ESICM Regional Conference Athens 2017: Management of Shock – Others

Right then – last session on other techniques/approaches to managing shock…..

Mechanical assist devices – Alain Combes

Classical indications for mechanical assistance:

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INTERMACS classification of indications for mechanical assist devices

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LVADs should be for stable patients – not for acute cardiogenic shock

IABP

What about IABP? SHOCK-2 trial Lancet 2013 —> no difference between control/balloon

Indication downgraded from I —> III: no indication for routine use in cardiogenic shock

Should it now be in the “Museum of Medicine” — along with the iron lung and swan ganz? 😉

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ESC/ – evidence now low

Tandem heart pVAFD

Not available in Europe – only US

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Difficult transeptal cannulation – fair number of issues with this device to be fair

Impella miniature intraaortic pump

Available in Europe

Up to 4L/min (Impella 5.0)

Issues

  1. Cost – 10-15K euros for few days use
  2. Concerns about haemolysis

Recent study – IABP v Impella —-> No difference in mortality

HeartMate PHP

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No data as of today for this pump

Major issues – only drain LV. Not of use in RV. New Impella for RV but cost ~20K euros

VA-ECMO

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Worth remembering that it’s low cost compared to Impella (but still 8-9K Euros per patient….)

Accepted indications:

A: ST-elevation with profound cardiogenic shock?

Paper —-> ST-elevation with profound cardiogenic shock

Close to 50% survival and 68% weaning in survivors

B: End stage DCM?

https://www.ncbi.nlm.nih.gov/pubmed/28471885

C: Fulminant myocarditis?

https://www.ncbi.nlm.nih.gov/pubmed/21336134

Most surviving without need for complex heart surgery/transplant

D: After cardiac surgery?

Old data but benefit —-> https://www.ncbi.nlm.nih.gov/pubmed/20106393

E: Post cardiac transplant?

https://www.ncbi.nlm.nih.gov/pubmed/21414795

What are the trends/emerging indications?

1. Septic shock with severe LV failure

Small study (n=14) but very unwell – SOFA score 18 with LVEF 16 and mean lactate 10

2. Pulmonary embolism

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3. Post-cardiac arrest

Post-resuscitation syndrome

Conflicting data on E-CPR —> benefit or no benefit

4. Combination – ECMO + Impella

Take home messages:

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Cristalloids or colloids? Balanced or not? – Luciano Gattinoni

Why do we give fluids?

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Review from 2013 in NEJM on resuscitation fluids —> here

So which fluid and what is the price to pay in terms of “health”?

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Low pressure

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Mechanics of fluid – no difference. Volume that creates a pressure

Issue is what price we pay by giving different fluids

CHEST trial – small differences in Cr. No standard deviations. Be careful interpreting data

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CONCLUSIONS:

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Individualising haemodynamic targets – Bernd Saugel

Precision medicine popular term – as is personalised medicine

e.g

http://www.nejm.org/doi/full/10.1056/NEJMp1500523#t=article

https://link.springer.com/article/10.1007/s00134-016-4471-8

https://www.ncbi.nlm.nih.gov/pubmed/26928384

 

Personalised medicine approach can be applied to haemodynamic management of ICU patients

https://www.ncbi.nlm.nih.gov/pubmed/28562384

 

Does personalising BP in the operating room improve outcomes?

https://www.ncbi.nlm.nih.gov/labs/articles/27792044/

Seems not to be important at first glance —-> MAP > 65 as food as one based on percentage reduction from baseline

But BP does not mean perfusion —-> autoregulation

https://annalsofintensivecare.springeropen.com/articles/10.1186/s13613-015-0085-5

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SSC recommends target of 65 BUT state ” when a better understanding of any pts condition obtained, BP target should be individualised”

Asfar et al NEJM 2014 – here

No difference in high v low target BP

BUT —-> Patients with chronic HT in the  low target group = increased RRT

 

What about SV/CO etc?

Pearse et al. Cardiac output guided management —> here

Maximisation of SV may not equate to optimisation

 

DO2 targeted?

Achievement of preoperative DO2 value associated with reduction in morbidity —> here

How to combine PERSONALISED treatment approached with PROTOCOLISED care?

 

What is the future?

Smaller sensors to record biosignals without heavy monitors/machines/cables

“Wearables”

 

Take home messages:

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ESICM Regional Conference Athens 2017: Management of shock – DRUGS

Vasopressors (A Gordon)

Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016 Authors Authors and affiliations

Comparison of Dopamine and Norepinephrine in the Treatment of Shock

Vasopressors for hypotensive shock (Cochrane review)

Catecholamines for shock – equally good or equally bad? – Singer

Issue with adrenaline is that lactate becomes hard to use as a target for therapy.

Association Between US Norepinephrine Shortage and Mortality Among Patients With Septic Shock

Vasopressin in shock – vasoconstrictor, V1 receptor on vascular smooth muscle, binds to V2 and oxytocin receptor. Septic shock – relative vasopressin deficiency

The VANISH Randomized Clinical Trial

Vasopressin versus Norepinephrine in Patients with Vasoplegic Shock after Cardiac Surgery: The VANCS Randomized Controlled Trial

Future trials on – angiotensin II, selepressin

Gordon – 1st line = noradrenaline. Will escalate to vasopressin (up to 0.06U/min). No dopamine.

Inotropes (A Mebazaa)

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Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance

  • the guidance advocates the use of lung ultrasound in the acute phase to help guide therapy

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

The Effectiveness of Inodilators in Reducing Short Term Mortality among Patient with Severe Cardiogenic Shock: A Propensity-Based Analysis

  • The initial use of inopressors alone appears to be associated with a poorer prognosis compared to a regimen of inopressors and inodilators in patients who are admitted for cardiogenic shock.

Pulmonary hypertension management (S Orfanos)

PULMONARY HYPERTENSION (GUIDELINES ON DIAGNOSIS AND TREATMENT OF)

Comprehensive Invasive and Noninvasive Approach to the Right Ventricle–Pulmonary Circulation Unit

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Prognostic factors and outcomes of patients with pulmonary hypertension admitted to the intensive care unit

Prostacyclin can reduce PVR and improve RV function but caution in LV failure. It can exacerbate V/Q mismatch leading to worsening gas exchange and hypoxaemia

Inhaled NO potent pulmonary vasodilator

Is there a safe plateau pressure in ARDS? The right heart only knows.

 

 

 

ESICM Regional Conference Athens 2017: How to monitor shock

Echocardiography (D Matamis)

Echo is not a haemodynamic monitoring tool – controversial. The speaker does feel that it is an excellent diagnostic tool.

Cases of pts with COPD and HCM with failure to wean from mechanical ventilator discussed. The managements were progressed using echocardiography.

Targeting occult heart failure in intensive care unit patients with acute chronic obstructive pulmonary disease exacerbation: Effect on outcome and quality of life

Takotsubo Cardiomyopathy

 

With the PAC (A Armaganidis)

The Pulmonary Artery Catheter A Critical Reappraisal

Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial.

Pulmonary artery catheters for adult patients in intensive care

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Volume status and fluid responsiveness (S Myatra)

Dynamic measures to guide fluid therapy

Use of ‘tidal volume challenge’ to improve the reliability of pulse pressure variation

Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients.

 

Volumetric variables including extravascular lung water (JL Teboul)

Comparison of values in critically ill patients for global end-diastolic volume and extravascular lung water measured by transcardiopulmonary thermodilution: a meta-analysis of the literature.

GEDV could overestimate LV preload in case of dilated RV

Extravascular lung water in critical care: recent advances and clinical applications

Less invasive hemodynamic monitoring in critically ill patients

 

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.
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Lactate and outcome?
  • Increased levels are associated with increased organ failure and mortality
  • Reduced clearance of lactate is associated with increased morbidity and mortality
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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:
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 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

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Need real-time measurement of peripheral perfusion

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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
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Can also assess brain perfusion:
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and