ventilation and respiratory centres - nhs wales ventilation and... · 2015. 10. 27. · •...

Ventilation and Respiratory Centres

Dr George Findlay

Consultant Intensivist

University Hospital of Wales

Cardiff

Clinical Disorders Associated with the Clinical Disorders Associated with the Development of ALI/ARDSDevelopment of ALI/ARDS

Direct insultCommon

Aspiration pneumoniaPneumonia

Less commonInhalation injuryPulmonary contusionsFat emboliNear drowningReperfusion injury

Indirect insultCommon

SepsisSevere trauma Shock

Less commonAcute pancreatitisCardiopulmonary bypassTransfusion-related TRALIDisseminated intravascular coagulationBurnsHead injuryDrug overdose

Atabai K, Matthay MA. Thorax. 2000.Frutos-Vivar F, et al. Curr Opin Crit Care. 2004.

Pulmonary Injury Sequence

• Endo/Epithelial Damage• Alveolar Cell Injury and/or loss• Capillary Congestion• Interstitial/Alveolar Edema & Haemorrhage• Protein Accummulation• Surfactant Deactivation• Atelactasis• Hyaline Membrane Formation• Inflammatory Cell Migration• Increased Protein Leak• Atelectasis

Deleterious effects of mechanical ventilation

• Ventilator induced lung injury - macroscopic– PIE– Pneumothorax– Pneumomediastinum– Pneumopericardium– Pneumoperitoneum– Subcutaneous

emphysema– Lung cysts

• Ventilator induced lung injury - microscopic– Lung oedema– Damage to alveolar-capillary

barrier– Surfactant dysfunction– Hyaline membranes– Histological features of ARDS– Fibrosis– Cytokine release

• Systemic sequelae– cardiac output– regional perfusion (gut, liver,

kidney)– bacterial translocation

• from lungs• from gut

– inflammatory mediators

Scope

• Non-ventilatory management• Ventilatory management• Role and function of respiratory centres

Non-ventilatory management• Basics really important

– Nutrition, bowel care, DVT prophylaxis, skin care, nosocomial infection avoidance (CVC, TT), positioning…..

– Staffing, regular review• Microbiology

– Samples/advice• Treat infection

– Antibiotics / antivirals• Get the basics right, avoid harm

Ventilatory management

Ventilator Induced Lung Injury

PositivePositive--pressure Mechanical pressure Mechanical VentilationVentilation

Currently, the only therapy that has been proven to be effectiveat reducing mortality in ALI/ARDS in a large, randomized,

multi-center, controlled trial is a protective ventilatory strategy.

Tidal volume and plateau pressure

VentilatorVentilator--induced Lung Injuryinduced Lung InjuryConceptual FrameworkConceptual Framework

Lung injury from:• Overdistension/shear - > physical injury• Mechanotransduction - > “biotrauma”

• Repetitive opening/closing • Shear at open/collapsed lung interface

Systemic inflammation and death from:• Systemic release of cytokines, endotoxin,

bacteria, proteases

“atelectrauma”

“volutrauma”

VentilatorVentilator--induced Lung Injuryinduced Lung Injury

Three different pathologic entities:• High-permeability type pulmonary edema • Mechanical over-inflation/distortion of lung structures• Lung inflammation “Biotrauma”

Rouby JJ, et al. Anesthesiology. 2004.


High-permeability type pulmonary edema• Main causative factor:

End-inspiratory lung volume >> peak inspiratory pressure “volutrauma more appropriate than barotrauma”

• Mechanisms altering the alveolar-capillary barrier permeability during MV involve:

- Increased transmural vascular pressure - Surfactant inactivation- Mechanical distortion and disruption of endothelial cells- Regional activation of inflammatory cells

Rouby JJ, et al. Anesthesiology. 2004.Ricard JD, et al. Eur Respir J. 2003.


Mechanical overinflation/distortion of lung structures• Emphysema-like lesions, lung cysts, and bronchiectasis• These lesions predominate in nondependent and caudal lung regions• The degree of overinflation is dependent on:

- Tidal volume- Peak airway pressure - Duration of mechanical ventilation- Time exposed to an Fio2 > 0.6

Rouby JJ, et al. Anesthesiology. 2004.


Lung inflammation “biotrauma”• Lung overinflation or overstretching produces regional and systemic

inflammatory response that may generate or amplify multiple-system organ failure.

• Factors converting the shear stress applied to an injured lung into regional and systemic inflammation are still incompletely elucidated but could include:

- Repetitive opening and collapse of atelectatic lung units- Surfactant alterations- Loss of alveolo-capillary barrier function- Bacterial translocation- Overinflation of healthy lung regions

Rouby JJ, et al. Anesthesiology. 2004.Dreyfuss D, et al. Am J Respir Crit Care Med. 2003.

ARDS Ventilation : “safe window”

Volume

Pressure

Zone ofOverdistention

“Safe”Window

Zone ofDerecruitmentand Atelectasis

Injury

Injury

• Overdistension Edema fluid accumulationSurfactant degradationHigh oxygen exposureMechanical disruption

• Derecruitment, AtelectasisRepeated closure / re-expansionStimulation inflammatory responseInhibition surfactantLocal hypoxemiaCompensatory overexpansion

After lavage,

PCV,

PEEP 15 cmH2O

Mean 23 cmH2O

PIP 33 cmH2O

Tidal Volume Strategies in ARDSTidal Volume Strategies in ARDS

Traditional Approach

High priority to traditional goals of acid-base balance and patient comfortLower priority to lung protection

Low Stretch Approach

High priority to lungprotectionLower priority to traditionalgoals of acid-base balanceand comfort

Practical Approach

• Identify cause of lung injury & treat• Best ventilatory care

– 6ml/kg IBW– PEEP initially by PEEP/FiO2 table– Resp rate (Ti/Te) by expiratory flow &

PaCO2– FiO2 < 0.6– Accept abnormal gases

Nothing normal about ARDS

• Permissive hypercapnia– What threshold? 7.25, 7.20, <<– No upper limit. Acidosis normally well tolerated– Consider damage by aiming for normocapnia

• Permissive hypoxia– Trade off between VILI and PO2– FiO2 and shunts– Accept PO2 > 6kPa. Not higher than 8kPa if high

pressure/volume

Issues for ventilated H1N1 patients (1)

• Persistent fever– Bacterial co-infection

• Culture / antibiotics / xray / US / CT– Continued viraemia

• Dose of oseltamivir/resistance/switch to zanamivir

– Thromboembolism• Doppler/CTPA/treat

• Refractory hypoxia– Slow to resolve primary lung injury– Secondary infection– Overdistension– Air leaks / pneumothorax– Pleural collections– Thromboembolic disease– RV dysfunction and pulmonary hypertension

Issues for ventilated H1N1 patients (2)

Respiratory Centres

Respiratory Centres

• Volume / outcome• ECMO limited• Therapies available

in larger centre– ECMO/NO/HFOV/Prone

• Capacity effects on smaller units

• Volume / outcome not same as transfer

• Concerns about transfer

• Evidence base– ECMO/NO/HFOV/Prone

For Against

Referral Time points

• 0-1 consecutive days ARDS– High risk

• pregnant, immunocompromised, chronic lung disease, obesity

– Need for rescue therapies– No level 3 bed locally– Calculate baseline scores

• P/F ratio, OI, LIS, GOCA

No coexisting disease that will cause death within 5 yrCoexisting disease that will cause death within 5 yr but not within 6 moCoexisting disease that will cause death within 6 mo

01

2

Associated diseasesA

UnknownDirect lung injuryIndirect lung injury

123

CauseC

Lung onlyLung + 1 organLung + 2 organsLung + ≥ 3 organs

ABCD

Organ failureO

Pao2/Fio2 ≥ 301Pao2/Fio2 200 -300Pao2/Fio2 101 – 200Pao2/Fio2 ≤ 100Spontaneous breathing, no PEEPAssisted breathing, PEEP 0-5 cmH2OAssisted breathing, PEEP 6-10 cmH2OAssisted breathing, PEEP ≥ 10 cmH2O

0123ABCD

Gas exchange

Gas exchange (to be combined with the numeric

descriptor)

G

DefinitionDefinitionScaleScaleMeaningMeaningLetterLetter

• P/F ratio – PaO2/FiO2• OI – FiO2 x 100 x Mean airway pressure / PaO2• LIS – Murray (CXR, P/F ratio, PEEP, Compliance)• GOCA


• 1-3 consecutive days ARDS– Unable to achieve TV </= 6ml/kg IBW– Unable to achieve plateau pressure </=

30cmH2O– Air leak present– Deteriorating score


• 3 -5 consecutive days ARDS– All patients with P/F ratio < 26.7kPa

• > 5-7 days– Discuss with centre but most likely to

continue with local treatment

Recommendations of EG Report

• the use of the P/F ratio in all patients in Critical Care with respiratory failure as a measure of respiratory compromise

• the adoption of a protective lung strategy for all patients at risk of ALI and ARDS

• the development by Critical Care Networks of clearly defined auditable pathways within a tiered framework of adult critical care services for patients with a P/F ratio ≤26.7KPa

Practical approach

• Score patients for lung injury• Basics right• Good ventilation

– ARDSnet, lung protection rather than normal gases

• Understand potential problems in H1N1– Secondary infection, viraemia, PE, fluid

• Use respiratory centres– Advice/transfer, early not late

After lavage,

Step up

After lavage,

Step down

[email protected]

Dynamic Multiscan CT: Results

healthy lung saline lavage ARDSstep-up step-down step-up step-down

V fast (%) 100 80 (75-84) 85 (80-90) 94 (93-96)V slow (%) 20 (16-25) 15 (13-17) 6 (4-6)Tc fast (s) 0.4 (0.3-0.4) 1.1 (0.7-1.6) 0.7 (0.6-0.8) 0.4 (0.3-0.4)Tc slow (s) 5 (4-6) 7 (5.5-10) 8 (6.3-10)

(5 pigs before and after induction of ARDS by lavage)(5 pigs before and after induction of ARDS by lavage)

Respiratory Therapy Concepts in ARDS :

• Conventional Ventilation :- PEEP, Fi02- Inverse Ratio- Low Volume Pressure Limited Ventilation- Perm. Hypercapnia - Prone positioning- NO Inhalation - Partial Liquid Ventilation

• Conventional Ventilation + HFJV• HFOV

Changing Lung Volume in CV:

Paw = Lung Volume !Inflation ≠ Deflation

6 ml/kg 12 ml/kgPIP (avg) 25 33

PEEP (avg) 6 6

Mortality 30% 39%

Ventilatordays

<

Organ failurefree days

<

IL-6 bloodlevels

<

ARDS network studyNew Eng J Med 2000;342:1301-8

Why HFOV ?

70 80 90 00Year

Tida

l V

olum

e (m

l/kg)

0

5

10

15

20

70 80 90 00Year

PEEP

0

10

20

30

40

5

0

HFOV

HFO

V

Pulmonary Injury Sequence:

•If we cannot prevent the injury sequence , then the target goal is to interrupt the sequence of events !

•High Frequency Oscillation does not reverse injury, but may interrupt the progression of injury

Pulmonary Injury Sequence Paradox

Necessity to achieve gas exchange but eliminate tidal breathing

“Use of mean airway pressure sufficient enough to maintain a constant intrapulmonary pressure above closing pressure, and eliminate the bi-phasic pressure swing, will alter the development of the pulmonary injury”

• Meredith K, et al , 1989 - baboons• Jackson C, et al, 1990 - ring tail monkeys• De Lemos, et al, 1992 - baboons

Pulmonary Injury Sequence:Pulmonary Injury Sequence:

HFOV:– Produces a more

uniform ventilation pattern

– Maintains normal architecture of the lungs during ventilation.

CMV lung biopsy

HFOV lung biopsy

Meredith et al

24 h

24 h

Optimized Lung Volume strategy:

1.) Increase Lung Volume above critical opening pressure to the Optimum and keep it there in Inspiration and Expiration !

Benefits: - homogenous gas distribution- reduced regional atelectasis- better matching of ventilation/perfusion- reduced oxygen exposure -? reduced VILI

HFOV Principle:

ET Tube

BIAS Flow

Patient

CDPAdjust Valve

Oscillator

Increase FRC with a “super CPAP system”

Mean Airway pressure 5 cm H2O

Optimized Lung Volume Strategy:Optimized Lung Volume Strategy:

CT Scan :ARDS pig model 30 kg

Mean Airway pressure 25 cm H2O



Mean Airway Pressure 40 cm H2O



CDP= FRC

CT 1 CT 2CT 3

Paw = CDPContinuousDistendingPressure

Optimized Lung Volume Strategy:

2.) Decrease Tidal Volumes to less or equal then dead spaceand increase frequency !

Benefits: - no excessive volume swings- reduced regional overinflation and stretching- reduced Volutrauma

HFOV Principle:

ET Tube

BIAS Flow

Patient

CDPAdjust Valve

Oscillator

Decrease TV’s to physiological dead space and increase frequency

GAS EXCHANGE IN HFOV

1.) Convection (Bulk Flow) Ventilation2.) Asymetrical Velocity Profile3.) Taylor Dispersion4.) Molecular Diffusion5.) Pendelluft6.) Cardiogenic Mixing

Chang HK. Mechanisms of gas transport during ventilation by HFOV, Brief Review, J Appl Physiol, 1984

Schindler M, et al. Effect of Lung Mechanics on Gas Transport During HFO. Pediatric Pulmonology, 1991

HFOV Principle:

CDP=FRC=Oxygenation

+ + + + +

- - - - -

AmplitudeDelta P =Tv =Ventilation

I

E

HFOV = CPAP with a wiggle !

Pressure transmission CMV / HFOV :Distal amplitude

measurements with alveolar capsules in animals, demonstrate it to be greatly reduced or “attenuated” as the pressure traverses through the airways.

Due to the attenuation of the pressure wave, by the time it reaches the alveolar region, it is reduced down to .1 - 5 cmH2O.

Gerstman et. al

HFOV Principle:Pressure curves CMV / HFOV

•There was no difference in overall mortality between patients primarily ventilated with HFOV and CMV

•Patients with an initial OI > 20 have a lower mortality with HFOV as compared with CMV (RR 0.48, 95% CI 0.30-0.75)

•Patients with the most severe ARDS appear to benefit most from HFOV as an early mode of ventilation. Future randomized controlled trials should concentrate on these more severe ARDS patients.

Conclusion. HFOV has beneficial effects on PaO2/FiO2 ratio and may be an effective rescue therapy in adults with severe oxygenation failure. Early institution of HFOV may be advantageousChest 2004;126;519-527

VILI in Pts With & Without Lung Protective Ventilatory Strategies

Ranieri et al JAMA 1999;282:54-61.

Prospective study comparing high frequency oscillatory ventilation versus Conventional mechanical ventilation in patients with ARDS

Shah S, Jackson SK, Findlay GP. Critical Care. University Hospital of Wales, Cardiff.

0

50

100

150

200

250

0 4 8 12 24 48 72

Time (Hours)

P/F

Rat

io (m

mHg

)

HFOVCMV

Presented at ATS, 2005Presented at ATS, 2005

Prospective study comparing high frequency oscillatory ventilation versus Conventional mechanical ventilation in patients with ARDS

Shah S, Jackson SK, Findlay GP. Critical Care. University Hospital of Wales, Cardiff.

IL6:Serum HFOV vs CMV

0

200

400

600

800

1000

1 2 3

Ti me

HFOV

CMV

IL 6: BAL CMV vs HFOV

0

200

400

600

800

1000

1 2

CMV BAL

HFOV BAL

Presented at ATS, 2005Presented at ATS, 2005

HFOV - Summary

• Ventilation in keeping with strategies of lung protection

• At least equivalent to CMV• Emerging data to show reduction in

biomarkers of VILI

Which patients ?

• ‘rescue’ therapy• Late application• Failing conventional

ventilation– High PEEP, peak,

FiO2, long Ti, prone, NO

• Early use• ALI not only ARDS• Prior to ‘aggressive’

conventional ventilation

Initial experience Present practice


• Adult ARDS late stage lung structural changes– Enlarged air

space– Septal

destruction– Fibrotic lesions

Rouby JJ, Inten Care Med 1993; 19:383


Twenty Years of One Year Follow Up of Lung Function (DLCO) in ARDS Survivors

Suchyta MR, ERS 1997

ventilation and respiratory centres - nhs wales ventilation and... · 2015. 10. 27. · •...

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