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?

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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