Definitions

The 1994 North American-European Consensus Conference (NAECC) criteria:• Onset - Acute and persistent• Radiographic criteria - Bilateral pulmonary infiltrates consistent with the

presence of oedema• Oxygenation criteria - Impaired oxygenation regardless of the PEEP

concentration, with a Pao2/Fio2 ratio 300 mmHg (40 kPa) for ALI and 200 mmHg (27 kPa) for ARDS

• Exclusion criteria - Clinical evidence of left atrial hypertension or a pulmonary-artery catheter occlusion pressure of 18 mm Hg.

Bernard GR et al., Am J Respir Crit Care Med 1994

Mortality from ARDSMortality from ARDS

ARDS mortality rates - 31% to 74%

The variability in the rates quoted is related to differences in the populations studied and in the precise definitions used.

The main causes of death are nonrespiratory causes (i.e., die with, rather than of, ARDS).

Respiratory failure has been reported as the cause of death in 9% to 16% of patients with ARDS.

Early deaths (within 72 hours) are caused by the underlying illness or injury, whereas late deaths are caused by sepsis or multiorgan dysfunction.

There is a controversy about the role of hypoxemia as a prognostic factor in adults. Nevertheless, in some studies, both Pao2/Fio2 ratio and Fio2 were variables independently associated to mortality.

Frutos-Vivar F, et al. Curr Opin Crit Care. 2004.Vincent JL, et al. Crit Care Med. 2003.

Ware LB. Crit Care Med. 2005.

Clinical Disorders Associated with the Development of ALI/ARDS

Direct insult

Common Aspiration pneumonia Pneumonia

Less common Inhalation injury Pulmonary contusions Fat emboli Near drowning Reperfusion injury

Indirect insult

Common Sepsis Severe trauma Shock

Less common Acute pancreatitis Cardiopulmonary bypass Transfusion-related TRALI Disseminated intravascular

coagulation Burns Head injury Drug overdose

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

Epidemiology

NIH, 1972 - Incidence of ARDS in the United States: 75 cases per 105 person.years population (approximately 150,000 cases per year)

International multi-center ALI/ARDS cohort studies, 1989 - 2002 • Incidence estimates of ALI/ARDS = 1.3 to 22 cases per 105 person.years

ARDS Network Study (NAECC definitions), 2003 - Incidence of ALI/ARDS in the United States: 32 cases per 105 person.years (range 16 - 64)

ARDS Network Study (NAECC definitions), 2003 - The average number of cases of ALI per ICU bed per year (2.2) varied significantly from site to site (range 0.7 - 5.8)

External forces applied on the lower lobes at end inspiration and end expiration in a patient in the supine position and mechanically ventilated with positive end-expiratory pressure.

• Large blue arrows: Forces resulting from

tidal ventilation

• Small blue arrows: Forces resulting from

positive end-expiratory pressure (PEEP)

• Green arrows: forces exerted by the

abdominal content and the heart on the

lung

Rouby JJ, et al. Anesthesiology. 2004.

aerated lung

consolidated lung

Vt

Vt

PEEP

The ARDS LungsThe ARDS Lungs

Positive pressure ventilation may injure the lung via several different mechanisms

VILI

Ventilator induced lung injury

Alveolar distension“VOLUTRAUMA”

Repeated closing and openingof collapsed alveolar units

“ATELECTRAUMA”

Oxygen toxicity

Lung inflammation“BIOTRAUMA”

Multiple organ dysfunction syndrome

Ventilator-induced Lung InjuryVentilator-induced 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”

How Much Collapse Depends on the Plateau

R = 100%

20

60

100

Pressure [cmH2O]20 40 60

Tota

l L

un

g C

ap

acit

y [%

]

R = 22%

R = 81%

R = 93%

00

R = 0%

R = 59%From Pelosi et alAJRCCM 2001

Some potentially recruitable units open only at high pressure

More Extensive Collapse But Lower PPLAT

Less Extensive Collapse But Greater PPLAT

PV Relationships(ARDS, Supine)

5 10 15 20 25

VL

(% TLC)

Ptp (cm H2O)0-5-10

FRC

TLC

Denver Health

Ventral Alveoli

Dorsal Alveoli

-15-20 30

ARDS Network Low VARDS Network Low VTT Trial Trial

Patients with ALI/ARDS (NAECC definitions) of < 36 hours

Ventilator procedures • Volume-assist-control mode• RCT of 6 vs. 12 ml/kg of predicted body weight PBW Tidal Volume

(PBW/Measured body weight = 0.83)• Plateau pressure 30 vs. 50 cmH2O• Ventilator rate setting 6-35 (breaths/min) to achieve a pH goal

of 7.3 to 7.45 • I/E ratio:1.1 to 1.3• Oxygenation goal: PaO2 55 - 80 mmHg/SpO2 88 - 95%

• Allowable combination of FiO2 and PEEP:

FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0 1.0 1.0 1.0

PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 18 20 22 24

The trial was stopped early after the fourth interim analysis (n = 861 for efficacy; p = 0.005 for the difference in mortality between groups)

ARDS Network. N Engl J Med. 2000.

ARDS Network: ARDS Network: Improved Survival with Low VImproved Survival with Low VTT

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0.0180160140120100806040200

Pro

po

rtio

n o

f P

atie

nts

Days after Randomization

Lower tidal volumesLower tidal volumesSurvivalSurvivalDischargeDischarge

Traditional tidal valuesTraditional tidal valuesSurvivalSurvivalDischargeDischarge

ARDS Network. N Engl J Med. 2000.

ARDS Network: Additional FindingsARDS Network: Additional Findings

In ALI and ARDS patients, 6 ml/kg PBW tidal volume ventilation strategy was associated with:• PaO2/FiO2 lower in 6 ml/kg low VT group• High RR prevented hypercapnia with minimal auto-PEEP (difference of

median intrinsic PEEP between the groups was < 1 cm H2O)• No difference in their supportive care requirements (vasopressors-IV fluids-

fluid balance-diuretics-sedation)• ~10% mortality reduction• Less organ failures• Lower blood IL-6 and IL-8 levels

ARDS Network. N Engl J Med. 2000. Parsons PE, et al. Crit Care Med. 2005.Hough CL, et al. Crit Care Med. 2005. Cheng IW, et al. Crit Care Med. 2005.

insp

exp

Open lung concept

%Opening and Closing Pressures in ARDS

50

Paw [cmH2O]

0 5 10 15 20 25 30 35 40 45 500

10

20

30

40 Opening pressureClosing pressureFrom Crotti et alAJRCCM 2001.

High pressures may be needed to open some lung units, but once open, many units stay open at lower pressure.

Recruitment Maneuvers (RMs)Recruitment Maneuvers (RMs)

Proposed for improving arterial oxygenation and enhancing alveolar recruitment

All consisting of short-lasting increases in intrathoracic pressures• Vital capacity maneuver (inflation of the lungs up to 40 cm H2O, maintained

for 15 - 26 seconds) (Rothen HU. BJA. 1999; BJA 1993.)

• Intermittent sighs (Pelosi P. Am J Respir Crit Care Med. 2003.)

• Extended sighs (Lim CM. Crit Care Med. 2001.)

• Intermittent increase of PEEP (Foti G. Intensive Care Med. 2000.)

• Continuous positive airway pressure (CPAP) (Lapinsky SE. Intensive Care Med. 1999. Amato MB. N Engl J Med. 1998.)

• Increasing the ventilatory pressures to a plateau pressure of 50 cm H2O for 1-2 minutes (Marini JJ. Crit Care Med. 2004. Maggiore SM. Am J Respir Crit Care Med. 2003.)

Lapinsky SE and Mehta S, Critical Care 2005

Other manoeuvres

• Prone positioning ventilation

• Prolonged inspiration

• Inverse ratio ventilation

Limit of open lung strategy

• To minimise VILI to the less damaged alveoli– need to minimise individual alveolar volume – cannot

measure this hence use pressure as surrogate– i.e max insp pressure (plateau pressure 30-32cm

H20)

– as PEEP increases and max pressure remains

unchanged ,TV will decrease • Alveolar ventilation will decrease• alv V: dead space vent ratio will decrease

PaCO2 increases - Resp acidosis

Increasing PaCO2• Management options

Increase resp rate

Minute volume

Delivered TV TV ml/kg Resp rate

6.4 L 640 ml 8 10

6.4 L 480 ml 6 14

6.4 L 320 ml 4 20

6.4 L 160 ml 2 40

Anatomical dead space 150ml

Increasing PaCO2• Permissive hypercapnia• Tracheal gas insufflation – attempting to reduce dead

space

Accompanying as alveolar ventilation decreases will require increasing FIO2 and eventually will result in alveloar hypoxia and arterial hypoxaemia

High frequency ventilation

• High frequency Jet ventilation– Delivers very short high pressure jets of air and relies

on passive exhalation

• High frequency flow interrupter:

• eg infant star – relies on high frequency interruption of flow , passive exhalation – normal circuit

• High frequency oscillatory ventilation

• pressurised circuit , uses a diaphragm piston unit to actively move gas in and out of the lungs – requires special non-compliant circuit , active expiration

3100B HFOV

High-frequency Oscillatory VentilationHigh-frequency Oscillatory Ventilation

High-frequency Oscillatory VentilationHigh-frequency Oscillatory Ventilation

Characterized by rapid oscillations of a reciprocating diaphragm, leading to high-respiratory cycle frequencies, usually between 3 and 9 Hz in adults(180 -600breaths per min), and very low VT (0.1-3ml/kg). Ventilation in HFOV is primarily achieved by oscillations of the air around the set mean airway pressure mPaw (35cm -45cm H2O).

High-frequency Oscillatory VentilationHigh-frequency Oscillatory Ventilation

• Active expiration

Pressurised circuit

35cm H20

90 cm

3-9 hz

0.1-3ml/kg

High-frequency Oscillatory VentilationHigh-frequency Oscillatory Ventilation

Pressure attenuation during HFOV

Pressure attenuation during HFOV

Distal airways

Increase the frequency:

What happens to TV: decreases

What happens to VILI: Decreases and hence wish to maximise this

What happens to PaCO2: Increases – alveolar MV decreases

Further questionsIf PaCO2 is rising and pH is < 7.25: What adjustments may be required?

1. Increase alveolar ventilation – how?

1. Increase amplitude

2. Decrease frequency

3. Remove ETT suction elbow

2. Decrease dead space

1. Introduce cuff leak

2. Tracheal gas insufflation

Further Questions:

What effect does this ventilation have on RV function:

Increase after load

Decrease preload

In which conditions would HFOV be contraindicated:

1. Severe obstructive airways disease

2. Intractable shock - must not be hypovolaemic (CVP at least 8mmHg)

3. Intracranial hypertension

Recruitment Manoeuvre prior to connection to HFOV

• May cause barotrauma , volutrauma and haemodynamic compromise– Hence these manoeuvres should not be attempted without a senior

member of the intensive care medical team being present

• recommended manoeuvre:

• Perform endotracheal toilet bfore manoeuvre

• Patient requires to be heavily sedated +/- paralysed

• should not be hypovolaemic or intractable shock

• Ventilator mode PCV

• High pressure alarm increased

• PEEP gradually increased to 25 cm H2O whilst observing haemodynamics

• Measure lung compliance and gradually reduce peep to level just above point that results in a loss in lung compliance

Final Questions

Diagnosis of pneumothorax:

• high index of suscpician

• Desaturation

• haemodynamic change

• Chest sounds difficult

• mPaw and ∆P may not change

• Decrease chest wiggle on side of pneumothorax

Abrupt rise in paCo2 and increase in ∆P -

. Airway obstruction

Change in resistance

High-frequency Oscillatory VentilationHigh-frequency Oscillatory Ventilation

Characterized by rapid oscillations of a reciprocating diaphragm, leading to high-respiratory cycle frequencies, usually between 3 and 9 Hz in adults, and very low VT. Ventilation in HFOV is primarily achieved by oscillations of the air around the set mean airway pressure mPaw.

HFOV is conceptually very attractive, as it achieves many of the goal of lung-protective ventilation.• Constant mPaws: Maintains an “open lung” and optimizes lung recruitment

• Lower VT than those achieved with controlled ventilation (CV), thus theoretically avoiding alveolar distension.

• Expiration is active during HFOV: Prevents gas trapping

• Higher mPaws (compared to CV): Leads to higher end-expiratory lung volumes and recruitment, then theoretically to improvements in oxygenation and, in turn, a reduction of FiO2.

Chan KPW and Stewart TE, Crit Care Med 2005