Transcript Slide 1

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 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
Indirect insult
Common
Aspiration pneumonia
Pneumonia
Sepsis
Severe trauma
Shock
Less common
Inhalation injury
Pulmonary contusions
Fat emboli
Near drowning
Reperfusion injury
Less common
Atabai K, Matthay MA. Thorax. 2000.
Frutos-Vivar F, et al. Curr Opin Crit Care. 2004.
Acute pancreatitis
Cardiopulmonary bypass
Transfusion-related TRALI
Disseminated intravascular
coagulation
Burns
Head injury
Drug overdose
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)
The ARDS Lungs
Vt
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.
aerated lung
• Large blue arrows: Forces resulting from
tidal ventilation
Vt
• Small blue arrows: Forces resulting from
consolidated lung
positive end-expiratory pressure (PEEP)
• Green arrows: forces exerted by the
abdominal content and the heart on the
lung
PEEP
Rouby JJ, et al. Anesthesiology. 2004.
Ventilator induced lung injury
Positive pressure ventilation may injure the lung
via several different mechanisms
Alveolar distension
“VOLUTRAUMA”
Repeated closing and opening
of collapsed alveolar units
“ATELECTRAUMA”
Lung inflammation
“BIOTRAUMA”
VILI
Multiple organ dysfunction syndrome
Oxygen toxicity
Ventilator-induced Lung Injury
Conceptual Framework
Lung injury from:
• Overdistension/shear - > physical injury
• Mechanotransduction - > “biotrauma”
“volutrauma”
• Repetitive opening/closing
• Shear at open/collapsed lung interface
“atelectrauma”
Systemic inflammation and death from:
• Systemic release of cytokines, endotoxin,
bacteria, proteases
Total Lung Capacity [%]
How Much Collapse Depends on the
Plateau
100
Less Extensive
Collapse But
Greater PPLAT
R = 93%
More Extensive
Collapse But
Lower PPLAT
60
R = 81%
Some potentially
recruitable units
open only at
high pressure
R = 59%
20
0
0
R = 0%
R = 22%
R = 100%
20
40
Pressure [cmH2O]
From Pelosi et al
AJRCCM 2001
60
PV Relationships
(ARDS, Supine)
Denver Health
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
VL
(% TLC)
FRC
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-20 -15 -10
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TLC
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
0
5
10

Ventral Alveoli



  
-5











Dorsal Alveoli
15 20 25 30
Ptp (cm H2O)
ARDS Network Low VT 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:
Improved Survival with Low VT
1.0
Proportion of Patients
0.9
0.8
0.7
0.6
0.5
Lower tidal volumes
Survival
Discharge
Traditional tidal values
Survival
Discharge
0.4
0.3
0.2
0.1
0.0
0
20
40
60
80
100
120
Days after Randomization
ARDS Network. N Engl J Med. 2000.
140
160
180
ARDS 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 fluidsfluid 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.
Open lung concept
exp
insp
Opening and Closing Pressures in ARDS
High pressures may be needed to open some lung units, but once open,
many units stay open at lower pressure.
50
40
Opening
pressure
Closing
pressure
%
30
20
From Crotti et al
AJRCCM 2001.
10
0
0
5
10 15 20 25 30 35 40 45 50
Paw [cmH2O]
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 12 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
High-frequency Oscillatory Ventilation
3100B HFOV
High-frequency Oscillatory Ventilation
Characterized by rapid oscillations of a reciprocating diaphragm, leading to highrespiratory 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 Ventilation
• Active expiration
Pressurised circuit
High-frequency Oscillatory Ventilation
0.1-3ml/kg
3-9 hz
35cm
H20
90 cm
Pressure attenuation during HFOV
Pressure attenuation during HFOV
Distal
airways
Increase the frequency:
What happens to TV:
What happens to VILI:
What happens to PaCO2:
decreases
Decreases and hence wish to maximise
this
Increases – alveolar MV decreases
Further questions
If 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 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