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Strategies for difficult ventilation…when good lungs go bad

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Strategies for difficult ventilation when good lungs go bad N Makris (Bucks Intensive Therapy Education) What have we already done.. Intubated our patient ... – PowerPoint PPT presentation

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Title: Strategies for difficult ventilation…when good lungs go bad


1
Strategies for difficult ventilationwhen good
lungs go bad
  • N Makris
  • (Bucks Intensive Therapy Education)

2
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)

3
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
5
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

6
Prone Ventilation How 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?..)

7
Prone Ventilation
  • Complications / Problems
  • Labour intensive
  • Accidental line/tube diplacement
  • Pressure sores
  • Nerve entrapment
  • Abdominal compression
  • Haemodynamic effects

8
Prone Ventilation Does 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

9
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

10
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

11

Cumulative Probability of Patient Survival After
Randomization.
12
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)

13
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

14
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

15
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

16
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

17
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

18

Fig 4 Effect of nitric oxide on PaO2/FiO2 ratio
at 24 hours.
19

Fig 2 Effect of nitric oxide on mortality.
20
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

21
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

22
Theoretical advantages
  • Smaller Vt limits alveolar distension
  • Higher mean airway pressure gives greater
    recruitment
  • Constant pressure during inspiration and
    expiration prevents atelectrauma

23
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

24
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

25
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

26
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

27
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

28
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

29
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

30
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)

31
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

32
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.
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