Strategies for difficult ventilation…when good lungs go bad

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Strategies for difficult ventilationwhen good
lungs go bad

• N Makris
• (Bucks Intensive Therapy Education)

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What have we already done..

• Intubated our patient
• Ventilator on any given mode, FiO2 1.0
• Set appropriate targets for ventilation
• Vt 6ml/kg PBW
• PaO2 gt8kPa
• pH gt7.15
• Tried recruitment manoeuvres
• Tried muscle relaxants
• Played around with IE ratios and ventilation
  mode
• (Called the boss)

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What are our options?

• Prone Ventilation
• Fluid restriction/ manipulation
• Nitric Oxide
• HFOV
• ECMO
• (Steroids)

4

• Zone A contains consolidation and atelectasis
  besy perfusion but poorest compliance
• Zone B highest compliance but poorest perfusion
• Zone C intermediate compliance and perfusion
  most prone to atelectrauma

Moloney E D , Griffiths M J D Br. J. Anaesth.
200492261-270
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If only

• It were possible to match up the areas of highest
  compliance ie best ventilation and best perfusion
• Reduce V/Q mismatch and improve gas exchange

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Prone VentilationHow does it work?

• Redistributes
• weight of mediastinum off the lungs
• Atelectasis, oedema and secretions from dependant
  part of lungs
• Increases
• Alveolar recruitment
• FRC
• Alters chest wall compliance and diaphragmatic
  excursion(Big Fish manoeuvre?..)

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Prone Ventilation

• Complications / Problems
• Labour intensive
• Accidental line/tube diplacement
• Pressure sores
• Nerve entrapment
• Abdominal compression
• Haemodynamic effects

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Prone VentilationDoes it work?

• Gattinoni et al, NEJM 2001.
• Multi centre RCT in Swiss and Italian ITUs
• Randomised 304 pts w ARDS/ALI to prone
  ventilation for gt6h/day or supine ventilation.
• Outcome measure mortality at 10days, ITU
  discharge and 6 months.
• No significant difference in mortality
• Oxygenation improved in 70 of patients proned
• No difference in accidental extubations

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Problems with the trial

• Only 40 of eligible patients were enrolled in
  the trial
• Stopped early after poor recruitment (no pun
  intended)
• Underpowered to detect difference (powered to
  detect 20 mortality benefit with 80
  probability)
• 12 patients randomised to supine group were
  proned
• 91 missed episodes of proning in 10 day trial
  period
• Mean Vt 10.3ml/kg in both supine and prone groups
  ie. not compliant w ARDSNET strategy

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Follow up studies

• Guerin et al, JAMA 2004
• Multi centre RCT, 791 pts randomised
• No difference in 28 day or 90 day mortality or
  ventilator free days between 2 groups
• Improved oxygenation in prone group
• Lower VAP risk in prone group 1.6 vs 2.1 episodes
  per 100 pt days
• Increased risk of endobronchial intubation, ETT
  obstruction and pressure sores in prone group

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Cumulative Probability of Patient Survival After
Randomization.
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Fluid Restriction

• FACTT (Fluids and Catheter Therapy Trial)
• Multicentre RCT in USA 1001pts randomised to 1 of
  4 groups within 48h of diagnosis
• CVC vs PAC
• Liberal vs conservative fluid
• Renal failure patients excluded
• Protocol driven CVP/PAOP targets, additionally
  targets for MAP, U/O, tissue perfusion
• In presence of shock (MAPlt60, appropriate fluid
  other therapies allowed)

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Results

• No outcome differences between CVC and PAC
• Higher rate of complications in PAC group
• 7 day fluid balance in liberal group 7L, approx
  even balance in conservative group
• Mortality similar in both groups
• 14.6 vs 12.1 ventilator free days at 28 days
• Earlier discharge from ITU in conservative group
• Slightly lower MAP and CI , slightly higher urea
  and creatinine but no increase in organ failure
  in conservative group

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Nitric Oxide

• How does it work?
• EDRF direct and indirect actions cause
  vasodilation via cGMP
• t½ a few seconds
• Inactivated by binding to Hb
• Inhibits platelet aggregation, neuro-transmitter
  , smooth muscle proliferation and leucocyte
  adhesion, free radical scavenger.
• When inhaled causes preferential vasodilation in
  ventilated alveoli
• Opens non-shunt pathways, improving oxygenation

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Nitric Oxide

• Highly toxic NO2 formed when NO reacts with O2
• Causes methaemoglobinaemia and pulmonary oedema
  in overdose
• Given in concentrations of 1-40ppm in ARDS
• Requires monitoring of NO and NO2 levels and
  scavenging of gases

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Expensive equipment alert

• No-one else has this kit
• It looks very expensive and has numbers on it
  no-one will understand
• They will think you are doing something really
  clever
• EVERYONE will understand how sick this patient is

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Nitric Oxide

• Does it work?
• Numerous RCTs, generally showing improved
  oxygenation in about 40-70 responders for
  12-24h
• gt20 improvement in PaO2 counts as response
• No demonstrable effect on ITU stay, ventilator
  free days or mortality

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Fig 4 Effect of nitric oxide on PaO2/FiO2 ratio
at 24 hours.
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Fig 2 Effect of nitric oxide on mortality.
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Prostacyclin

• PGI2 is also a potent vasodilator
• Has a half life of 2-3mins
• Can be continuously nebulised at up to
  50ng/kg/min
• Increases surfactant release and has minimal
  toxicity
• But is dissolved in alkaline glycine buffer which
  can cause airway inflammation
• Improves oxygenation as effectively as iNO
• No improvement in mortality

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HFOV

• Gas in the lung is oscillated around a constant
  mean airway
• Large airway pressure changes in trachea
  attenuated in alveoli
• Typical settings
• Amplitude 20-100cm H2O
• Rate 100-300/min
• Vt 1-3ml/kg
• First established for use in pediatrics cases of
  neonatal ARDS

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Theoretical advantages

• Smaller Vt limits alveolar distension
• Higher mean airway pressure gives greater
  recruitment
• Constant pressure during inspiration and
  expiration prevents atelectrauma

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Multicenter Oscillatory Ventilation for ARDS
Trial (MOAT)

• Exclusion criteria
• Weight lt 35 kg
• Severe COPD or asthma
• Intractable shock
• Severe airleak
• Nonpulmonary terminal diagnosis
• FiO2 gt 0.80 for more than 2d
• Primary outcomes at 30 and 90 days
• Dead
• Alive on ventilator
• Alive off ventilator

• Multicentre RCT published 2002
• HFOV (n75)vs conventional ventilation (n73)
• Inclusion criteria
• gt16 years
• PaO2/FiO2 lt 200 while on PEEP gt 10
• Bilateral pulmonary infiltrates on CXR
• No evidence of left atrial HTN

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Results

• Improved oxygenation index predicted survival
  irrespective of mode of ventilation
• Trend towards survival (37 vs 52 mortality)
• Similar trial (Boden et al) stopped recruiting
  early because of these results

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Criticisms

• Inadequately powered to assess mortality
• ARDSNET ventilation not adhered to in
  conventional ventilation arm
• Mean Vt8ml/kg ABW, 10.6ml/kg IBW
• Mean Plateau pressure 38cm H2O at 48h
• OSCAR trial still recruiting

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Extra-Corporeal Membrane Oxygenation

• Modification of cardiac bypass
• Blood passes through membrane oxygenator
• Can be veno-venous (preferred) or arterio-venous
• Main risks are of anticoagulation and infection

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Conventional ventilation or ECMO for Severe Adult
Respiratory failure (CESAR) trial

• RCT ,published 2009
• ECMO at Glenfield vs CV at numerous sites n90
  for each arm
• Inclusion criteria
• Age 18-65 years
• Reversible pathology
• No contraindication to anticoagulation
• IPPV lt 7 days
• Optimum conventional treatment tried - Murray
  score gt3 or uncompensated hypercapnea, pHlt7.2

• Exclusion criteria
• Duration of high pressure and/or high FiO2
  ventilation gt7 days
• Intra-cranial bleeding
• Any other contra-indication to limited
  heparinisation
• Patients who are moribund and have any
  contra-indication to continuation of active
  treatment

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Outcome measures

• Primary death or severe disability at six months
• Secondary
• - Nature and duration of ventilation and
  other
• organ system support
• - Length of ICU and hospital stay
• - Blood product use
• - Cost effectiveness

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Results

• Death/ severe disability at 6months
• 37 in ECMO group
• 53 in CV group
• ARR of 16 ? NNT of 6.25
• RRR of 31
• P 0.03
• Death at 6months
• 33 vs 45 P0.07

• 22 of 90 patients randomised to ECMO did not
  receive it due to improvement in respiratory
  function or death prior to commencement

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Limitations

• Non-standardized ventilation protocol
• 30 of patients in CV arm did not receive lung
  protective strategy
• 103 pts screened patients excluded from study due
  to unavailability of ECMO bed
• Mortality in those who received CV not
  significantly different to those who received
  ECMO (48.5 for ECMO versus 43.1 for MV) P
  0.64)

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Summary

• Prone ventilation
• Safe, improves oxygenation for a while, no
  mortality benefit
• NO, PGI2
• Safe, improves oxygenation for a while, no
  mortality benefit
• HFOV
• Safe, improves oxygenation, no mortality benefit
  proven yet, await OSCAR
• ECMO
• Not widely available, not particularly safe,
  appears to improve mortality

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References

• Protective ventilation of patients with acute
  respiratory distress syndrome. Moloney E D ,
  Griffiths M J D Br. J. Anaesth. 200492261-270
• Effects of Systematic Prone Positioning in
  Hypoxemic Acute Respiratory Failure
• Guerin, C. et al. JAMA 20042922379-2387
• The National Heart, Lung, and Blood Institute
  Acute Respiratory Distress Syndrome (ARDS)
  Clinical Trials Network. Comparison of two
  fluid-management strategies in acute lung injury.
  N Engl J Med 20063542564-2575
• High-Frequency Oscillatory Ventilation for Acute
  Respiratory Distress Syndrome in Adults Derdak
  et al American Journal of Respiratory and
  Critical Care Medicine Vol 166. pp. 801-808,
  (2002)
• Peek GJ, Mugford M, Tiruvoipati R, Wilson A,
  Allen E, Thalanany MM, Hibbert CL, Truesdale A,
  Clemens F, Cooper N, Firmin RK, Elbourne D CESAR
  trial collaboration. Lancet. 2009 Oct
  17374(9698)1351-63.