Difficult Ventilation and HFOV Antony Tobin SVHM antony.tobin@svhm.org.au

What%is%the%problem%in%ARDS%

•  Can’t%ven7late%v%can’t%oxygenate%•  alveolar%ven7la7on%v%V/Q%•  Usually%can’t%oxygenate%

The%Problem%in%ARDS%

•  Diffuse%pulmonary%infiltrates%

•  Posterior%collapse%•  V/Q%mismatch/shunt%•  Reduced%compliance%–%s7ff%lungs%

V/Q mismatch V/Q <1 there is little change in pO2 until V/Q = 0.2

pO2 changes little for V/Q over 10

most change is between 0.1 and 1

CO2 curve is more linear so that increases in ventilation of prevent hypercapnia

0.1 1 10

pCO2

pO2

O2 content

40

100

20

ARDS – reduced lung compliance and low mean airway pressure result in airspace collapse and hypoxia

Increasing mean airway pressure recruits alveoli reducing shunt and V/Q mismatch so improving oxygenation

Mean Airway Pressure = Oxygenation

Alveolar%Mechanics%in%ARDS%and%the%effect%of%Mean%Airway%pressure%

%Steinberg AJRCCM 2004;169:57-63%

Evidence%Based%approach%to%ven7la7on%in%ALI%NEJM%2000;342:1301W8%

%•  Volume%and%Pressure%Limited%ven7la7on%

– 7dal%volume%goal%6mg/kg%ideal%body%weight%–  Inspiratory%Plateau%pressure%<%30%cmH20%– Lower%Vt%to%4%or%5%ml%/kg%to%maintain%%Pplat%<30%cmH20%

– PEEP?%

Higher versus Lower Positive End-Expiratory Pressures in Patients with the Acute Respiratory

Distress Syndrome N Engl J Med 2004;351:327-36.

•  549 ALI/ARDS patients to high or low PEEP •  PEEP set according to algorithm •  Mean PEEP 8.3+3.2 v 13.2+3.5cm H20 •  No difference in mortality or liberation from

ventilator •  For protective ventilation (Vt,6ml/kg and Pplat

limit of 30) higher PEEP conferred no benefit

Higher versus Lower Positive End-Expiratory Pressures in Patients with the

Acute Respiratory Distress Syndrome N Engl J Med 2004;351:327-36.

%

Higher versus Lower Positive End-Expiratory Pressures in Patients with the Acute Respiratory

Distress Syndrome N Engl J Med 2004;351:327-36.

•  But patients in higher PEEP older with lower P/F ratio

•  High PEEP algorithm changed after first 171 patients

•  Subsequent high PEEP patients had lower adjusted mortality

•  Trial terminated early based on all data – may have been different if only latter group analysed

High PEEP turns

NNT = 28

Higher'vs'Lower'Posi.ve'End2Expiratory'Pressure'in'Pa.ents'

With'Acute'Lung'Injury'and'Acute'Respiratory'Distress'

Syndrome'Briel't'al'JAMA'2010%

•  In%pa7ents%with%ARDS(PF<200),%higher%levels%of%PEEP%were%associated%with%a%rela7ve%mortality%reduc7on%of%10%%(absolute%difference,%4%;%number%needed%to%treat,%25).%%

•  In%contrast,%pa7ents%with%acute%lung%injury%but%without%ARDS%may%not%benefit%or%may%actually%experience%harm%from%higher%PEEP%levels.%%

Plateau'Pressure'v'Recruitment'with'PEEP?'

•  Rodents ventilated with three modes: •  High Pressure

(45 cmH2O), High Volume •  Low Pressure (negative

pressure ventilator), High Volume

•  High Pressure (45 cmH2O), Low Volume (strapped chest and abdomen)

Dreyfuss,D ARRD 1988;137:1159

Plateau'Pressure'v'Recruitment'with'PEEP?'

Dreyfuss Am J Respir Crit Care Med Vol 157. pp 294–323, 1998

Neuromuscular'Blockers'in'Early'Acute'Respiratory'

Distress'Syndrome'Papazian'NEJM'2010'

•  In%severe%ARDS%(PF<120)%early%administra7on%of%a%neuromuscular%blocking%agent%for%48hrs%%improved%90Wday%survival%(31.6%v%40.7%)%%and%increased%the%7me%off%the%ven7lator%without%increasing%muscle%weakness.%%

•  Improved%oxygena7on%•  Reduced%barotrauma%

But%muscle%relaxants%worsen%lung%compliance%and%CO2%will%worsen!?%

The damaging pressure and distension relates to the alveoli membrane…..in spontaneous breathing the pressure measured at the upper airway does not reflect the trans alveoli membrane pressure. Low levels of pressure support, combined with large negative inspiratory pressures may result in TVs and trans-alveoli pressures that may induce VILI.

Prone'ven.la.on'reduces'mortality'in'pa.ents'with'acute'

respiratory'failure'and'severe'hypoxemia:'systema.c'review'

and'meta2analysis'–'Sud'Int'Care'Med'2010'

•  Prone%ven7la7on%reduces%mortality%in%pa7ents%with%severe%hypoxemia%(PF%<100)%

•  Associated%with%increased%risks%tube%blockage,%pressure%areas%

•  No%mortality%benefit%for%lesser%severity%of%hypoxia%

Recruitment%Manoeuvres%

•  There%is%not%evidence%to%make%conclusions%on%whether%recruitment%manoeuvres%reduce%mortality%or%length%of%ven7la7on%in%pa7ents%with%ALI%or%ARDS%Hodgson'Cochrane'2009'Apr'15;(2):CD006667.%

•  This%open%lung%strategy%was%associated%with%greater%ameliora7on%in%some%systemic%cytokines,%improved%oxygena7on%and%lung%compliance%over%seven%days.%Hodgson'Crit'Care.'2011;15(3):R133'

•  PHARLAP'

Staircase Recruitment

•  385 patients with non-sepsis ARDS •  Randomised to NO 5 ppm or not

Low-dose inhaled nitric oxide in patients with acute lung injury: a randomized controlled trial.

Taylor RW JAMA 2004;291(13):1603-9.

Normal Nitric Oxide

Off Vent 10.6 10.7

Mortality 20% 23%

Alive (Tpiec)

11.9 11.4

Alive (Ext)

17.0 16.7

Inhaled%nitric%oxide%•  No%evidence%of%reduced%mortality%•  Improves%oxygena7on%•  May%increase%renal%failure%in%adults%Cochrane%2010%Jul%7;(7):CD002787%

•  Low%dose%associated%with%reduced%long%term%injury?%–%improved%sta7c%lung%func7on%tests%Dellinger%Crit%Care.%2012%Mar%2;16(2):R36%

Dose–Response Characteristics during Long-Term Inhalation of Nitric Oxide in Patients with Severe

Acute Respiratory Distress Syndrome Herwig Gerlach et al. Am J Respir Crit Care Med Vol 167. pp 1008–1015, 2003

Randomised to 10ppm (n=20 or conventional Rx Initially best response was at 10ppm By day 4 dose response curve was left shifted with best at 1ppm Higher doses led to deterioration in pO2 in some Did not effect duration of mechanical ventilation or ICU LOS

APRV%–%largely%evidence%free%zone%

Other%•  Restrict%fluids/diuresis%–%Yes%%

–  N%Engl%J%Med.%2006%Jun%15;354(24):2564W75%

•  B2%agonists%–%No%–  Lancet.%2012%Jan%21;379(9812):229W35%

•  Steroids%–%No%•  Drain%effusions%–%maybe%•  Decompress%abdomen%–%maybe%•  Op7mise%–%cardiac%output/Hb%–%probably%•  ECMO/HFOV%

Summary of ventilation

•  Limit plateau pressure to 30cm/H20 •  Aim for tidal volume of 6ml/kg ideal body weight •  Set PEEP according to ARDSnet at minimum but higher PEEP

may be better especially in severe ARDS •  Tolerate saturations > 88% depending on other delivery variables •  Tolerate hypercapnia •  Unclear whether higher plateau pressures acceptable if tidal

volumes restricted (influence of pulmonary v extrapulmonary restriction)

•  Recruitment manoeuvres may be beneficial

HFOV in Adults

Antony%Tobin%Intensive%Care%Unit%St%Vincent�s%Hospital%Melbourne%

Sensormedics 3100B

Conven7onal%ven7la7on%

•  Ven7la7on%determined%by%rate%and%7dal%volume%(pressure%&%compliance)%

•  Oxygena7on%by%PEEP/MAP%and%FiO2%

30

MAP

PEEP

IP

Conven7onal%ven7la7on%

•  Increase%PEEP%to%raise%MAP%and%recruit%lung%•  As%MAP%increased%ven7la7on%is%generally%reduced%due%to%reduced%inspiratory%pressure%

•  Trade%off%between%oxygena7on%and%ven7la7on%

30 MAP

PEEP

IP

HFOV%W%a%vibra7ng%CPAP%circuit%

“Piston”%vibra7ng%at%5W8Hz%

Fresh%Gas%supply%

To%the%pa7ent%

Valve%to%control%airway%pressure%WW

CPAP%

HFOV%v%CMV%

•  High%pressure%CPAP%with%superimposed%high%frequency%low%volume%�breaths�%

•  Tidal%volumes%are%less%than%dead%space%•  Allows%high%pressures%and%adequate%ven7la7on%

30

MAP

PEEP

IP

The%effect%of%HFOV%on%lung%recruitment%Carney%D%CCM%2005%33(3):S122%%

CMV%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%HFOV%

What%does%it%look%and%sound%like%

Why%use%HFOV%

•  Rescue%– Unable%to%oxygenate%– Unable%to%ven7late%

•  Minimise%injury%to%lungs%– Limit%7dal%volumes%– Open%lung%ven7la7on%

How%may%Ven7la7on%cause%Harm? •  Biophysical Trauma

– Barotrauma – pneumothorax – Volutrauma - lung overdistension – Low volume trauma- Atelectotrauma

•  Biochemical Trauma

•  Oxygen Toxicity

Zones of Injury

Overdistension

Zone of shear forces

Atelectasis

Minimising%Harm%with%conven7onal%ven7la7on%

•  Limit%7dal%Volume%to%reduce%Alveolar%overWdistension%– Vt%6ml/kg%ideal%body%weight%– Plateau%Pressure%<=%30%

•  Maintain%End%Expiratory%Volume%to%minimise%atelectotrauma%and%minimise%FiO2%

– High%PEEP%– High%Mean%airway%pressure%–%rate,%I:E%

HFOV%looks%Ideal%

•  UltraWlow%VT%– 1W4%mls%in%animal%models%

•  High%Constant%mean%airway%pressure%– Maintains%open%lung%– Allows%lower%FiO2%

High%frequency%oscilla7on%in%pa7ents%with%acute%lung%injury%and%acute%respiratory%distress%syndrome%%

%S%Sud%BMJ%2010%340:2347%%

•  6%randomised%studies%4%adult,%2%paediatric%•  Total%of%365%pa7ents%with%160%deaths%(43%)%

–  PaO2%higher%–  Lower%mortality%RR%0.77:0.61W0.98%–  Treatment%failure%less%likely%–  Harm%and%complica7ons%similar%

•  No%difference%in%effect%between%adults%and%paediatric%sudies%•  High%frequency%oscilla7on%might%improve%survival%and%is%unlikely%

to%cause%harm.%%

equally applied in treatment groups. We assessed thequality of evidence for clinical outcomes, includingmortality, treatment failure, and adverse events,according to recommendations of the GRADE work-ing group.41

We contacted authors of all included trials to requestadditional data and to clarify methods as necessary.

Outcomes

We considered the following clinical outcomes: hospi-tal or 30 day mortality (primary outcome), six monthmortality, duration of mechanical ventilation, ventila-tor-free days to day 28 or 30, health related quality oflife at one year, and treatment failure leading to cross-over to the other arm or discontinuation of the studyprotocol (secondary outcomes). We accepted authors’definitions of treatment failure, which could includesevere oxygenation failure, ventilation failure, hypo-tension, or barotrauma (pneumothorax, pneumome-diastinum, subcutaneous emphysema). We alsoconsidered physiological outcomes measured at 24,48, and 72 hours after randomisation: oxygenation,measured by the ratio of partial pressure of arterial

oxygen (PaO2) to inspired fraction of oxygen (FiO2)(PaO2/FiO2 ratio); oxygenation index (OI, defined as100!mean airway pressure/(PaO2/FiO2 ratio)); venti-lation, measured by partial pressure of carbon dioxide(PaCO2); and mean airway pressure. Finally, we con-sidered adverse events including barotrauma, hypo-tension, obstruction of endotracheal tube fromsecretions, and technical complications and equipmentfailure in patients treated with high frequency oscilla-tion (including unintentional system air leaks and pro-blems with the oscillatory diaphragm, humidifier, andalarm systems).21 42

Whenever possible, we analysed patients accordingto their randomly assigned group for all clinical andphysiological outcomes.

Statistical analysis

We conducted meta-analyses using random effectsmodels in Review Manager (RevMan) 5.0 (CochraneCollaboration, 2008) and statistical tests of publicationbias using the metabias command in Stata 9.2 (2006;StataCorp,College Station, TX). Randomeffectsmod-els incorporate variation both within and between stu-dies and typically provide wider confidence intervalswhen heterogeneity is present. We reported continu-ous outcomes using weighted mean difference (a mea-sure of absolute change) or ratio ofmeans (ameasure ofrelative change)43 and binary outcomes as risk ratios.We considered (two sided) P<0.05 as significant andreported individual trial and summary results with95% confidence intervals.We assessed heterogeneity between studies for each

outcome using the I2 measure44 45 and used publishedguidelines for low (I2=25-49%), moderate (I2=50-74%),and high (I2!75%) heterogeneity.45

To assess publication bias we examined funnel plotsof treatment effect versus study precision and usedBegg’s rank correlation test46 and a modified Macas-kill’s regression test.47 Given the low statistical power

Table 3 | Additional interventions or rescue treatments and funding in trials of high frequency oscillation and conventional mechanical ventilation included insystematic review

High frequency oscillationConventional mechanical

ventilationSedation and paralysis applied

equally to both groupsProtocols for ventilatorweaning and extubation

Funding*(industry support)

Arnold et al,48 1994 NR NR No NR Yes

Derdak et al,51 2002 Nitric oxide, 4/75; proneposition, 2/75, high dosesteroids, 1/75

Nitric oxide, 8/73; proneposition, 3/73; high dosesteroids, 4/73

No No Yes

Shah et al,55 2004† None None Yes NR No

Bollen et al,49 2005 NR NR NR No Yes

Papazian et al,53 2005 All patients ventilated inprone position

All patients ventilated inprone position

Yes No No

Samransamruajkit et al,54

2005Nitric oxide, 1/7 Nitric oxide, 0/9 Yes No No

Demory et al,50 2007 Prone position for 12hbeforeHFO in supine position

Pronepositionfor12hprior toCMV in supine position

Yes No No

Mentzelopoulos et al,52 2007‡ All patients received trachealgas insufflation. Steroids forARDS, 20/27

Steroids for ARDS, 21/27 No (27/27 HFO v 17/27 CMVpatients paralysed)

Yes No

NR=not reported, ARDS=acute respiratory distress syndrome.*Industry funding (CareFusion, formerly Sensor Medics) included partial support of study or provision of Sensor Medics 3100B HFO ventilators.†Conference abstracts, with supplementary information provided by primary investigators.

Arnold 1994

Derdak 2002

Shah 2004

Bollen 2005

Mentzelopoulus 2007

Samransamruajkit 2005

Total (95% CI)

Test for heterogeneity: !2=0.00, "2=3.36,

df=5, P=0.64, I2=0%

Test for overall effect: z=2.12, P=0.03

0.83 (0.43 to 1.62)

0.72 (0.50 to 1.03)

0.87 (0.37 to 20.4)

1.30 (0.66 to 2.55)

0.61 (0.36 to 1.04)

0.67 (0.18 to 2.42)

0.77 (0.61 to 0.98)

13.0

42.6

7.9

12.5

20.6

3.4

100.0

0.1 0.2 0.5 1 2 5 10

FavoursHFO

FavoursCMV

Risk ratio(95% CI)

Risk ratio(95% CI)

Weight(%)

10/29

28/75

6/15

16/37

11/27

2/6

73/189

Highfrequencyoscillation

12/29

38/73

6/13

8/24

18/27

5/10

87/176

Conventionalmechanicalventilation

Fig 2 | Hospital or 30 day mortality in patients with acute lung injury/acute respiratory distresssyndrome allocated to high frequency oscillation or conventional mechanical ventilation

RESEARCH

page 4 of 11 BMJ | ONLINE FIRST | bmj.com

%High%frequency%oscilla7on%in%pa7ents%with%acute%lung%injury%and%

acute%respiratory%distress%syndrome%(ARDS)%

%S%Sud%et%al%BMJ%2010%340:2347%%

HFOV%Principles%

•  Oxygena7on%controlled%by%%– mean%airway%pressure%–  FiO2%%–  Same%as%conven7onal%ven7la7on%

•  CO2%controlled%by%– Amplitude%of%oscilla7ons%(delta%P)%–  Frequency%of%Oscilla7ons%–  I:E%and%Cuff%leak%

Principles%

•  High%pressure%CPAP%with%superimposed%high%frequency%low%volume%�breaths�%

•  Tidal%volumes%are%less%than%dead%space%so%gas%exchange%occurs%by%different%methods%to%conven7onal%ven7la7on%

the peripheral particles diffuse radially,promoting axial gas exchange with ex-pired alveolar gas (6). This phenomenonis particularly evident at the airway bifur-cations where there is skewing of theinspiratory profile compared with a moresymmetric expiratory velocity profile (7).The airway bifurcation phenomenonstreams fresh gas toward the alveoli alongthe inner airway walls while “alveolar”gas is streamed away from the alveolialong the outer wall, and hence plays animportant role in the longitudinal con-vective transport mechanisms duringHFOV (8).

Taylor proposed that the longitudinaldispersion of tracer molecules in a diffu-sive process is augmented by radial trans-port mechanisms when laminar flow isapplied in both the absence (6) or pres-

ence of turbulent eddies and secondaryswirling motions (9). Fredberg (10) sub-sequently used a semiempiric analysis topredict that the combination of Taylordispersion and molecular diffusion (aug-mented dispersion) accounts for almostall gas transport during HFOV.

Time-constant inequalities and phaselags between lung regions may set upbulk convective currents recirculating airbetween neighboring lung units (11–13).In vitro (14) and computational (15) lungmodels have shown that gas exchangeduring HFV may be markedly improvedby the interaction of flow between asyn-chronous neighboring airways and hasbeen graphically illustrated with strobo-scopic filming techniques (2, 13). Asym-metries in inertance and compliance ofperipheral airways and lung units are

more important determinants of pendel-luft than are asymmetries in resistance(16).

The superimposition of the rhythmic,strong contractions of the heart may fur-ther promote peripheral gas mixing bypromoting the generation of flow withinneighboring parenchymal regions ratherthan at the airway opening (17). The con-tribution of cardiogenic oscillation dur-ing HFOV has not been quantified, al-though it has been suggested thatcardiogenic mixing may account for up tohalf of the oxygen uptake in the presenceof totally apneic respiration (18). Collat-eral ventilation occurring through non-airway connections between neighboringalveoli has also been proposed as an ad-ditional mechanism of gas transport dur-ing both conventional and HFOV. The

Figure 1. Gas transport mechanisms and pressure damping during high-frequency oscillatory ventilation (HFOV). The major gas-transport mechanismsoperating during HFOV in convection, convection–diffusion, and diffusion zones include: turbulence, bulk convection (direct ventilation of close alveoli),asymmetric inspiratory and expiratory velocity profiles, pendelluft, cardiogenic mixing, laminar flow with Taylor dispersion, collateral ventilation betweenneighboring alveoli, and molecular diffusion (see text for details). The extent to which the oscillatory pressure waveform is damped is influenced by themechanical characteristics of the respiratory system. Atelectatic alveoli will experience higher oscillatory pressures than normally aerated alveoli, whereasincreased peripheral resistance increases the oscillatory pressures transmitted to proximal airways and neighboring alveolar units (adapted with permission(2), © 2005 Massachusetts Medical Society).

S136 Crit Care Med 2005 Vol. 33, No. 3 (Suppl.)

Paw is created by a continuous bias flow of gas past the resistance (inflation) of the balloon on the mean airway pressure control valve. FiO2 is controlled by O2 blender on the side

CO2%Control%%

•  CO2%is%in%some%ways%analogous%to%conven7onal%ven7la7on%

•  Alveolar ventilation during CMV is defined as: •  F x Vt

•  Alveolar Ventilation during HFV is defined as: •  F x Vt 2

•  Therefore, changes in volume delivery have a more significant affect on CO2 elimination than frequency

•  Importantly frequency is inversely proportional to Vt so as frequency is reduced Vt goes up

Regula7on%of%stroke%volume%

Stroke volume

•  The stroke volume is determined by the diaphragm •  The stroke volume will increase if

–  The amplitude increases by increasing the power (higher delta P) –  The frequency decreases (longer cycle time)

•  Aim to use high deltaP and high frequency

Primary control of CO2 is by the stroke volume produced by the Power Setting which controls the amplitude or delta P.

•  The % Inspiratory Time also controls the time for movement of the piston, and therefore can assist with CO2 elimination.

•  Increasing % Inspiratory Time will also affect lung recruitment by increasing delivered Paw.

Secondary control of PaCO2 is the set Frequency.

Alarms%

Founda7on%Principles%

•  Target%pH%>%7.25%W%35%(permissive%hypercapnia)%•  U7lise%the%highest%possible%frequency%to%minimise%7dal%volume%and%only%decrease%for%CO2%control%if%delta%P%maximal%

•  Aim%for%satura7ons%88W95%%or%PaO2%55W80%to%minimise%the%risk%of%oxygen%toxicity%

•  Rapid%7tra7on%to%achieve%oxygena7on%ini7ally%with%observa7on%over%hours%to%determine%the%effects%of%weaning/ven7latory%changes%

Ini7al%Setngs%Fessler%H%CCM%2007%35(7):1649%

•  Bias%Flow%=%40L/min%•  Inspiratory%7me%=%33%%•  Amplitude%(delta%P)%=%90cmH20%•  Mean%airway%pressure%

– mPaw%+%5%on%conven7onal%or%34cmH20%•  FiO2%=%100%%•  Frequency%based%on%pH%

–  pH%<7.1%=%4Hz%–  pH%7.1%W7.19%=%5Hz%–  pH%7.2W7.35%=%6Hz%–  pH%>7.35%=%7Hz%

Oxygena7on%•  Use%ini7al%recruitment%manoeuvre%%•  Set%high%alarm%to%55,%Turn%off%piston%•  Raise%mPaw%to%45,%Hold%for%45sec%•  Reduce%to%mPaw%to%34%and%reset%high%alarm%•  If%SpO2%>%range%–%decrease%FiO2%every%5%min%7ll%SpO2%<%95%then%observe%for%2%hours%

•  Titrate%FiO2%and%Paw%according%to%table%

CO2%Control%

•  Aim%for%pH%7.25%W7.35%with%highest%frequency%•  If%pH%>%7.35%%

–  increase%f%by%1%Hz%every%2%hours%to%15%–  If%f%=%15%Hz%decrease%delta%P%by%5W10cmH2O%every%1W2hrs%

•  If%pH%<%7.25%%–  if%delta%P%<%90,%increase%delta%P%to%by%5W10%cmH20%every%1W2%hrs%to%max%of%90%cmH20%

–  If%delta%P%=%90%decrease%f%by%1%Hz%every%2%hours%•  If%f%<7%and%pH%<7.25%%

–  introduce%cuff%leak%(increase%mPaw%by%5%and%introduce%cuff%leak%7ll%mPaw%back%to%previous%level)%

Other%

•  Pa7ents%should%be%deeply%sedated%•  May%need%intermivant%bolus%muscle%relaxant%•  Small%breaths%(<5cmH2O)%should%be%tolerated%•  Once%started%should%run%for%at%least%12%hours%•  HOB%>30%degrees%•  Use%heated%humidifier%•  InWline%suc7on%

Transi7on%back%to%CMV%•  When%%

–  FiO2%<%0.5%– mPaw%=%22W24%cmH2O%–  stable%for%24hours%

•  Ini7al%setngs%%–  Vt%=%6mlkg,%%–  FiO2%=%0.5,%%–  PEEP16cmH2O%–  RR%20W25%

•  Check%ABGs%awer%30min%%

Example%of%Response%to%HFOV%

6.9

7

7.1

7.2

7.3

7.4

7.5

pH after change to HFOV

0

50

100

150

200

250 PF Ratio after Change to HFOV

Prior%to%transi7on%to%HFOV,%on%BIPAP%(34/14%Vt%260%–%300ml,%RR%22%–%pH%7.16,%CO2%57,%Po2%55%HCO3%20%on%NO%10ppm)%%Back%onto%BIPAP%(26/12%FiO2%60%)%awer%76%hours%of%HFOV%

HFOV%

HFOV%

BIPAP% BIPAP%

When%do%I%consider%HFOV%

•  Consider%early%–%won’t%work%day%7%•  ARDS/Diffuse%lung%disease/APO%

– Disease%where%s7ff%lungs%the%problem%•  Oxygena7on%failure%

–  %unable%to%maintain%FiO2%<=%0.6%•  Ven7la7on%failure%%

–  pH<7.25%with%%–  Vt%of%>=%6ml%and%%–  plateau%>=30%cmH2O%

Strategies%for%Inadequate%O2%

•  Seda7on%and%Paralysis%•  Recruitment%manoeuvre%•  High%PEEP,%reduced%I:E,%op7mise%circula7on%•  Nitric%Oxide%•  ?Prone%•  Inverse%Ra7o%•  Oscillator%•  Accept%lower%SpO2%•  Accept%higher%pressure/volumes%•  ECMO%%

Ques7ons?%