All posts by segun olusanya

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

New Technology in Ventilation 25th September 2017 #LIVES2017

In respiratory failure, there is regional variability in oxygenation (and perfusion)- imaging can be used to monitor this. Point of care ultrasound for instance ncbi.nlm.nih.gov/pmc/articles/P…

Electrical Impedance tomography can monitor regional changes as well ncbi.nlm.nih.gov/pubmed/25843526

Oesophageal manometry can help us monitor transpulmonary pressure nejm.org/doi/full/10.10… – however is only used in about 1% of ARDS patients according to the LUNG-SAFE study jamanetwork.com/journals/jama/…

Respiratory muscle functioning can be done using the NAVA device journals.sagepub.com/doi/pdf/10.117… – this may end up being key to keeping intrapleural driving pressure low (Amato)

Mechanical power can be roughly calculated at the bedside as a product of driving pressure and respiratory rate- this may become our key targeted variable in future (Amato)ncbi.nlm.nih.gov/m/pubmed/27620…

However both driving pressure and mechanical power remain static measures of lung mechanics. In future we’ll need dynamic bedside tools.

Ventilator dissynchrony remains a problem and contributes to mortality…. ncbi.nlm.nih.gov/pubmed/25693449

 

And of course there’s ECMO. Some patients still require ventilation while on ECMO and the reasons for this will vary- for some it will be gas exchange, for others it will be muscular (Camporotta).

There remain several unanswered questions in the ECMO population- how to wean, who needs (and doesn’t need) mechanical ventilation… hopefully answers will come.

 

The future may well be closed-loop ventilation, such as that seen with the Hamilton ventilators in their ASV mode.

youtube.com/watch?v=4uOFPG…

 

 

 

The ICU Airway- 25th September 2017 #LIVES2017

 

10-20% of the ICU population will be difficult to intubate- and this can lead to significant morbidity and mortality, as the excellent UK NAP4 audit showed NAP4: Executive summary | The Royal College of Anaesthetists

3% of patients will have an intubation related cardiac arrest…

It’s been suggested that we treat every ICU patient as a difficult intubation. Assess the airway beforehand- the MACHOCA score has been recommended The MACOCHA score is feasible to predict intubation failure of … – NCBI

Tips to optimise intubation?

Should we use VL first line? Maybe- but MACMAN says no thebottomline.org.uk/summaries/icm/…

And what about high flow oxygen as apnoeic oxygenation? Maybe ncbi.nlm.nih.gov/pubmed/25479117 or maybe not? emcrit.org/pulmcrit/apnei…

Or combine HFNC with non-invasive ventilation for the ultimate oxygenator? bmjopen.bmj.com/content/6/8/e0…

 

So some controversies remain- hopefully with more data to come we can make ICU intubation safer.

Beta-agonists/Beta Blockers- why and when? (25th Sept 2017) #LIVES2017

  1. IN ACUTE MYOCARDIAL INFARCTION- BETA STIMULANTS OR BETA BLOCKERS?

Brief summary: If the patient’s haemodynamics are stable, leave them alone! If they are in cardiogenic shock, consider inotropic support while getting them to the cath lab immediately (based on the new ESC guidelines academic.oup.com/eurheartj/arti…)

So why discuss beta blockade at all? Well, initial trials suggested a benefit of beta blockade during AMI (circ.ahajournals.org/content/early/…), however later trials failed to show a benefit (acc.org/~/media/Clinic…) leading to a downgrade of the original recommendation. There may still be a benefit in patients with established low EF who are having an MI, though.

Timing of beta blocker administration may also be an issue (the earlier the better, as suggested by ncbi.nlm.nih.gov/pubmed/27052688)

Patient in shock? Planning to use inotropes? It’s recommended to monitor the cardiac output, as well as other markers of organ perfusion.

Should we use catecholamines, inodilators, or both? This study suggests a benefit from combined inodilator/catecholamine therapy (journals.plos.org/plosone/articl…)

However adrenaline is associated with a WORSE outcome in cardiogenic shock (ncbi.nlm.nih.gov/pubmed/27374027)- increases troponin, creatinine and urea.

ESC guidelines recommend weaning vasopressors as soon as possible based on that data.

Patients can be risk stratified using biomarkers (ST2, BNP) journals.lww.com/ccmjournal/Abs…
Questions from the audience included choice of inotropes (combination agents recommended over catecholamines alone, based on above data) and whether there was still a role for PDE-III agents (milrinone, enoximone) and levosimendan.

Regarding the latter- there has been no mortality benefit so far, however they are better than using adrenaline alone.

 

2: BETA AGONISTS IN SEPTIC SHOCK

Jean-Louis Vincent started off with a fantastic aide memoire on inotropic action:

Screen Shot 2017-09-30 at 22.30.52

Inotropes have varying effects on the cardiovascular system- they are not all the same. They also have profound metabolic effects – such as the lactataemia seen with adrenaline…

Screen Shot 2017-09-30 at 22.32.03

Their effects may be dose dependent, as seen with isoprenaline ncbi.nlm.nih.gov/pmc/articles/P… and dobutamine link.springer.com/article/10.100…

Inotropes may help to recruit the microcirculation and reduce the inflammatory response in critical illness. According to JLV, inotrope induced myocardial infarction is rare in the ICU! If we are worried about tachycardia, ivabradine may have a role in obtunding that while allowing the other catecholaminergic effects to continue…

Individualised therapy seemed to be the take home message here.

 

3. BETA BLOCKERS IN SEPTIC SHOCK

There’s a link between hypoxia and inflammation nejm.org/doi/full/10.10… – by increasing oxygen delivery beta blockade may reduce the inflammatory response.

However beta adrenergic stimulation improves flow in sepsis ncbi.nlm.nih.gov/pmc/articles/P… – so why is beta bl0ckade being talked about?

Well, there’s rat data showing that early beta blockade improves outcomes in sepsis ncbi.nlm.nih.gov/m/pubmed/19829… and then there is human data suggesting that prior treatment with beta blockers improves outcomes in septic shock journals.lww.com/ccmjournal/Abs…

Then came this- the Morelli paper showing improved mortality with esmolol in septic shock ncbi.nlm.nih.gov/pubmed/24108526

So how does it work? It may reduce cardiac output but overall tissue perfusion seems preserved ncbi.nlm.nih.gov/pubmed/27411452

So who would benefit? Daniel De Backer suggests:

-High contractility

-Low cardiac output state

-Non-fluid responders

-Diastolic dysfunction

– Individuals with systolic anterior motion of the mitral valve on echocardiography- De Backer reckons up to 30% of septic shock will have this!

(So basically do an echo to find out!)