TR in defibrillator leads as opposed to pacing leads, and if there are more than one right ventricular lead.
3. In a series of 41 patients undergoing TV surgery for severe TR believed to be caused by a lead, leaflet impingement was found in 16, leaflet adherence in 14, leaflet perforation in 7, and leaflet entanglement in 4 cases. It appears that the posterior and the septal leaflets may be more vulnerable to injury than the anterior leaflet.
4. A multicenter prospective study currently underway has enrolled 300 patients undergoing cardiac implantable electronic device (CIED) implantation to investigate whether significant TR is caused by the presence of these endocardial leads, with transthoracic echocardiograms obtained within 30 days before and 12 months after implantation.
5. Intravascular hardware and damage to the TV predisposes the patient to endocarditis and thrombosis, either of which can lead to TV dysfunction causing regurgitation or stenosis.
6. Dyssynchronous left ventricular electromechanical activation induced by left bundle branch block or right ventricular pacing is a well-recognized cause of mitral regurgitation. Whether a similar mechanism operates for TR is controversial. Most studies suggest that the physical presence of the lead itself plays the primary, if not the entire role in TV dysfunction, as the percentage of paced beats does not correlate with worsening TR.
7. CIED leads cause echocardiographic imaging artifacts and signal attenuation, due to their high acoustic impedance and reflectivity, resulting in underestimation of TR by color-flow Doppler mapping especially during transthoracic echo, and somewhat less so during transesophageal echo. The regurgitant jet tends to assume an eccentric, rather than a central trajectory, resulting in loss of color-flow Doppler signal, and hence underestimation of regurgitation. In patients eventually found to have severe TR due to CIED leads, only 63% were correctly diagnosed by transthoracic echo during the preoperative study, whereas all were found to have severe TR by preoperative or intraoperative transesophageal echo. Sensitivity of transthoracic echo to detect severe TR can be increased by incorporating hepatic vein assessment (color flow and spectral Doppler).
8. Three-dimensional echocardiography offers improved spatial definition of the interaction between lead and valve and/or subvalvular apparatus, and it is the imaging modality of choice for assessment of CIED lead–TV interaction.
9. There are no prospective data to support TR in the absence of device or endovascular infection as an indication for transvenous lead extraction, hence its absence from the Heart Rhythm Society guideline statement of 2009. However, excess mortality associated with severe TR has been estimated to be 40-75% in patients with CIEDs. When operative risk is low, patients with lead-related severe TR would be expected to benefit from an intervention. If the right ventricle and tricuspid valve annulus are dilated or TV leaflets are damaged, tricuspid valve repair or replacement plus lead removal, relocation, or replacement should be considered. If the right ventricle, tricuspid annulus, TV leaflet appear intact, transvenous lead extraction alone should be considered first.
10. The future of CIEDs in which endocardial leads are absent (leadless pacing) or nontransvalvular (as in His bundle pacing) is likely to be associated with a reduction in lead-related cardiac dysfunction

Published in JACC 2017

ESICM Partners Webinar - Dynamic Measures: What is new in fluid management?

Please leave comments


 

Do we really need to limit tidal volume in everybody

Below is video recording of pro- con debate on this topic. See what you think and comment on the presentations.This was presented in Brussels during the ISICEM Symposium, March 2017.
It also raises the issue if we should look for " a middle of the road" solution by applying this strategy to only high risk -ARDS patients by using for example the LIPS score .
Is the right strategy in the middle, using a score trying to  identifying high risk patients, or should we take an all or nothing approach in non-ARDS hypoxemic respiratory failure?
Use earphones as the audio is not great. I am planning to edit with Camtasia Studio and attach separately recorded audio of higher quality. Stay tuned.



 

Is LIPS really predictive of ARDS..... look at the overlap in the slide in a surgical population

ECCO2R in patients with acute respiratory failure

Carbon dioxide (CO2) which is twenty times more diffusible and has different physiological features compared to oxygen, still continues to occupy one of the most important physiological parameters in intensive care practice and can often act like double-edged sword. Hypercapnia may have deleterious effects on cardiac, brain and lung function. In contrast, it has also been shown that acidosis secondary to CO2 elevation may have an anti-inflammatory effect and consequently permissive hypercapnia may prevent progression of lung injury. However, this immunosuppressive effect can increase the tendency for bacterial super-infection (1).

Over last decade, artificial support systems called Extracorporeal Carbon Dioxide Removal or ECCO2R have increasingly become popular devices used to control CO2 levels. Indications include not only optimisation of lung protection in acute respiratory distress syndrome (ARDS) management, but also for type 2 respiratory failure induced by exacerbations of severe asthma and chronic obstructive pulmonary disease (COPD) or temporarisation as a bridge to lung transplantation (2-5). The main characteristics that separate ECCO2R from other extra-corporeal life support (ECLS) techniques, is the need for significantly reduced calibre of cannulae required for vascular access (due to the low blood flow requirement through the extra-corporeal gas exchange membrane to remove CO2).

This recent article by Morelli et al (6) in the journal Intensive Care Medicine highlights that there is a lack of current evidence (small, single centre studies) for the general application of ECCO2R to daily practice. The main clinical indications at present are in ARDS and COPD.

Initially the use of ECCO2R was introduced into ARDS through the need to prevent excessive hypercapnia as a result of low tidal volume lung protective strategies. Zapol et al. introduced the concept of applying ECMO in order to prevent ventilator induced lung injury (VILI) (7). Further evidence came from the Xtravent study by Bein et al. where ultraprotective ventilation strategies, specifically with the use of ECCO2R suggested a trend towards improved survival (8). As a result, there are two large ongoing prospective multicentre randomised control studies (SUPERNOVA and REST) in France and the UK examining the safety and feasibility of such a strategy. It is expected that, within the next five years, the results of these studies will provide valuable guidance regarding the evidence based application of the combination of ultra protective ventilation and ECCO2R in acute respiratory failure.

The other use of ECCO2R is in the support and prevention of invasive mechanical ventilation (IMV) in patients with acute type 2 respiratory failure. It does not only avoid endotracheal intubation in these patients, but also reduces respiratory work, the need for sedation and as a result, further CO2 production. In a similar fashion, ECCO2R may be also be a supportive strategy as a bridge to lung transplantation  in the maintenance of respiratory muscle strength. In addition, ECCO2R may improve pulmonary hypertension and right heart function and improve myocardial efficiency (9).

However it should be emphasised clearly that, even if ECCO2R helps intensivists in the situations described above, there could be some inevitable drawbacks for patients related to utilising these devices. The expense of lowering CO2 can sometimes increase hypoxaemia, as a result of atelectasis with low tidal volume associated low airway pressures and ventilation-perfusion mismatch and there may be recourse to ECMO in some patients treated with ECCO2R. Furthermore, due to the low blood flows used through the extracorporeal circuit, there is increased risk of thrombosis within the catheter and gas exchange membrane (10).

To conclude, due to observational designs, low patient numbers, controversial results and some disadvantages such as hypoxemia, current studies do not demonstrate  the efficiency and applicability of ECCO2R. More robust studies are needed to determine its efficacy in daily practice with these patients.

This article review was submitted by EJRC members Dr Burcin Halacli and Dr Brijesh Patel (Royal Brompton Hospital), on behalf of the NEXT committee.

References
1.     Ismaiel NM, Henzler D (2011) Effects of hypercapnia and hypercapnic acidosis on attenuation of ventilator-associated lung injury. Minerva Anestesiol 77:723–733
2.     Gattinoni L, Agostoni A, Pesenti A et al (1980) Treatment of acute respiratory failure with low-frequency positive-pressure ventilation and extracorporeal removal of CO2. Lancet 2:292–294
3.     Tajimi K, Kasai T, Nakatani T, Kobayashi K (1988) Extracorporeal lung assist
for patient with hypercapnia due to status asthmaticus. Intensive Care
Med 14:588–589
4.     Sklar MC, Beloncle F, Katsios CM et al (2015) Extracorporeal carbon dioxide removal in patients with chronic obstructive pulmonary disease: a systematic review. Intensive Care Med 41:1752–1762
5.     Schellongowski P, Riss K, Staudinger T et al (2015) Extracorporeal CO2 removal as bridge to lung transplantation in lifethreatening hypercapnia.
Transpl Int 28:297–304
6.     Morelli A, Del Sorbo L, Pesenti A, Ranieri VM, Fan E. Extracorporeal carbon dioxide removal (ECCO2R) in patients with acute respiratory failure. Intensive Care Med. 2017 Apr;43(4):519-530.
7.     Zapol WM, Snider MT, Hill JD et al (1979) Extracorporeal membrane oxygenation in severe acute respiratory failure. A randomized prospective
study. JAMA 242:2193–2196
8.     Bein T, Weber-Carstens S, Goldmann A et al (2013) Lower tidal volume strategy (≈3 ml/kg) combined with extracorporeal CO2 removal versus “conventional” protective ventilation (6 ml/kg) in severe ARDS: the prospective randomized Xtravent-study. Intensive Care Med 39:847–856.
9.     Karagiannidis C, Strassmann S, Philipp A, Müller T, Windisch W (2015) Veno-venous extracorporeal CO2 removal improves pulmonary hypertension in acute exacerbation of severe COPD. Intensive Care Med 41:1509–1510
10.     Fanelli V, Ranieri MV, Mancebo J et al (2016) Feasibility and safety of
low-flow extracorporeal carbon dioxide removal to facilitate ultraprotective
ventilation in patients with moderate acute respiratory distress
syndrome. Crit Care 20:36

What’s new in refractory status epilepticus?

Refractory status epilepticus (RSE) is defined by persistent seizures, resistant to first-line (benzodiazepines) and second-line (“classic” anticonvulsant therapy, suchas valproate, phenytoin/fosphenytoin or levetiracetam), usually requiring general anesthesia and continuous electroencephalogram (EEG) monitoring . This is of particular importance since up to 43  % of patients with status epileptics will progress to RSE. Rossetti and Bleck recently proposed an update on the management of status epilepticus .

This article reviews the recent literature on convulsive RSE in adults, aiming to summarize advantages/disadvantages and comparative studies of “standard” intravenous anesthetics (propofol, midazolam, barbiturates) and describe the emerging use of the alternative anesthetic agent, ketamine. An algorithm is p[roposed for the management of RSE in the ICU.

Note the option and role of ketamine.

Hemodynamic Monitoring:what is new in 2017

Here is a  link to the audio of the entire (Non- Invasive) Hemodynamic Montoring in perioperative setting and in the ICU in critically ill intubated and non- intubated patients at ISICEM  37th Meeting Brussels , Belgium . It's somewhat of an exhaustive review.I will publish the slides later, as I am sending this ad hoc from the Starbucks at Brussels Central train Station. 

At the end, I felt somewhat let down as I could not pinpoint either Xavier Monnet or Ivor Douglas what single test to use on on critically ill septic patients to asses PLR, particularly in intubated patients without arrhythmia's, sedated and not over- breathing the ventilator (either on VCV- AC and PC- AC).

Both speakers also had a significant conflicts of interest. Xavier Monnet with Precision Medical and Ivor Douglas with Cheetah Medical, both heavily sponsored for there research in the field. 
Nevertheless, I think you will take away clinical useful information from most of the talks. 

Keep in mind that the latest and newest drug or test often doesn't stand the test of time.  An important article from the New Yorker ,  highlights the point I am trying to make here .Will NICOM or etCO2  as CO ( cardiac output ) surrogate measurement technique to assess FLR  fall prey to " regression to the mean ",  as happens for most clinical interventions and diagnostic tests?  Bioimpedance is a noteworthy example in this category. I am afraid the answer will be eventually ...yes. 

(More thoughts of the decline effect, New Yorker) 

A few pratical and clinical helpful messages can be taken away form this session: 

1) Provided you believe the results, act accordingly to what the device tells you (consistency). Unfortunately, I have not found the +LR and -LR ratios for either etCO2 and NICOM. I asked the question, neither researchers could give me an answer.

2) Probably, the most useful result you can get, applied to the current "slow data-point collection" NICOM device is a negative result ( I supect NICOm has a good NPV but I cannot prove this based on the literature). This is important because further aggressive fluid administration will avoid  further damage to the glycocalyx and capillary leak  

3) Repeated fluid boluses guided by a positive result on NICOM ( assuming an unrealistic 100% accuracy - probably more in the 60- to 70% range), may still cause an overshoot. 
Is the infliction point for CO on the Frank-Starling (FS) curve the end- point  for optimal tissue perfusion and oxygenation?
What is the ideal CO for an individual patient ? (something these devices cannot tell us ). We are already high on the FS ("flat part") curve once the test becomes negative. Do we need to go this far ?  

4) Maintenance fluids after initial volume resuscitation (this is  after the usual 30 ml/kg in the hypotensive septic patient and +/- pressor use initially) should be abandoned in favor of clinical assessment and FLR.Either etCO2 ( but specific conditions will need to be met and thsi will be a topic of another blog entry) or NICOM maybe a useful CO surrogate marker, although PPV/SVV techniques can still  be used in the right clinical context. 
Unchecked/unmonitored use of maintenance fluids is associated with increased mortality.

5) "Rapid NICOM" (not clinically available yet ) may be the most single useful test in the near future for FLR ( flid responsiveness).

6) Because of the well studied variable accuracy ( >30-40%) of various noninvasive hemodynamic monitoring techniques, trending results does not necessarily improve clinical decision making. Accuracy is not independent of interpretation of trending results.   

Programme Hemodynamic Non- Invasive Montoring 37th Symposium 2017, Brussels, Belgium 

Norepinephrine Shortage and Mortality

This  important study, presented yesterday in Brussels at the 37th ISICEM and same time publication in JAMA,  raises  the concern that national drug shortages could be placing potentially large numbers of patients in jeopardy, such as an increased risk of death from septic shock.


Potential pitfalls of the study are addressed in the Editorial.  

Driving Pressure: An Important Parameter to Prevent ARDS/VILI

I will write more about this in the next blog, but the concept of driving pressure ( Pdr = Vt/Crs- Vt;  tidal volume, Crs; compliance respiratory system ) is important in VILI and is and independent risk factor. Just ventilating at 6 ml/kg does not assure decreased risk of VILI if done with Pdr> 12. This is an important bedside concept we will need to incorporate in our clinical thinking.

The following presentation is a nice and simple introduction:

Driving Pressure in ARDS

Capnography during Cardiac Arrest

Here is some useful info on etCO2 during cardiac arrest as well as some references pointing out benefits and limitations of the technique, as well as use in practice. etCO2 during CPR is certainly a useful​ adjunct.

The AHA Guidelines only label this as a Class  IIB recommendation and needs to be used with additional clinical parameters . Also, be able to troubleshoot the device as other factors can be involved giving an inaccurate reading .

Here are some references with additional info:

Heradstveit BE, Sunde K, Sunde GA, Wentzel-Larsen T, Heltne JK. Factors complicating interpretation of capnography during advanced life support in cardiac arrest–a clinical retrospective study in 575 patients. Resuscitation. 2012 Jul;83(7):813-8. doi: 10.1016/j.resuscitation.2012.02.021. Epub 2012 Feb 25. PubMed PMID: 22370007.

Kolar M, Krizmaric M, Klemen P, Grmec S. Partial pressure of end-tidal carbon  dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care. 2008;12(5):R115. doi: 10.1186/cc7009. Epub 2008 Sep 11. PubMed PMID: 18786260; PubMed Central PMCID: PMC2592743.

Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med. 1997 Jul 31;337(5):301-6. PubMed PMID: 9233867. [Free Full Text]

Comparative Effectiveness of Vancomycin and Metronidazole

Among patients with severe disease, 30-day all-cause mortality was significantly lower for those who were treated with oral vancomycin than for those who were treated with metronidazole (15% vs. 20%); 30-day mortality did not differ significantly among patients with mild-to-moderate disease. Also, CDI relapse rates did not differ between treatment groups in either stratum of disease severity.

Comparative Effectiveness of Vancomycin and Metronidazole for the Prevention of Recurrence and Death in Patients With Clostridium difficile Infection


Real life data show that metronidazole is still given frequently in patients with severe disease.


Here is a risk calculator for moderate- severe disease requiring oral vancomycin

NOACs in Surgery

This a video from the European Society of Intensive  Care Medicine on monitoring , time of holding and restarting of NOACs in relation to surgery and treatment/reversal  with various degrees of bleeding. A couple of important points:

1) Apixaban does not affect coagulation parameters, as all other NOAC's do to a variable extend (but never correlate with degree of anticoagulant effect) . dTT and PT/PTT will only tell you if there is treatment effect if elevated, but it says nothing about the actual levels of the drug . A normal PT/PPT and TT in a patient taking an unknown NOAC , can have significant elevated drug levels and be coagulopathic when the drug was apixaban.
2) There is no role for a FFP during bleeding with any of these drugs ....you will have to give liters and liters and deplete the bloodbank in the process
3) Thromboelastograms will become more and more important, especially now that rivaroxiban is approved in conjunction with DAPT in ACS
4) Be very careful with NOACs in Stage D HFrEF patients, as they often have wide swings in renal function and a large number of them have cardio-renal syndrome class II. I still prefer VKA as drug of choice. Moreover, these patients were not studied in the various trials
5) Although not mentioned in this Webinar: NOAC's are contraindicated in patients with mechanical valves ( until further trials available)  !

Attached is also an article from JACC on the relation of NOAC's and coagulation parameters.

Laboratory Measurement of the Anticoagulant Activity of the Non–Vitamin K Oral Anticoagulants

Webinar 2016 Sepsis Guidelines ESICM

Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants

Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants https://t.co/oTvhHIDTbJ pic.twitter.com/0VQ3S22orA

— Critical Care (@Crit_Care) February 15, 2017

Link of the article to my ReadCube

Should We Intubate During In -Hospital Cardiopulmonary Resuscitation: Conventional Wisdom vs Big Data

Intubation during arrest was associated with worse outcomes.

The 2015 American Heart Association Advanced Cardiovascular Life Support guidelines deemphasize advanced airway placement as a component of initial resuscitation. Out-of-hospital–arrest data suggest lower survival among patients who are intubated in the field (NEJM JW Emerg Med Feb 2013 and JAMA 2013; 309:257). To determine whether this applies to in patients, investigators examined resuscitations of more done 108,000 patients in a US registry.

Seventy percent of patients were intubated during their code events; most (95%) of these intubations occurred within 15 minutes of resuscitation. Patients with initial nonshockable rhythms (i.e., pulseless electrical activity [PEA] or asystole) were more likely to be intubated than were those with ventricular fibrillation or tachycardia (69% vs. 53%).

In a time-matched propensity analysis, patients who were intubated during resuscitation were significantly less likely to survive to discharge than those who were not (16% vs. 19%) and were less likely to be discharged with good functional status (11% vs. 14%). In subgroup analyses, associations between intubation and these outcomes were not seen in patients who had preexisting respiratory insufficiency but were more pronounced for patients with initial shockable rhythms.

Comment by Patricia Kritek, MD. , American College of Chest Physicians (Critical Care Board Review Course):

This observational study raises important questions about an established practice: Attempt at intubation can interrupt chest compressions or slow defibrillation, potentially delaying these life-saving interventions, particularly for patients with ventricular fibrillation or tachycardia.  However the results still could be confounded by underlying differences between the intubated and non-intubated groups that were not captured by the statistical technique of propensity matching.  Therefore, I am not ready to abandon efforts to intubate patients with in-house arrest, especially those with PEA or asystole moreover, when respiratory failure is the cause of an arrest, early advanced airway management is important as a potential remedy to the underlying pathophysiology.

The accompanying editorial in JAMA  is enlightening and highlights the pitfalls, but also the strengths of this analysis.

Is There Any Benefit at all to Hypothermia in In-Hospital Cardiac Arrest

Data from a large cohort examining the the benefit of hypothermia in adult in- hospital arrest found no benefit. As a matter of TTM( targeted temperature management) was associated with a lower likelihood of survival to hospital discharge and a lower likelihood of a favorable neurological outcome in both shockable and non- shockable rhythms . An RCT is certainly warranted in this group. The data are consistent with a prospective study in the pediatric population ( the latter did have a major flaw of initiating TTM on average 5 hours after ROSC )

Association Between Therapeutic Hypothermia and Survival After In-Hospital Cardiac Arrest

No Benefit from Therapeutic Cooling After Pediatric In-Hospital Cardiac Arrest

One-year outcomes were similar with therapeutic hypothermia or therapeutic normothermia.

The efficacy of therapeutic hypothermia (target temperature, 33.0°C) versus therapeutic normothermia (target temp 36.8°C) in improving outcomes after out-of-hospital cardiac arrest in children is similar in clinical trials. To compare the efficacy of these interventions after in-hospital pediatric cardiac arrest, researchers randomized 329 children aged 48 hours to 18 years to either intervention (maintained for 120 hours) after in-hospital arrest.

The primary outcome was 12-month survival with favorable neurobehavioral outcomes. All participants had previously normal neurobehavioral assessment, received chest compressions for at least 2 minutes, and remained dependent on mechanical ventilation after return of circulation.

There were no between-group differences in the primary outcome, and the rates of survival at 12 months between the hypothermia and normothermia groups were also similar (49% and 46%, respectively). The trial was stopped after a review of interim efficacy results due to an assessment of futility.

COMMENT

Despite these authors' valiant attempt to control the therapeutic interventions, some variables might have affected the outcomes. For example, it took approximately 5 hours to initiate the interventions after the return of circulation. Would outcomes have been different if the interventions had been carried out more quickly? Are these target temperatures the correct ones? 

Therapeutic Hypothermia after In-Hospital Cardiac Arrest in Children

Lower Oxygen Saturation Goals Are Safe in Mechanically Ventilated Patients

Targeting to 88%–92% did not cause harm.

The optimal oxygenation goal for patients who are receiving invasive mechanical ventilation remains unclear. Clinicians usually target resolution of hypoxemia and pay little attention to weaning levels of oxygen once 100% saturation has been achieved. However, harms caused by hyperoxia, including effects on cardiac function and lung parenchyma, are of concern.

To assess the safety of a lower oxygenation target, investigators randomized 104 patients who were receiving invasive mechanical ventilation to either a conservative strategy (peripheral oxygen saturation, 88%–92%) or a liberal strategy (peripheral oxygen saturation, >95%) for the duration of ventilator support. Positive end expiratory pressure (PEEP) levels were determined by treating physicians who were not blinded to the intervention. Three quarters of enrolled patients had medical diagnoses. Mean fraction of inspired oxygen (FiO2) at randomization was 0.44.

No differences were detected between groups in organ dysfunction or mortality. Mean saturation in the conservative arm was 93.4% (vs. 97.0% for the liberal arm), and more arterial blood gases were drawn. These two findings suggest some clinician discomfort with targeting lower oxygen saturation levels. Patients in the conservative arm were more likely to have episodes of severe desaturation, although these events were rare in both groups.

This study reassures us that a lower oxygen saturation target is not harmful. Whether this practice confers benefit is unclear, but these results should allow researchers to comfortably conduct larger randomized, controlled trials with lower oxygen saturation goals.

Conservative versus Liberal Oxygenation Targets for Mechanically Ventilated Patients. A Pilot Multicenter Randomized Controlled Tria

Surviving Sepsis - Guidelines 2016

A lot has been written about this and this is not hot of the press , but the video gives a nice summary and comparison with the previous guidelines

The 2012 versus the 2016 Guidelines Video

A User Guide to the 2016 Surviving Sepsis Guidelines

Webinar from ESICM on Hypothermia post Cardiac Arrest: 33 vs 36 degrees ..or just fever control?

Interesting how we change our minds after a one hour lecture. The original 33 degree Hypothermia trial had a major flaw: the control arm had a high incidence of uncontrolled fever, common post cardiac arrest. Not exactly the control group you want. 
I suspect ultimately fever control is all that is needed , but device therapy will likely accomplish this better then medical therapy alone.

Setting up APRV on the PB 840 Ventilator

I have been so used working with the Drager ventilator where setting the Phigh and Plow, as well as Thigh and Tlow is easy and intuitive.  However in other ventilators particular in the Puritan-Bennett 840 you  have to go into settings and use the locks to demonstrate your T low.  
Every time I camera in and asked a respiratory therapist,  they state that they cannot set T low . This not the case . Also the difference adding PSV is that you have to subtract the difference between Phigh and Plow and then add PS to the pressure difference to set the level of PS you want. This is explained pretty well in the video. Also RR has to be kept between 6-12 BPM ( look at Thigh and Tlow when changing this)  and PEFR can be nicely demonstrated, magnified in freeze frame mode. I: E ratio becomes totally irrelevant when PSV is added.


Here is a good summary overview on how to manipulate the various parameters :

APRV Management

Discussion high Tv and lung protective strategy in APRV

APRV  discussion 

Severe hypercapnia and outcome of mechanically ventilated patients with ARDS

Limitation of tidal volumes (<8ml/kg ideal body weight) and airway pressure is used as a lung protective strategy during MV in patients with ARDS . However, this strategy may result in high partial pressure of carbon dioxide in arterial blood (PaCO2) levels. The biological effects of hypercapnia in critically ill patients are conflicting. It remains unclear if, on balance, hypercapnia per se has any effect on organ function and survival. 

In patients with severe hypercapnia, the PaO2/FiO2 ratio was significantly lower and peak airway pressure, plateau airway pressure, and PEEP were higher than in patients with a maximum PaCO2 of <50 mmHg. The relationship between PaCO2 and ICU mortality demonstrated a U-shaped curve, with patients with very low and high PaCO2 having an increased risk of death. Mortality was significantly higher in patients with a maximum PaCO2 of ≥50 mmHg during the first 48 h of MV (62.5%) than in patients with a maximum PaCO2 of <50 mmHg (49.6%). The incidence of barotrauma, renal dysfunction, and cardiovascular dysfunction was significantly higher in patients with a maximum PaCO2 of ≥50 mmHg compared to patients with a maximum PaCO2 of <50 mmHg (p<0.05). 

After adjustment for baseline variables including age, SAPS II at ICU admission, corrected minute ventilation, use of pressure/ volume limitation strategy (PLS), presence of acidosis, driving pressure, PaO2/FiO2 ratio, and study period, the presence of severe hypercapnia remained independently associated with a higher risk for ICU mortality (OR 1.93, 95% CI 1.32–2.81; p = 0.001). Even when limiting analysis to patients receiving PLS (and matched for all other variables), severe hypercapnia was associated with higher ICU mortality compared to patients with a maximum PaCO2 of <50 mmHg (OR 1.58, CI 95% 1.04–2.41; p = 0.032). Acidosis or the combination of hypercapnia and acidosis independently increased the risk of ICU mortality.

Conclusion:

Patients receiving lung-protective ventilation with a tidal volume of ≤6 ml/kg had a high incidence of severe hypercapnia. Although patients receiving lung-protective ventilation have a lower mortality, hypercapnia appears to be independently associated with worse outcomes in patients with ARDS. The authors challenge the notion that severe hypercapnia is safe and prospective trials are required to ascertain if hypercapnia is indeed ‘permissive’. 

Link to original article in ESIM 2017


My comment: 

Although a retrospective study, it raises the issue if we should apply early APRV - with benefits of improved oxygenation, circumventing the problem of 6 ml/kg Tv, and lower paCO2, as this is less of problem in this mode, This actually one of the points that Nader Habashi makes about APRV. It should not be used as a rescue mode. Its interesting to look at the animal long model in this mode, where there is no repeat collapsing and reopening of recruitable lung tissue and with in general little problem controlling paCO2. I think the time has come to compare in a RCT APRC versus VCV-AC and /or PC-AC in moderate to severe ARDS. My humble opinion and I tend to go very early to APRV already in ARDS. An RCT will give us the answer to this important question. 

Predicting NIV failure in hypoxemic patients: the HACOR score

Non-invasive ventilation (NIV) is applied worldwide to patients with hypoxemic respiratory failure. It is often applied as an attempt to avoid invasive mechanical ventilation. However, the application of NIV is often ad hoc and non-evidence based. Duan et al. have developed a scoring system which accurately predicts patients that would be at risk of NIV failure such that the clinician can plan for the decision to implement invasive mechanical ventilation.

Results:
1.    Heart rate, Acidosis (pH), Consciousness (GCS), Oxygenation, and Respiratory rate (HACOR) were independent predictors of NIV failure in the test cohort.
2.    HACOR score is out of 25 with differential weighting of each scale:

3.    At 1 hour of NIV, odds ratio of NIV failure is 1.73 for every 1-point increase in HACOR score of test cohort.
4.    Patients with NIV failure show a higher HACOR score at 1, 12, 24, and 48 hours of NIV.
5.    HACOR score improves in patients with NIV success and remains unaltered in patients with NIV failure.
6.    The diagnostic accuracy for NIV failure of a HACOR score above 5 at 1 hour of NIV was 81.8% (test cohort) and 86% (validation cohort).
7.    This remained above 80% regardless of NIV duration, diagnosis, age, or disease severity (APACHE 2 score).
8.    Patients who failed NIV and were intubated early (within 12 hours) had a HACOR > 5 at NIV initiation and 1 hour NIV than those intubated later (after 12 hours of NIV). Interestingly, early intubation in this study had a significantly lower mortality than late intubation in those with NIV failure.


Conclusions:
1.    HACOR is a potentially useful bedside tool for the prediction of NIV failure.
2.    HACOR score accurately predicts NIV failure in patients with hypoxemic respiratory failure in this single centre study.
3.    A HACOR score >5 at 1hour of NIV highlights patients with a >80% risk of NIV failure regardless of diagnosis, age, and disease severity.
4.    The authors imply the utility of HACOR to assess the need for early to improve mortality.

ORIGINAL ~ Predicting NIV failure in hypoxemic patients: the HACOR score

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Comments:
There is some risk of circularity bias here, and some parameters assigned high points in the HACOR score (e.g., GCS score <13, PaO2/FiO2 <125) seem like obvious triggers for intubation. Nevertheless, the HACOR components make clinical sense and the score predicted failure well. The HACOR score is a reasonable tool to use when you are unsure about whether to use NIV

Echocardiographic Analysis of Heart Failure

Here are essential parameters needed for evaluation of HFpEF in resting echocardiographic studies.

 Additional data are derived from Valsalva and Leg Raising Manoeuvres not shown. Also speckle tracking and Global Longitudinal Strain is shown provides additional data on mycardial function.

HCM Japanese Variant

APRV Workshop by Dr. Nader M. Habashi, MD, FACP, FCCP

One of the best reviews are found around.  Interestingly how he only works with  2 variables, Phigh and Thigh.

The Way Forward

Addressing Physician Burnout

Early Intubation associated with decreased survival in cardiac arrest

Findings do not support early tracheal intubation for adult in-hospital #cardiacarrest https://t.co/y8gitYJuzu

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Reduce the risk of iatrogenic anaemia by returning blood to the patient when sampling - now possible with Proxima https://t.co/oc1qgQdtGG pic.twitter.com/ueamb7NErb

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Early enteral #nutrition in critically ill: @ESICM clinical practice guidelines. #FOAMed https://t.co/PokbfrTdAZ pic.twitter.com/lksV5pGXMA

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