The acute respiratory distress syndrome (ARDS)

The immunology of ARDSpermeability and the influx of protein-rich fluid into the alveolar space edema formation  Damage to type I alveolar cells allows both increased entry of fluid int

The Acute Respiratory Distress

Syndrome (ARDS)

J Christopher Farmer

A bad day in the ICU…now what?

F I O 2 = 1.0, PEEP = 15 cm H 2 O, SpO 2 = 85%

What is ARDS?

Clinical diagnostic criteria for ARDS

ALI versus ARDS

Acute Lung Injury

 Ventilator-associated lung injury

 Underlying injury made worse by mechanical (mainly) effects of MV

 VASI

 Ventilator-associated systemic inflammation

 Biotrauma

The continuum of ARDS

fibrosis & alveolar destruction

ARDS histopathology

Typical histological findings of ARDS include alveolar

inflammation, thickened septae and protein leak (pink), hyaline membranes, congestion and decreased alveolar volume

Risk Factors for ARDS

Pulmonary

 Aspiration pneumonia

 Infectious pneumonia

 Smoke or toxic gas inhalation

 Trauma with lung contusion

 Near drowning

 Acute eosinophilic pneumonia

 BOOP

Risk Factors for ARDS

 Fulminant hepatic failure

 Multiple bone fractures with fat emboli syndrome

 Blood transfusion

 Sepsis

 Post upper airway obstruction

 Drugs (bleomycin)

Pulmonary function in ARDS

The immunology of ARDS

permeability and the influx of protein-rich fluid into the alveolar space

edema formation

 Damage to type I alveolar cells allows both increased entry of fluid into the alveoli and decreased clearance of fluid from the alveolar space

 Damage to type II cells results in decreased production of

surfactant with resultant decreased compliance and alveolar collapse

The immunology of ARDS

the development of ARDS also involves…

 Tumor necrosis factor (TNF) and other cytokines

 Leukotrienes

 macrophage inhibitory factor, platelet factors, and others

 platelet sequestration and activation

 An imbalance of proinflammatory and anti-inflammatory cytokines

The heterogeneity of ARDS

Effects of Recruitment Maneuvers to

Promote Homogeneity within the Lung

Malhotra: NEJM 357: 1113, 2007

Panels A through D show the progressive resolution of infiltrates after application of

inflations of increasing pressure (reprinted from Borges, et al)

The theoretical answer: Promote alveolar

recruitment

 The Problem: a uniformly applied positive insufflating

pressure/breath only opens some alveoli during a timed respiratory

cycle

 The Physiologic dilemma:

 Variable/altered alveolar time constants

 That is, the amount and duration of PPV needed to “recruit” a collapsed alveoli varies from one lung unit to another

 Underinflation in some alveoli and overinflation in others

 Or, failure to maintain alveolar opening (cycling)

 The Solution: “not too much and not too little and only in the right

places!”

Conventional Ventilation as Compared with

Protective Ventilation

Malhotra: NEJM 357: 1113, 2007

This example shows that conventional ventilation at a tidal volume of 12 ml per kilogram of body weight and an

end-expiratory pressure of 0 cm of water (Panel A) can lead to alveolar over-distention (at peak inflation) and collapse (at the end of exhalation) Protective ventilation at a tidal volume of 6 ml per kilogram (Panel B) limits over-inflation and end-

expiratory collapse by providing a low tidal volume and an adequate positive end-expiratory pressure (Adapted from

Tobin)

Hotchkiss, Crit Care Med 2002

Ventilator-Associated Lung Injury (VALI)

Tears in alveolar blood/airspace barrier

69 year old, septic, ARDS, died day 3, PCV, Ppeak 53, PEEP 17

Normal Rat Lungs and Rat Lungs after Receiving High-Pressure

Mechanical Ventilation at a Peak Airway Pressure of 45 cm of Water

Malhotra: NEJM 357: 1113, 2007

After 5 minutes of ventilation, focal zones of atelectasis are evident, in particular at the left lung apex After 20 minutes of ventilation, the lungs are markedly enlarged and congested; edema fluid fills the tracheal cannula

Lung Recruitment Options to Conventional

MV for Severe ARDS

1 Continue conventional MV with until plateau pressure/PEEP maximized/

optimized

2 Move towards inverse ratio ventilation

3 Begin inhaled nitric oxide or prostacyclin

4 Prone positioning

5 Recruitment maneuvers

 30-40 cm H 2 O PEEP for 30-60 secs

6 Consider alternative modes of MV

 High frequency oscillatory ventilation (HFOV)

 Airway pressure release ventilation (APRV), or Bilevel ventilation (BIPAP)

Mechanical ventilation strategies

Goals:

1 Ensure adequate oxygenation and ventilation

2 Prevent lung injury

3 Promote lung healing

Protective strategies – low tidal volumes and PEEP

Benefits of PEEP:

Increased end-expiratory lung volume

Recruitment of unventilated alveoli

Decreased perfusion of unventilated areas Increased V/Q matching Decreased intrapulmonary shunt

Adverse effects of PEEP:

ALI/barotrauma

Decreased venous return

MV in ARDS

MV in ARDS

 Decreasing inspiratory flow prolongs T I In ARDS, this gives more time for the more diseased units to be recruited

 Pressure controlled ventilation has not been shown to be superior

 In VCV, inspiratory flow is usually delivered as square or

decelerating wave and in PCV always decelerating

 Advantages of VCV guaranteed V T and V E and disadvantage lack of control of airway pressure and patient intolerance

 Advantages of PCV controlled airway pressure and patient

tolerance and disadvantages unfamiliarity and non-guaranteed VTand VE

Tidal volume in PCV

ARDSNet: The use of PEEP and FIO2

Malhotra: NEJM 357: 1113, 2007

Inverse Ratio Ventilation in ARDS

increased mean airway pressure

Prone ventilation in ARDS/ALI

pressure sores

BIPAP: APRV with spontaneous

breathing

HFOV

HFOV - Pressure wave in proximal

HFOV: How does it work?

augmentation during spontaneous breathing

Facilitated diffusion

PaCO2

PaO2

lamina develop with differential flow velocities

Oxygenation with HFOV

Machine adjustable parameters:

Ventilation during HFOV

CV (“bulk flow”) VE = f x VT

HFOV (“facilitated diffusion”) VE = f x V T 2

small changes in TV have greater effect during HFOV

When should HFOV be initiated?

? (or PEEP > 15?)

3 If patient requiring paralysis for oxygenation

4 Earlier intervention better

How should HFOV be initiated?

1 Adequate sedation, analgesia

(paralysis during transition?)

2 Set mPaw 3-5 cm H2O> mPaw on CV (initial 5 cm H2O ETT

cuff-leak)

3 Set ∆P at @ “20 + PaCO2” (range 55-90)

4 Set Hz at 5 (unless compartment

syndromes, obesity, etc) (range 3 - 8 Hz)

5 Set TI% at 33% and bias flow @ 30 lpm

Unresolved Issues in HFOV

“protective lung” ventilation?

other “open lung” approaches (e.g APRV, HFPV/VDR)?

mortality and ventilator-free days

Inhaled Vasodilators in ARDS

HTN

required

Other Therapies in ARDS

ketoconazole, ibuprofen have been tried in RCT with negative results

survival benefit for steroids

Prognosis in ARDS

1990

 In the first three days, the underlying disease

 Later, nosocomial infections and sepsis account for most of the deaths

and usually asymptomatic

Poor Prognostic Factors in ARDS

antagonist)

Case study #1

A 60 year old man (70 kg IBW) was admitted for RML

pneumonia and has required mechanical ventilation for 24

Case study #2

A 60 year old man is admitted to the ICU for severe respiratory distress that developed during a blood

Your next steps are…

Case study #3

A 60 year old man (70 kg IBW) has been in the ICU with severe ARDS for 2 days His current ventilator setting are

Case study #4

A 60 year old man has been in the ICU with severe ARDS

Your next steps are…

Case study #5

A 60 year old man has been in the ICU with severe ARDS

Your next steps are…