Category Archives: Respiratory

Myth Busters! #LIVES2020

5 False beliefs in acute and chronic respiratory failure

Pr Alexandre DEMOULE

  1. ARDS pts should be intubated promptly
  2. Intubation can be safely delayed in ARDS patients
  3. In COPD, NIV is contra-inducated in case of coma
  4. In cancer pts, do everything not to intubate
  5. Response to prone position predicts the outcome

ARDS pts should be intubated promptly

Time to intubation has no impact on mortality

In COPD, NIV is contrainidcated in case of coma

  • NOT AT ALL, in cases of hypercapnic coma, do a NIV trial

In cancer pts, do everything not to intubate

Response to PRONE position predicts the outcome

When lactate is normal the circulation is adequate

Prof J Bakker

The ten pitfalls of lactate clearance in sepsis

Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients With Septic Shock
The ANDROMEDA-SHOCK Randomized Clinical Trial


  • The clinical context we create from an increased lactate is: tissue hypoperfusion/hypoxia
    • This is on a macrocirculatory level
  • Lactate levels frequently remain abnormal during the first 24h of admission in survivors of septic shock
  • Mildly elevated lactate levels are associated with increases in mortality and abnormal microcirculation
  • Lactate levels need context
    • Markers of peripheral/microcirculatory perfusion
  • Lactate levels do not denote a state of perfusion

Adrenaline improves outcome after cardiac arrest?

Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospital data registry

A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest

2019 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations


  • Survival to hospital admission x 3 higher
  • More survivors to discharge
  • More neurologically favourable survivors
  • More brain-injured survivors


False beliefs about duration of antibiotic therapy

J De Weale (twitter)

The FALSE beliefs

  1. Antibiotic duration needs to be ‘fixed’
    • No Biological rationale
    • Bacteria don’t calculate the days exposed
  2. Short courses are less effective
    • Longer courses do not protect against complications
    • BUT some infections do require longer treatment
  3. I need a biomarker to determine duration
  4. Antibiotics need to be continued until clinical symptoms have subsided
  5. An antimicrobial course should always be completed.


  • Inappropriate antimicrobial use in the ICU is unacceptably high
  • Duration important contributor
  • Management often based on incorrect assumptions
  • “7-days course” current dogma for most infections
  • Individualized therapy is the future
  • AI to refine therapy duration

Prof’s De Weale’s slideset (I like the design)

Prognostication of individual survival chances is not possible? Machine learning is the answer

Prof Mihaela van der Schaar (twitter)

Machine learning can enable:

1) Delivering precision medicine at the patient level
2) Understanding the basis and trajectories of health and disease
3) Informing and improving clinical pathways, better utilize resources, and reduce costs
4) Transforming population health and public health policy

False beliefs in the management of fever

F Schortgen

Fever is not hyperthermia

Treating fever has never been proven to improve patient comfort

Effect of Shivering on Brain Tissue Oxygenation During Induced Normothermia in Patients With Severe Brain Injury

Antipyresis is NOT necessarily good for haemodynamic stabilistation and tissue oxygenation


New developments that every intensivist should know about…..


Prof S Price


2020 Acute Coronary Syndromes (ACS) in Patients Presenting without Persistent ST-Segment Elevation (Management of) Guidelines

  • Rapid rule in/rule out algorithms now recommended to use ESC 0h/1h algorithm ( or 1h/2h algorithm (second best option) if a hs-cTn test with a validated algorithm is available
  • If elective non-invasive/invasive imaging is needed after the rule-out of MI, invasive angiography is the best option in those with a very high clinical likelihood of UA. Stress testing with imaging or CCTA is best in those with low-to-modest clinical risk.
  • Rhythm monitoring for up to 24 h or to PCI (whichever comes first) is recommended for those at low risk for arrhythmias and monitoring >24h if at increased risk
  • Early routine invasive approach within 24 hours for NSTEMI based on hs-cTn measurements, GRACE score >140, dynamic/new STT changes.

Clinical application of the 4th Universal Definition of Myocardial Infarction

Temporary circulatory support for cardiogenic shock


EJ Nossent

Potential therapies

Pirfenidone for idiopathic pulmonary fibrosis: analysis of pooled data from three multinational phase 3 trials

Efficacy and Safety of Nintedanib in Idiopathic Pulmonary Fibrosis

Nintedanib for Systemic Sclerosis–Associated Interstitial Lung Disease

Nintedanib in Progressive Fibrosing Interstitial Lung Diseases

Take home message

  • ILD is not one disease
  • Acute excacerbation in every type of ILD
  • The landscape is changing; finally…
  • Position antifibrotic therapy fibrotic ILD not clear yet; immunosuppressants.

From the disease lung fibrosis to criteria, towards phenotyping, towards personalized medicine.


Prof S Koch



EID risk is increasing due to climate change and loss of biodiversity
-> we need to adress this now

Neurological manifestation of Covid-19 occur in ~ 36%

Cerebrovasculare Manifestions occur in ~ 5% of Covid-19 patients based on
–pathological coagulation or hyperinflammation
–includes younger patients or patients with typical riskfactors
–leads to more severe outcome
-> check carefully coagulation parameters and risk factors

Altered conscious state is seen in ~ 65% of Covid-19 ICU patients
–based on encephalopathy or seizures
-> EEG monitoring, MRI


S Loer

Optimizing preoperative fluid therapy Encourage use of clear carbohydrate drinks up until 2 h prior to surgery!

  • Less catabolism
  • Less postoperative nausea and vomiting
  • Less insulin resistance
  • Less perioperative anxiety

Intraoperative fluids

Impact of intraoperative goal-directed fluid therapy on major morbidity and mortality after transthoracic oesophagectomy: a multicentre, randomised controlled trial

Perioperative goal-directed therapy: what’s the best study design to investigate its impact on patient outcome?

Anesthesia-induced immune modulation

Post-op delirium

Postoperative delirium: perioperative assessment, risk reduction, and management

Post-op pain

How to personalize PEEP and tidal volume in ARDS?

By Dr Tomasso Mauri, University of Milan

  • ARDS is a heterogenous disease with several sub-phenotypes. Therefore, it makes sense to personalize ventilatory management.
  • To personalize the management, we need individualized bedside monitoring –
    • Respiratory mechanics, Esophageal pressure, Electrical impedance tomography are some of the bedside tools available for monitoring

Personalizing PEEP in patients with potential lung recruitability:

  • Goals of PEEP – Stabilize recruitment and avoiding VILI
  • PEEP when set between closing and opening pressure provides stable recruitment
  • Stable recruitment –> decreases inflammation
  • PEEP personalized using one of P/F ratio, Esophageal Pressure (EP), Electrical Impedance tomography (EIT) or Recruitment/Inflation index (R/I)
  • Recruitment correlated with P/F at PEEP 5 (low P/F – higher potential for recruitment)
  • Heavy lung (more oedema) -> higher EP -> higher potential for recruitment; choose the PEEP associated with zero transpulmonary pressure at end expiration
  • Assessment of volume of recruitment between lower and higher PEEP (5-15 cmH2O) levels used to calculate R/I index (>0.5 indicates higher potential for recruitment); use the double PV loop method
  • EIT aids in dynamic assessment of tidal volume in the dependent lung (EIT ventilation/EIT perfusion) – personalizing PEEP based on this leads to homogenous V/Q -> evolving technology.

Personalizing tidal volume in ARDS:

  • Height can help calculate PBW to get 6ml/kg tidal volume, but not the size of the baby lung
  • Better estimate the size of the baby lung is the compliance (=tidal volume/driving pressure)
  • Driving pressure = Tidal volume/Compliance (baby lung)
  • Driving pressure <14 cmH2O is associated with reduced mortality
  • Start at 6ml/kg tidal volume, personalize the PEEP and measure driving pressure -> aim is to keep driving pressure under 15 cmH2O and Plateau under 30 cmH2O
  • With very low tidal volumes, CO2 can accumulate causing respiratory acidosis – consider ECCO2-R in such a situation
  • Tidal volume, once selected after personalizing the PEEP, must be maintained for 48 hours or until spontaneous breathing established

Assessing and optimizing respiratory drive at the bedside

Irene Telias, Canada

Respiratory drive is the output of respiratory centers that control the magnitude of inspiratory effort

Why assess respiratory drive?

  • Derangements are frequent
  • Can have adverse consequences on diaphragm/lungs/ sleep

Respiratory control is complex

  • Chemoreflex – pH, pCO2 and pO2 via central and peripheral chemoreceptors control the output of the respiratory center
  • Multiple factors modify the drive in ICU patients (inflammation, metabolic demands, mechanical ventilation etc)


  • Respiratory center cannot be monitored directly. Respiratory drive is a surrogate
  • Measures of respiratory drive can be used to estimate inspiratory effort and vice versa


  • Electrical activity of the diaphragm (EAdi)
  • Mechanical activation of diaphragm (Diaphragm Ultrasound)
  • Esophageal or gastric pressure measurement
  • P0.1 or Pocc
  • P0.1 specific for respiratory drive
  • Respiratory rate is not a good measure of the drive (except when it is <17 or >30 in ICU patients)

How is it done?

  • Majority of vents do it
  • P0.1 is the drop in airway pressure in the first 100 msec; Pocc is the drop in airway pressure during an end expiratory occlusion maneuver
  • P0.1 – Surrogate of respiratory drive, validated

High Respiratory drive

  • P0.1 > 3.5 – 4 cmH2O– High respiratory drive
  • Identify modifiable factors (adjust flow and tidal volume, reduce dead space, treat infection, pain etc)
  • PEEP and FiO2 adjustment
  • Sedation and analgesia

Low respiratory drive

  • 1 <1 cmH20
  • Typically, in patients recovering from respiratory failure – usually on high levels of PS – causes apnea and disrupted sleep
  • Reduce PS or use other modes