Ventilation strategies, targets and goals in acute respiratory failure
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Transcript of Ventilation strategies, targets and goals in acute respiratory failure
Ventilation strategies, targets and goals in acute respiratory failure
Peter C. RimensbergerPediatric and Neonatal ICU
University Hospital of GenevaSwitzerland
1) To support or manipulate gas exchange by
ameliorating alveolar ventilation (pCO2) and
oxygenation (pO2)
2) to restore or maintain adequate functional residual
capacity in order to prevent or reopen atelectasis and
to improve oxygenation lung compliance;
3) to reduce work of breathing in the presence of high
airway resistance and/or reduced compliance, when
spontaneous breathing becomes ineffective.
Common physiological objectives of mechanical ventilation
Defined Clinical Targets and Goals
Acceptable or “best” Strategies
Ventilation Modes
Adjunctive Therapies
Patient with his specific disease
Derecruitment with „shallow“ tidal volumes
Bendixen HH New England J Med 1963; 269:991-996
The targets 45 years ago: Good pO2, normal pCO2
Recruitment with large tidal volumes
Concept of low Vt or peak pressure limitation and « high » PEEP
Adapted from Suzuki H Acta Pediatr Japan 1992; 34:494-500
HFOV
CMV
Airway pressure (cmH2O)
Vo
lum
e
Normal lung
ARDS
Often resulting in
hypercapnia
Normocapnia possible
Allowable Vt?
ARDS network trial (Vt 6 vs. 12 ml/kg)
Mortality: 31 vs. 38 (p < 0.007)
n = 861
PIP: 32 vs. 39 cmH2O Pplat: 25 vs. 33 cmH2O
NEJM 2000;342:1301-1308
Vt of 6 ml/kg (with limitation of plateau pressures to 30 cmH2O) is better than Vt of 12 ml/kg
High PEEP is probably better than low PEEP
Girard TC and Bernard GR Chest 2007;131;921-929
Tidal Volume: A risk factor for ALI in patients who did not have ALI at the onset of mechanical ventilation
50
40
30
20
10
0
Pro
port
ion
of A
LI (
%)
< 9 > 12
Tidal Volume (ml/kg PDW)
n = 66
9 to 12
n = 160
p < 0.001
n = 100
Mean Vt 10.9 ± 2.3
Gajic O et al. Crit Care Med 2004; 32:1817-1824
Is there a safe Pplat, below which there is no beneficial effect of tidal volume reduction?
Hager DN et al. AJRCCM 2005; 172:1241-45
Gattinoni L A JRCCM 2001; 164:1701–1711
Recruiting pressure (CPAP, SI or Pplat)
before RMbefore RM after RMafter RM
Halter JM AJRCCM 2003, 167:1620-6
alveoli per fieldalveoli per field
inspirationinspiration expirationexpiration
I – EI – E
Maintaining pressure (CPAP or PEEP)
Frerichs I, Dargaville P, Rimensberger PC (manuscript in preparation)
right lung dependent region
normal lung
injured lung
post surfactant lung
Regional «homogeneity» on the deflation limbright lung nondependent region
normal lung
injured lung
post surfactant lung
Cheifetz I, Respiratory Monitoring in Roger’s Textbook of Pediatric Intensive Care Medicine
Oxygen Targets?
Oxygenation Index Predicts Outcome in Children with Acute Hypoxemic Respiratory Failure
Trachsel AJRCCM 2006
Severity of oxygenation failure at any point in time during AHRF correlates with duration of mechanical ventilation and mortality. This is best reflected by oxygenation index which shows a direct correlation to outcome in a time-independent manner.
from Cheifetz I, Respiratory Monitoring in Roger’s Textbook of Pediatric Intensive Care Medicine
O2 delivery = 1.3 x CO x Hb x SpO2
Oxygen content in mixed venous blood 1.3 x Hb x SvO2
The classical focus in ventilated patients
CO2
O2
P.Rim 2006
20
0
15
5
15
10
15
15
25
20
Prevalentrecruitment
Balance
Prevalentoverdistention
Constant VT : Plateau - PEEP []
PEEP [cm H2O]
0
10
20
30
40
50
Air
way
pre
ssu
re [
cmH
2O
]
PEEP
Plateau
L. Gattinoni, 2003
Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32
“Functional” Recruitment
P/F-ratio, oxygen delivery and quasi-static Crs during PEEP steps
P
tby the pO2 response ?
CT-aerationpoorly areated
poorly areatednormal
normal
At ZEEP and2 PEEP levels
Diffuse CT-attenuations
Focal CT-attenuations
Rouby JJ AJRCCM 2002;165:1182-6
Anatomical recruitment versus overdistention
P.Rim 2006
20
0
15
5
15
10
15
15
25
20
Prevalentrecruitment
Balance
Prevalentoverdistention
Constant VT : Plateau - PEEP []
PEEP [cm H2O]
0
10
20
30
40
50
Air
way
pre
ssu
re [
cmH
2O
]
PEEP
Plateau
L. Gattinoni, 2003P.Rim 2006
Constant VT : PaCO2 and PaO2
Prevalentrecruitment
Balance
Prevalentoverdistention
0 5 10 15 20
PEEP [cmH2O]
0
20
40
60
80
100
[mm
Hg
]
PaCO2
PaO2
L. Gattinoni, 2003
Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32
“Functional” Recruitment
P/F-ratio, oxygen delivery and quasi-static Crs during PEEP steps
P
t
by the pO2 response ?
2
1
–
2
1
–
PEEP 20
1
1
1
1
1
1
Prevalent overinflation = dead space effect
PEEP 5
Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32
“Functional” Recruitment
P/F-ratio, oxygen delivery and quasi-static Crs during PEEP steps
P
t
by the pO2 response ?
RV FRC
PV
R
TLC
Lung Volume
Permissive Hypercapnia:A target or an undesirable consequence?
Protection by Reduced Lung Stress or by Therapeutic Hypercapnia?
Laffey JG Am J Respir Crit Care Med 2000; 162: 2287–2294
Bigatello LM at al. Curr Opin Crit Care 2001, 7:34–40
Bigatello LM at al. Curr Opin Crit Care 2001, 7:34–40
Mariani G, Cifuentes J, Carlo WA Pediatrics 1999;104:1082-1088
Normocapnia 35-45 mmHg
Clinical experience: Premature infants, 600 à 1200 g, < 24 hrs on MV
Permissive Hypercapnia 45-55 mmHg
Carlo W et al. J Pediatr 2002;141:370-5
Minimal ventilation to prevent BPD
Carlo W et al. J Pediatr 2002;141:370-5
Minimal ventilation to prevent BPD
vs.
PCO2 target >52 mm Hg
PCO2 target <48 mm Hg
Hypoventilation with moderate hypercapnia seems safe. However, certain categories of patients are at risk, including those with head trauma, high intrathoracic pressure, hemodynamic instability, myocardial irritability, and dysfunction.
The safety of a very high PaCO2 is not proven.
It is still unclear how low a value of arterial pH can be considered safe.
The beneficial effect of permissive hypercapnia on patient outcome is still controversial.
HYPERCAPNIA in pediatric ARDS
Fabre J et al. Pediatrics 2007;119:299
In the preterm infant: Acceptable is Normocarbia or Moderate Hypercarbia
Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32
The pO2 response and cardiorespiratory interactions ?
RV FRC
PV
R
TLC
Lung Volume
No benefit of iNO on survival of ARDS
0
10
20
30
40
50
60
70
Lundin Dellinger Troncy Michael Dobyns
30 d
ays
mo
rta
lity
(%)
iNo
Placebo
Pathophysiological benefits of iNO treatment in ALI / ARDS
PaO2 low
right and left ventricular dysfunction may improve
VA
TSQ
Q
Redistribution of pulmonary blood flow towards well ventilated lung units
– V/Q mismatch
– PVR
NO
NO
PaO2
VA
TSQ
Q
Pressure gradient TI = 44 mmHg
RV-dilatation (before iNO)
Pressure gradient TI = 21 mmHg
Improved RV-size / function (on iNO)
High PVR with increased PAP
RV-dilatation and dysfunction
LV / LA-compression / dysfunction
Reduced cardiac output
Reduced DO2
MOF
Indications
1. Severe ARDSOptimally ventilatedPaO2 12 kPa on FIO2 1.0
2. Right-sided cardiac failureSignificant RSCF: MPAP > 24 mmHg, TPG > 15,PVR > 400 dynes-scmMust support systemic circulation: inotropes, etc.Beware adverse effects on the left ventricle
UK guidelines for the use of iNO
Cuthbertson BH Intensive Care Med (1997) 23: 1212-1218
(= P/F ratio of < 100)
Airway pressure (cmH2O)
Vo
lum
e
Normal lung
ARDS
Settings
Individualized settings are “dictated” by the defined goals and targets this gives the strategy to be chosen
Individualized Vt
Will need adjustment of respiratory rates (with appropriate Ti and Te)
Go for a PEEP trial
Individualized PEEP
1) Oxygenation O2 delivery (hemodynamics) O2 consumption (metabolism rates) SvO2
2) CO2 MValv Ventilation efficiency alveolar deadspace in the balance with the degree of allowable hypercapnia
Vent settings: Vt 4 – 6 ml/kg, rate adjustment (I-E ratio 1:1), PEEP 5, Pplat <30
FiO2 > 40% increase PEEP (PEEP trial)
O2 , CO2 , CrsO2 , CO2 , Crs
FiO2 > 40% Reduce PEEP ev. decrease FiO2
Ev. adjust Vt
Algorithm-guided approach (oxygenation/ventilation)
If FiO2 > 60% (1) try prone position: response if P/F increase > + 40%
and / or compliance increase > 25%(2) try iNO 8 to 12 ppm: stop if no response after 10 minutes
response if P/F > + 15%
Algorithm-guided approach (hemodynamic)
Hemodynamic targets: no signs of hypoperfusion SvO2 targets > 65%
yes
Negative fluid balance
no
Overdistention?
Fluid challenge
no
Reduce PEEP
yes
iNO (10 – 20 ppm) Verify response cardiac US
Pulmonary Hypertension ?(with RV dilatation)
from Cheifetz I, Respiratory Monitoring in Roger’s Textbook of Pediatric Intensive Care Medicine
O2 delivery = 1.3 x CO x Hb x SpO2
Oxygen content in mixed venous blood 1.3 x Hb x SvO2
The classical focus in ventilated patients
CO2
O2
The pO2 targets in specific patients
• Extremely preterm / preterm / full term;
• Newborn with septic shock;
• Preterm infant with significant PDA;
• Persistent Pulmonary Hypertension of the Newborn: FiO2 setting based on pre- or post-ductal area ?
Why do we tolerate SpO2 between 70-80% in cyanotic cardiopathy, and not in the preterm infant ?
Target SpO2 : Pre- and/or Post ductal ?
DA Pre-ductal : higher SpO2
Post-ductal : lower SpO2
Persistent Pulmonary Hypertensionof the Newborn/Preterm :
• Premature Rupture of the Membranes• Sepsis• Severe HMDRA
RVLV
PA
DO2= 1.3 x AoFlow x Hb x SpO2
Evidence for a benefit of SpO2 < 90-95% in the preterm infant ?
1. Physiologic data• Evidence for deleterious
effects of high PaO2
(>80mmHg?)• Increase the risk of ROP and
respiratory morbidity (Askie LM. Cochrane, 2001)
• Risk of hyperoxemia with SpO2 range 90-95% ?SpO2
PaO2 (mmHg)
90
95
42 110 Jubran A. Crit Care, 1999
Evidence for a benefit for SpO2 < 90-95% in the preterm infant ?
O2 consumption
O2 delivery = 1.3 x AoFlow x Hb x SpO2
PvO2
Fetal circulation
PaO2 = 18 mmHg !SaO2 = 60 % !
O2 Delivery
= 1.3 x AoFlow x Hb x SpO2
Evidence for a benefit for SpO2 < 90-95% in the preterm infant ?
• Lack of evidence for hypoxia in hypoxemic preterm infants (Petrova A et al.
Pediatr Crit Care Med, 2006) • Prospective study
• 10 preterm infants 24-32 weeks GA
• Mesurement of tissular oxygenation (NIRS, brain and kidney) when SpO2 < 80% ;
No tissular hypoxia(Tissular SO2 and Fractional O2 Extraction : Adequate)
Evidence for a benefit for SpO2 < 90-95% in the preterm infant ?
Tin W et al. Arch Dis Child Fetal Ed, 2001 • Retrospective study
• 295 preterm infants < 28 weeks GA
• Comparison of different policies:
– Target SpO2 70-90% vs 88-98%
Tin W et al. Arch Dis Child Fetal Ed, 2001
Outcome of the preterm infants according to the policy of target SpO2
Tin W et al. Arch Dis Child Fetal Ed, 2001
Respiratory outcome (1)
Tin W et al. Arch Dis Child Fetal Ed, 2001
Respiratory outcome (2)
Target SpO2 ?
• Hyperoxemia can occur for SpO2 ranges between 90-
96%;
• Physiologic evidence suggest that O2 delivery can
be normal when SpO2 is lower than 88%, providing
adequate cardiac output and hemoglobin concentration;
• Clinical data suggest that target SpO2 between 70
and 90% may reduce ROP, O2 need without increasing
neurological impairment in very preterm infants.
Tin W, et al: Arch Dis Child Fetal Neonatal Ed 84:F106, 2001
Target SpO2 in the preterm infant ?
Take home message
SpO2:
Preductal SpO2, instead of postductal, should be monitered during the first days after birth;
Target SpO2 should not be > 95%
Target SpO2 < 92% may be preferred in extremely preterm infants