ESICM Regional Conference Athens 2017: How to assess perfusion

First session this morning. Talks focusing on SvO2, ScvO2, PCO2 gap, lacate and measurement/assessment of peripheral perfusion

Again a fair amount of focus on the microcirculation…..

Massimo Antonelli – SvO2/ScvO2, PCO2 gap

“Shock is the clinical expression of circulatory failure that results in inadequate cellular O2 utilisation”
Vincent et al. NEJM 2013
Aim of treatment: restoring lost balance between O2 demand from peripheral tissue and O2 supply
What are the signs of tissue hypoperfusion?
Clinical indices
Mottled skin, altered mental status, diuresis <0.5ml/kh/hr, hypotension/tachycardia etc
Haem parameters:
Increased O2ER and anaerobic threshold —-> SvO2/ScvO2/Lactate
Inadequate DO2 —-> CO/Hb/PCO2 gap
Impaired peripheral perfusion with normal macro-haemodynamics —-> microcirculation e.g. sublingual
  • SvO2 = VO2 from the whole body, ScvO2 = VO2 from mostly brain and upper arms
  • Absolute values are not interchangeable but trends over time are the same
  • Sedation may influence both measurements
  • Septic patients may have abnormally high measurements
Rivers – early GDT —> suggested a benefit to targeting ScvO2 (amongst other variables….)
But ARISE/ProCESS/PROMISE ——> not replicated…although corrected ScvO2 higher in Arise/Process/Promise compared to Rivers – are we speaking about same populations when comparing studies?
What are the drawbacks of using ScvO2?
ScvO2 often high in septic pts ——> VO@ decreased in septic shock patients
Unclear the impact of microcirculatory impairment e.g. DeBacker ICM 2010
Venous admixture?
What about the elevated PCO2 gap (A-V)?
Nice review here by Vallet in ICM 2013 and in LITFL here
PCO2 gap is marker of inability of adequate venous flow
Elevated PCO2 gap means that:
  1. CO is not sufficient under conditions of suspected tissue hypoxia
  2. Microcirculatory flow is not high enough or adequately distributed to clear the CO2 excess even in the presence of a normal CO

“PCO2 gap should be considered as a marker of the ability of an adequate venous blood flow to remove the CO2 excess rather than as a marker of tissue hypoxia”

Mallet et al. Minerva Anesth 2015

Can we use it clinically?
Yes e.g. in tandem with lactate —-> https://www.ncbi.nlm.nih.gov/pubmed/25792204
Take home messages:
  1. DO2 is important when O2 consumption is dependent on it
  2. Very low SvO2/ScvO2 are markers of tissue hypoxia and should be corrected
  3. Sepsis alters normal DO2/VO2 relationship such that ScvO2 may not always be a good marker of tissue hypoxia
  4. CO2 gap may unmask those patients who are going to develop tissue hypoxia and should be considered a marker of low flow state

Interesting question from the floor:

Q: Should we be worried about patients post-CABG with low SvO2 (e.g. PAC-measured)?

A: Low SvO2 not always a marker patient is unwell e.g. when exercising, SvO2 can drop to 25%. So need to assess on case-by-case basis

Andrew Rhodes – Lactate as a marker of perfusion

Sepsis remains a huge problem – recent paper this year: bit.ly/sepsisjama

 Surviving Sepsis Campaign (SSC) targets:

  • CVP
  • MAP
  • UO
  • ScvO2
 BUT – ARISE/PROMISe/PROCESS —> can do it but doesn’t improve outcome (despite not being as sick/no signal of harm)
Lactate is a surrogate marker of inadequate tissue perfusion. But lots of causes of high lactate e.g.
Screen Shot 2017-06-16 at 14.28.08
Lactate and outcome?
  • Increased levels are associated with increased organ failure and mortality
  • Reduced clearance of lactate is associated with increased morbidity and mortality
Screen Shot 2017-06-16 at 14.11.14
Best lactate cutoff for predicting poor outcome was 1.5:
Mortality below 1.5 = 17%, above 1.5 > 60% —-> bit.ly/lactatesepsis
Similar in children —-> bit.ly/lacatepaeds
So — does measuring lactate improve pt outcomes?
Serial measurement is more useful than single measurement – sensitivity/specificity of single lacate level has been debated
 But problems…..
How can we use lactate to guide resuscitation?
RCT by Tim Jansen on lactate to guide resuscitation – especially nice protocol ncbi.nlm.nih.gov/pubmed/20463176
(**But – no difference in lactate between control/intervention group after treatment…..**)
Effect replicated in RCT by Chinese group:
One protocol suggested by the speaker:
Screen Shot 2017-06-16 at 14.27.44
 SSC 2016: “We suggest guiding resus to normalise locate in patients with elevated locate levels as a marker of tissue perfusion” – weak recommendation, low quality of evidence
But what percentage reduction should we aim for and how should we do that? Still unclear…..
Take home messages:
  1. Lactate remains the best biomarker for risk assessment
  2. Low lactate clearance is a good predictor of mortality
  3. At the present time, lactate clearance alone has not been proven to be an adequate end point for resuscitation
  4. Further trials are needed to demonstrate the efficacy of lactate clearance as a primary endpoint in the resuscitation of severe sepsis or septic shock

Jacques Duranteau – Peripheral perfusion

Again – emphasis on the importance of the microcirculation

IMG_0888

Need real-time measurement of peripheral perfusion

Screen Shot 2017-06-16 at 14.53.45

Mottling score predicts survival in septic shock —-> https://t.co/4rWohL2jPn 

Subjective assessment of peripheral perfusion may be useful —-> ncbi.nlm.nih.gov/pubmed/19237899
Nurses can reliably assess microcirculation at the bedside with high sens/spec —> bit.ly/2rmW0Mp
Can use TTE to measure AKI – “resistive index” in kidney at bedside
Screen Shot 2017-06-16 at 14.48.32
Can also assess brain perfusion:
Screen Shot 2017-06-16 at 14.53.23
and