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


Balance


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


Balance


0 5 10 15 20

PEEP [cmH2O]

0

20

40

60

80

100

[mm

Hg

]

PaCO2

PaO2

L. Gattinoni, 2003




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




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

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


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


• 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)


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


Respiratory outcome (1)


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

Ventilation strategies, targets and goals in acute respiratory failure

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