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Ventilation strategies, targets and goals in acute respiratory failure

Ventilation strategies, targets and goals in acute respiratory failure. Peter C. Rimensberger Pediatric and Neonatal ICU University Hospital of Geneva Switzerland. Common physiological objectives of mechanical ventilation.

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Ventilation strategies, targets and goals in acute respiratory failure

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  1. Ventilation strategies, targets and goals in acute respiratory failure Peter C. Rimensberger Pediatric and Neonatal ICU University Hospital of Geneva Switzerland

  2. Common physiological objectives of mechanical ventilation 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.

  3. Patient with his specific disease Defined Clinical Targets and Goals Ventilation Modes Acceptable or “best” Strategies Adjunctive Therapies

  4. The targets 45 years ago: Good pO2, normal pCO2 Recruitment with large tidal volumes Derecruitment with „shallow“ tidal volumes Bendixen HH New England J Med 1963; 269:991-996

  5. Normal lung CMV Volume ARDS Airway pressure (cmH2O) HFOV Adapted from Suzuki H Acta Pediatr Japan 1992; 34:494-500 Concept of low Vt or peak pressure limitation and « high » PEEP Allowable Vt? Often resulting in hypercapnia Normocapnia possible

  6. ARDS network trial (Vt 6 vs. 12 ml/kg) n = 861 Mortality: 31 vs. 38 (p < 0.007) PIP: 32 vs. 39 cmH2O Pplat: 25 vs. 33 cmH2O NEJM 2000;342:1301-1308

  7. Girard TC and Bernard GR Chest 2007;131;921-929 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

  8. Tidal Volume:A risk factor for ALI in patients who did not have ALI at the onset of mechanical ventilation p < 0.001 50 40 30 20 10 0 Mean Vt 10.9 ± 2.3 n = 100 n = 160 Proportion of ALI (%) n = 66 < 9 9 to 12 > 12 Tidal Volume (ml/kg PDW) Gajic O et al. Crit Care Med 2004; 32:1817-1824

  9. 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

  10. after RM before RM alveoli per field inspiration expiration I – E Maintaining pressure (CPAP or PEEP) Halter JM AJRCCM 2003, 167:1620-6 Recruiting pressure (CPAP, SI or Pplat) Gattinoni L A JRCCM 2001; 164:1701–1711

  11. right lung dependent region right lung nondependent region normal lung normal lung injured lung injured lung post surfactant lung post surfactant lung Regional «homogeneity» on the deflation limb Frerichs I, Dargaville P, Rimensberger PC (manuscript in preparation)

  12. Oxygen Targets? Cheifetz I, Respiratory Monitoring in Roger’s Textbook of Pediatric Intensive Care Medicine

  13. Oxygenation Index Predicts Outcome in Children with Acute Hypoxemic Respiratory Failure 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. Trachsel AJRCCM 2006

  14. The classical focus in ventilated patients O2 CO2 O2 delivery = 1.3 x CO x Hb x SpO2 Oxygen content in mixed venous blood 1.3 x Hb x SvO2 from Cheifetz I, Respiratory Monitoring in Roger’s Textbook of Pediatric Intensive Care Medicine

  15. P t “Functional” Recruitment by the pO2 response ? P/F-ratio, oxygen delivery and quasi-static Crs during PEEP steps Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32

  16. normal poorly areated normal poorly areated CT-aeration Anatomical recruitment versus overdistention At ZEEP and 2 PEEP levels Diffuse CT-attenuations Focal CT-attenuations Rouby JJ AJRCCM 2002;165:1182-6

  17. P t “Functional” Recruitment by the pO2 response ? P/F-ratio, oxygen delivery and quasi-static Crs during PEEP steps Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32

  18. 1 1 2 2 1 1 1 1 1 1 – – PEEP 5 PEEP 20 Prevalent overinflation = dead space effect

  19. P t “Functional” Recruitment by the pO2 response ? P/F-ratio, oxygen delivery and quasi-static Crs during PEEP steps PVR RV FRC TLC Lung Volume Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32

  20. 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

  21. Bigatello LM at al. Curr Opin Crit Care 2001, 7:34–40

  22. Bigatello LM at al. Curr Opin Crit Care 2001, 7:34–40

  23. Clinical experience:Premature infants, 600 à 1200 g, < 24 hrs on MV Normocapnia 35-45 mmHg Permissive Hypercapnia 45-55 mmHg Mariani G, Cifuentes J, Carlo WA Pediatrics 1999;104:1082-1088

  24. Minimal ventilation to prevent BPD Carlo W et al. J Pediatr 2002;141:370-5

  25. Minimal ventilation to prevent BPD vs. PCO2 target >52 mm Hg PCO2 target <48 mm Hg Carlo W et al. J Pediatr 2002;141:370-5

  26. HYPERCAPNIA in pediatric ARDS 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.

  27. In the preterm infant: Acceptable is Normocarbia or Moderate Hypercarbia Fabre J et al. Pediatrics 2007;119:299

  28. The pO2 response and cardiorespiratory interactions ? PVR RV FRC TLC Lung Volume Lichtwarck-Aschoff M AJRCCM 2000; 182:2125-32

  29. 70 60 50 40 iNo 30 days mortality (%) Placebo 30 20 10 0 Lundin Dellinger Troncy Michael Dobyns No benefit of iNO on survival of ARDS

  30. NO VA NO Q S Q S Q T Q T PaO2 • Redistribution of pulmonary blood flow towards well ventilated lung units • V/Q mismatch  • PVR   right and left ventricular dysfunction may improve Pathophysiological benefits of iNO treatment in ALI / ARDS VA PaO2low

  31. RV-dilatation (before iNO) Pressure gradient TI = 44 mmHg

  32. Improved RV-size / function (on iNO) Pressure gradient TI = 21 mmHg

  33. RV-dilatation and dysfunction LV / LA-compression / dysfunction Reduced cardiac output Reduced DO2 MOF High PVR with increased PAP

  34. UK guidelines for the use of iNO Indications 1. Severe ARDS Optimally ventilated PaO2 12 kPa on FIO2 1.0 2. Right-sided cardiac failure Significant RSCF: MPAP > 24 mmHg, TPG > 15, PVR > 400 dynes-scm Must support systemic circulation: inotropes, etc. Beware adverse effects on the left ventricle (= P/F ratio of < 100) Cuthbertson BH Intensive Care Med (1997) 23: 1212-1218

  35. Normal lung Volume ARDS Airway pressure (cmH2O) 2) CO2  MValv  Ventilation efficiency  alveolar deadspace  in the balance with the degree of allowable hypercapnia Settings Individualized Vt Will need adjustment of respiratory rates (with appropriate Ti and Te) Go for a PEEP trial Individualized PEEP Individualized settings are “dictated” by the defined goals and targets  this gives the strategy to be chosen 1) Oxygenation  O2 delivery (hemodynamics) O2 consumption (metabolism rates)  SvO2

  36. FiO2 > 40% increase PEEP (PEEP trial) O2 , CO2 , Crs O2 , CO2 , Crs Reduce PEEP ev. decrease FiO2 FiO2 > 40% • If FiO2 > 60% • 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 (oxygenation/ventilation) Vent settings: Vt 4 – 6 ml/kg, rate adjustment (I-E ratio 1:1), PEEP 5, Pplat <30 Ev. adjust Vt

  37. no yes Overdistention? no yes Negative fluid balance Fluid challenge Reduce PEEP Pulmonary Hypertension ? (with RV dilatation) iNO (10 – 20 ppm)  Verify response cardiac US Algorithm-guided approach (hemodynamic) Hemodynamic targets: no signs of hypoperfusion SvO2 targets > 65%

  38. The classical focus in ventilated patients O2 CO2 O2 delivery = 1.3 x CO x Hb x SpO2 Oxygen content in mixed venous blood 1.3 x Hb x SvO2 from Cheifetz I, Respiratory Monitoring in Roger’s Textbook of Pediatric Intensive Care Medicine

  39. 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 ?

  40. Target SpO2 : Pre- and/or Post ductal ? • Persistent Pulmonary Hypertension • of the Newborn/Preterm : • Premature Rupture of the Membranes • Sepsis • Severe HMD RA RV LV Pre-ductal : higher SpO2 DA PA Post-ductal : lower SpO2 DO2= 1.3 x AoFlow x Hb x SpO2

  41. SpO2 95 90 PaO2 (mmHg) 110 42 Evidence for a benefit of SpO2 < 90-95% in the preterm infant ? • 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% ? Jubran A. Crit Care, 1999

  42. O2 delivery = 1.3 x AoFlow x Hb x SpO2 PvO2 O2 consumption Evidence for a benefit for SpO2 < 90-95% in the preterm infant ?

  43. Fetal circulation PaO2 = 18 mmHg ! SaO2 = 60 % ! O2 Delivery = 1.3 x AoFlow x Hb x SpO2

  44. 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)

  45. 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%

  46. Outcome of the preterm infants according to the policy of target SpO2 • Tin W et al. Arch Dis Child Fetal Ed, 2001

  47. Respiratory outcome (1) • Tin W et al. Arch Dis Child Fetal Ed, 2001

  48. Respiratory outcome (2) • Tin W et al. Arch Dis Child Fetal Ed, 2001

  49. 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.

  50. Tin W, et al: Arch Dis Child Fetal Neonatal Ed 84:F106, 2001

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