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?
Mottled skin, altered mental status, diuresis <0.5ml/kh/hr, hypotension/tachycardia etc
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
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:
- CO is not sufficient under conditions of suspected tissue hypoxia
- 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?
Take home messages:
- DO2 is important when O2 consumption is dependent on it
- Very low SvO2/ScvO2 are markers of tissue hypoxia and should be corrected
- Sepsis alters normal DO2/VO2 relationship such that ScvO2 may not always be a good marker of tissue hypoxia
- 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:
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.
Lactate and outcome?
- Increased levels are associated with increased organ failure and mortality
- Reduced clearance of lactate is associated with increased morbidity and mortality
Best lactate cutoff for predicting poor outcome was 1.5:
So — does measuring lactate improve pt outcomes?
Serial measurement is more useful than single measurement – sensitivity/specificity of single lacate level has been debated
How can we use lactate to guide resuscitation?
(**But – no difference in lactate between control/intervention group after treatment…..**)
Effect replicated in RCT by Chinese group:
One protocol suggested by the speaker:
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:
- Lactate remains the best biomarker for risk assessment
- Low lactate clearance is a good predictor of mortality
- At the present time, lactate clearance alone has not been proven to be an adequate end point for resuscitation
- 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
Need real-time measurement of peripheral perfusion
Mottling score predicts survival in septic shock —-> https://t.co/4rWohL2jPn
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
Can also assess brain perfusion: