Category Archives: Circulation

Advanced Critical Care Echocardiography Course- Day 1

Introduction (De Backer)

Consensus statement on training in 2014 https://www.ncbi.nlm.nih.gov/pubmed/24615559  – this is the basis of the ESICM’s European Diploma in advanced critical care EchoCardiography (EDEC) https://www.esicm.org/education/edec-2/

CICM Levels of training https://onlinelibrary.wiley.com/doi/full/10.1002/ajum.12127

So what does advanced CCE measure compared to basic?

-Colour doppler looking at flow patterns and valvular lesions,

-spectral doppler for quantifying valvular abnormalities, measuring cardiac output and measuring intracardiac pressures

-Heart lung interactions

TEE is recommended as essential in EDEC

 

TOE Views (Vieilland- Baron)

http://www.echo-rea.uvsq.fr/echocardiographie-en-reanimation/langue-en/open-educational-resources/the-most-common-echocardiographic-views/03-transesophageal-echocardiography-the-most-common-views-248923.kjsp?RH=1354638851042

Practice online with the Toronto Virtual TEE simulator http://pie.med.utoronto.ca/tee/

LV Systolic function- Vieillard-Baron

-LV Dilation suggests a chronic injury

-LV Systolic dysfunction does not mean cardiogenic pulmonary oedema

-LV systolic function is a combination of contractility and afterload

-RWMA is ischaemia until proven otherwise

LV Systolic Function- Vignon

At the advanced level we are going way beyond “eyeballing” ejection fraction…

 

LV Systolic function- Dessap

Assess in all views:

Visual impression
LV EF (Ideally Simpson’s method of discs)
LV FAC

Don’t forget the importance of afterload!
Good images can be obtained with TTE 90% of the time.

If you are still struggling, strain is becoming more widely available…

LV Diastolic function- McLean

This is an area without much evidence in the critically ill…

ASE recommendations for LV diastolic dysfunction https://asecho.org/wp-content/uploads/2016/03/2016_LVDiastolicFunction.pdf

Applications of diastolic dysfunction guidelines in sepsis https://annalsofintensivecare.springeropen.com/articles/10.1186/s13613-017-0342-x

How to measure Diastolic function- Slama

This is really hard!

Problem with these tools is that mitral flow/pulmonary venous flow/Propagation velocity are all rather load dependent
Ea (e’) is probably least of these

EDEC Accreditation structure (De Backer)

Register here https://www.esicm.org/education/edec-2/

Pericardial disease and echo (Paul Mayo)

Twitter thread here https://twitter.com/iceman_ex/status/1177950552526864384

Whatever you do don’t forget that tamponade is a CLINICAL diagnosis!!

Many thanks to all the amazing speakers for sharing their knowledge.

TTM @ #EuAsia19

Optimal depth, timing and duration based on recent clinical trials (K Sunde)

Cardiac arrest is a complex disease

  • several different causes (many untreatable, irreversible, extreme challenging)
  • large heterogeneity
  • challenges the system due to the limited/crucial time-intervals (hypoxia/extreme ischemia)
  • large differences in quality of care within and inbetween systems (both during ALS and in post resuscitation care)
  • very high mortality

Depth and Timing

ILCOR Statement 2003 –

Unconscious adult patients with spontaneous circulation after out-of hospital cardiac arrest should be cooled to 32-34°C for 12-24 hrs when the initial rhythm was VF.

For any other rhythm, or cardiac arrest inhospital, such cooling may also be beneficial.

Outcome, timing and adverse events in therapeutic hypothermia after out-of-hospital cardiac arrest.

  • timing, speed and duration of hypothermia had no impact on outcome!

Confounding aspects regarding early/fast cooling

  • the lack of protection against a drop in core temperature is due to a larger and deeper brain injury! (link)
  • If you are really “dead” you are colder and it is very easy to cool you fast! (link)

Intra-Arrest Transnasal Evaporative Cooling: A Randomized, Prehospital, Multicenter Study (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness) link

Duration of TTM

Targeted Temperature Management for 48 vs 24 Hours and Neurologic Outcome After Out-of-Hospital Cardiac Arrest

Prolonged targeted temperature management in patients suffering from out-of-hospital cardiac arrest

Conclusion

  • Cardiac arrest is complex, with large heterogeneity and very high mortality
  • Large differences in quality of care within and inbetween systems
  • Concerning pathophysiology and TTM: depth, speed and duration impacts on the reperfusion injury/brain injury
  • We are concluding based on pragmatic trials not optimizing the intervention tested or considering the ongoing pathophysiology!
  • Outcome assessment: cognitive function/QoL years after the arrest!

Haemodynamic Management During Targeted Temperature Management (Huang CH)

Multiple reasons for haemodynamic instability post-cardiac arrest

Haemodynamic Response Correlated to Outcome – Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest.

Cardiovascular Response & Haemodynamic Changes In Hypothermia Treatment

  • Changes in CV β-adrenoceptor (reduced response)
  • Bradycardia
  • Increase in stroke volume
  • Reduced intravascular volume during hypothermia is by 10– 35%

Lower heart rate is associated with good one-year outcome in postresuscitation patients (link)

Survivors Have Higher Mean Arterial Pressure (link)

Lowest value of DAP over the first 6 h after ICU admission for predicting unfavourable neurological outcome at 3 months (link)

Postresuscitation hemodynamics during therapeutic hypothermia after out-of-hospital cardiac arrest with ventricular fibrillation: A retrospective study

Taiwanese Protocol

LIVES2018: Respiratory variations of the IVC- Cholley

Inferior Vena Cava may appear congested when it’s dilated without any respiratory variation collapsed with very small diameter through the respiratory cycle, or compliant and vary through respiratory cycle. But how IVC looks like depends on how the patientis breathing, spontaneouslyvs mechanically ventilated.

During spontaneous breathing, in inspiration there is a decrease in pleural pressure, partially transmitted to the heart chambers with a decrease in Right Atrial Pressureand increase in Venous Return (the lower the RAPthe easier the venous return). Because of this decrease in RAP there is a decrease in IVC transmural pressure the size (diameter) and a decrease in size of IVC.

To give numbers, a 40% variation in spontaneouslybreathingpatients is usually associated to preload responsiveness: patient will respond to fluids (but it does not mean that he needs fluids: gives only if associated hypotension/poor perfusion).

 IVC2

In patients with positive pressure ventilation physiology is completely reversed: you put positive pressure in the thorax, this is partially transmitted to the heart chambers whit an increase in RAP, an increase in IVC transmural pressure and in IVC diameter. We expect a dilated and non compliant Vena Cava due to the impeded venous return, collapsible vena cava is an abnormal finding. If you observe a compliant Vena Cava n a patient on MV, changing diameter with ventilation, actually increasing diameter with insufflation due to raised pressure in thorax impeding venous return and flattening in expiration with pressure release), this means that probablythis patient has volume in the veins that can be recruited. A > 12-18% variation in mechanically ventilated patientis usually associated to preload responsiveness(Feissel et al. 2004 http://bit.ly/2Cvm6Fp; Barbier et al. 2004 http://bit.ly/2Pb8R3p).

IVC2

In patients with elevated Intra-Abdominal Pressure IVC is not interpretable anymore.

The endpoint of resuscitation is improve tissue perfusion, not to increase IVC diameter. The respiratory variations in large vessels just attest that there is some stressed volume that can be recruited: is vein collapses there is room to expand a little more and by increasing the stressed volume there is an high probability to increase the venous return and cardiac output if you think this in needed.And remember: IVC measurement really simple but not make the vena cava say what it can’t say.

IVC3

Pictures from Cholley B talk at #LIVES2018

From theory to practice – ARDS: An old syndrome, new organ interactions #EuAsia18

The lung and the kidneys (Ostermann)

When kidney function lost, –> reduced clearance , fluid overload, acidosis BUT also inflammation, cytokine release and cell death

The distant organ effects of acute kidney injury

AKI causes a higher degree of capillary leakage within the lungs

Ventilator induced kidney injury

IMG_3154

Bench-to-bedside review: Ventilation-induced renal injury through systemic mediator release – just theory or a causal relationship?
Mechanical ventilation as a mediator of multisystem organ failure in acute respiratory distress syndrome.

Fluid management with a simplified conservative protocol for the acute respiratory distress syndrome

IMG_3155IMG_3154

Lung brain interactions (Oddo)

ARDS in the brain-injured patient: what’s different?

IMG_3158 IMG_3157

Issues to consider

  • Oxygenation
  • PEEP
  • CO2/TV

Hyperoxia in intensive care, emergency, and peri-operative medicine: Dr. Jekyll or Mr. Hyde? A 2015 update
Cerebro-pulmonary interactions during the application of low levels of positive end-expiratory pressure.

Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates.
Screen Shot 2018-04-14 at 11.30.11

Heart lung interactions (Cecconi)

IMG_3159

Is tidal volume challenge the new PLR? Use of ‘tidal volume challenge’ to improve the reliability of pulse pressure variation

Or end-expiratory hold?
Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients.

 IMG_3162