1. Causes of Respiratory Failure I Lung tissue –Pneumonia –Pulmonary hemorrhage –Pulmonary edema –Respiratory distress syndrome (hyaline membrane disease)

2. HMD wet lung congenital pneumoniameconial aspiration

3. Adults and children: Acute respiratory distress syndrome (ARDS) Newborn: Infant respiratory distress syndrome (iRDS) Mortality: 25 - 35% CLD: 15 - 25% Ventilator induced lung injury Mechanical ventilation Oxygenation Lung volumes Pulm. compliance

4. 4-day-old, 26-week gestation infant 2-day-old, 38-week gestation infant MRI signal intensity from non-dependent to dependent regions The water burden of the lung makes the lung of the preterm infant, despite surfactant treatment,vulnerable to VILI Adams EW AJRCCM 2002; 166:397–402

5. Nonhomogeneous Lung Disease A strategy that is effective in opening damaged areas may result in overinflation and trauma to more normal areas of the lung. The pathophysiology shared by these diseases is nonuniform lung involvement where certain lung units are nearly normal while other areas are markedly abnormal.

6. Diffuse “Homogeneous” Lung Disease The goals of assisted ventilation in this group of patients are to improve lung inflation, compliance and ventilation/perfusion matching while avoiding barotrauma or compromise of cardiac output.

7. The best approach = The extended sigh (stepwise increase and decrease of PEEP using the lowest VT possible) Required Monitoring: SaO2, PaO2 PaCO2 and/or endtidal CO2 Hemodynamics

8. "static" compliance: static PIP (Pplat) - PEEP tidal volume Cst = PEEP titration The oxygenation response: Can it be used? Recruitment Overdistension Burns D J Trauma 2001;51:1177-81

9. 20/5 Steps of 5 cmH2O to 35/20 20/5 Pressure control ventilation PEEP 5 PEEP 10 PEEP 15 PEEP 20 PEEP titration: O 2 and CO 2 response in a lung injury model of surfactant depletion ETT disconnection

10. O 2 -improvement = Shunt improvement = PaO 2 VA PaCO 2 a) recruitment PaO 2 PaCO 2 VA b) flow diversion

11. PEEP5 15 1 1 1 1 1 1 O 2 -improvement does not exclude overinflation Gattinoni L (2003) Prevalent overinflation = dead space effect PaO 2 and PaCO 2 increase

12. Airway pressure (cmH 2 O) Volume (l) (surfactant depleted lung) ALI severe (A)RDS Allowable V t and disease severity

13. Transition from CMV to HFOV 1)Pplat approaching 25 cmH2O after PEEP trial (recruitment) and / or PEEP > 12 cmH2O 2) Reduction of Vt < 5 required to match Pplat limits 3) “uncomfortably” high pCO2 or low pH (level dependent from additional pathologies)

14. 1. HFOV uses very small VTs. This allows the use of higher EELVs to achieve greater levels of lung recruitment while avoiding injury from excessive EILV. CMV HFOV CMV HFOV Rationale for HFOV-based lung protective strategies 2. Respiratory rates with HFOV are much higher than with CV. This allows the maintenance of normal or near-normal PaCO2 levels, even with very small Vts.

15. Suzuki H Acta Pediatr Japan 1992; 34:494-500 The concept of volume recruitment during HFO

16. Continuous blood gas monitoring during HFO CDP: 13 CollapseOverdistention 121110911

17. Causes of Respiratory Failure II Lung hypoplasia syndromes –Congenital diaphragmatic hernia –Potter syndrome –prolonged rupture of membranes –Hydrops fetalis The common variable in this group of infants is small, often abnormal lungs. This is associated to: -Difficult CO2 elimination -Pulmonary hypertension (PPHN)

18. Congenital diaphragmatic hernia iNOHFOECMO Gentle ventilation (peak pressure limitation) “Permissive” hypercapnia  resp acidosis May worsen PPHN “Versus” VILI (baro- volutraumatisme)

19. Congenital diaphragmatic hernia Bohn D Am J Respir Crit Care Med 2002; 166: 911–915 Accept ductal shunting as long as RV function is not impaired!

20. Total Survivors ECMO Bohn D Am J Respir Crit Care Med 2002; 166: 911–915 Survival rates in CDH

21. Sakri H Pediatr Surg Int (2004) 20: 309–313 The Scandinavian Experience with CDH Surfactant (-) NO +/- (Cardiac US!) HFOV +++ (early) ECMO (-) “Geneva” attitude

22. Causes of Respiratory Failure III Conducting airways Aspiration (before or after birth) Congenital malformation Tracheal fistula

23. Extra- and intrathoracic airway obstruction Stridor From Pérez Fontán JJ, 1990 + +

24. Classical pathological conditions that may lead to a difficult to ventilate situation Severe airway compression / malacia No PEEP PEEP 10cmH 2 O courtesy from Quen Mok, Great Ormond Street Hospital for Children, London

25. Severe airway compression Once you can ventilate these patients (with high PEEP) they are usually difficult to extubate My advice: Keep a high PEEP on spontaneous ventilation, reduce pressure support and extubate from a high PEEP (ev. to CPAP or NIV)

26. External PEEP in obstructive lung disease (PEEP-trial) VT = 6 mL/kg RR = 6/min VT = 6 mL/kg RR = 9/min VT = 9 mL/kg RR = 6/min VT = 9 mL/kg RR = 9/min Caramez MP Crit Care Med 2005; 33:1519 –1528

27. External PEEP in obstructive lung disease (PEEP-trial) “paradoxical” response Biphasic response Classical overinflation response Caramez MP Crit Care Med 2005; 33:1519 –1528

28. Duval E Pediatric Pulmonology 2000: 30:350–353 HFOV in severe airway obstruction

29. Causes of Respiratory Failure IV Air leak syndromes Pneumothorax Bronchopulmonary fistula PIE

30. CMV HFOV CMVHFOV PIP PEEP Tracheal pressure (cmH2O) EndinspirationEndexpiration Classical indication for HFV - because of small pressure swings

31. PIE, bronchopleural fistula, pneumothroax Recruit to improve oxygenation and in order to lower the FiO2 needed – then reduce the airway pressures to the lowest level needed (air leak will often cease) References: Shen Chest 2002;121;284-6 Mayes Chest. 1991; 100:263-4 Rubio Intensive Care Med. 1986;12:161-3 One sided intubation or airway blocking by inserted balloon catheters is almost never required even in severe airleak (this was just a nice idea to get a case report)

32. Causes of Respiratory Failure V Pulmonary perfusion Congenital heart disease Persistent fetal circulation

33. 31 6/7 wks GA, 1000 g GA (small for GA) 1 course of prenatal steroids 12 hours before delivery Presents with respiratory distress at birth: RR 64, indrawing, SO2 84% at RA CPAP trial with fast increasing O2 requirements (> 60%) Venous and arterial umbilical catheter First art BGA: pH 7.09, PCO2 11 kPa (83 mmHg), pO2 4.36 Intubation Vent settings: TCPL, RR 60, PEEP 5, PIP 18 Poor sats persists: SO2 78% under FiO2 80%

34. PIP 24, PEEP 8, RR 60 no real change in SO2 (SaO2 82 %, FiO2 100%) Art BGA: pH 7.11, pCO2 10 kPa, pO2 3.33, BE –3.6 A: Surfactant? B: HFOV? C: Other? Switch to HFOV: CDP 19, Pressure Ampl 46, Freq 12 Hz SO2 80 %, FiO2 100% Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8

35. A: Surfactant? B: Increase CDP? C: Other? CDP 19, Pressure Ampl 46, Freq 12 Hz SO2 80 %, FiO2 100% Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8

36. CDP 19, Pressure Ampl 46, Freq 12 SO2 80 %, FiO2 100% Art BGA: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8 CDP 14, Pressure Ampl 34, Freq 15 SO2 92 %, FiO2 can be lowered fast to 40% Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6 Diagnosis and what next?

37. CDP 14, Pressure Ampl 34, Freq 15 SO2 92 %, FiO2 40% Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6

38. CDP 14, Pressure Ampl 34, Freq 15 Hz SO2 92 %, FiO2 can be lowered fast to 40% Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6 CDP 13, Pressure Ampl 30, Freq 15 Hz SO2 91 %, FiO2 can be furter lowered to 25% Art BGA: pH 7.42, pCO2 4.4, pO2 3.50, BE –2 SO2 78 % SO2 74 % CDP 13, Pressure Ampl 25, Freq 15 Hz SO2 94 %, FiO2 can be furter lowered to 21% Art BGA: pH 7.39, pCO2 4.87, pO2 3.59, BE –2.3 iNO 8 ppm Echo cardiac

39. 6 hours later (after refixation of ETT) rapid drop in saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30) BGA: A)Increase in airway pressures for recruitment? B)Surfactant C)Increase iNO concentration D)Other

40. CDP 13, Pressure Ampl 25, Freq 15 Hz

41. CDP 13, Pressure Ampl 25, Freq 15 Hz, FiO2 100%, iNO 12 ppm Stepwise increase in CDP up to 20 SO2 72% pre and postductal Art BGA: pH 7.22, pO2 3.56, pCO2 8.0, BE - 3 Gradually increase in P-Ampl to 46 Surfactant SO2 varies around 65 to 75% on FiO2 100%, iNO 12 ppm Art BGA: pH 7.1, pCO2 5.0, pO2 2.36, BE - 5 Lactate: 2.2 4.5

42. CDP 20, Pressure Ampl 48, Freq 10 Hz, FiO2 100%, iNO 12 ppm SO2 varies around 55 to 75% Art BGA: pH 6.97, pCO2 10.0, pO2 2.86, BE – 12, Lactate 8.6 A)Increase iNO, B) switch to CMV C) change HFO settings, D) second dose of surfactant

43. CDP reduction from 20 to 14 Sat immediately improves to 90%, allowing to reduce FiO2 to 60 then 40 % Anticipate!A) I have to reduce iNO B) I lower further CDP C) I change other settings – which one? D) Excellent work, I need a coffee now! Reduce pressure amplitude immediately when lowering CDP (coming of overdistension will render oscillation swings more effective!) Pressure amplitude from 48 to 30 (visible wiggeling) Art BGA: pH 7.39, pCO2 3.4, pO2 6.26, BE – 10 CDP reduction from 14 to 10, P-amplitude to 24, FiO2 to 21%

45. PPHN with: 1)R-L shunt across the FO  severe hypoxemia 2)RV dilatation and failure  poor CO 1) Moderate mainly postductal hypoxemia + ev R-L shunt FO 2) In general good CO NO yes NO may lead to L-R shunt with pulmonary flooding Open ductus Closed ductus

46. R-L shunt and RV dilatation before iNO

47. Shunt inversement under iNO

48. RDS and PPHN in the newborn infant: Nitric oxide effect Right to left shunt without iNOLeft to right shunt on iNO PA Ao Duct PA Ao Duct Indication: not poor postductal oxgygenation but signs of poor cardiac output

49. Take home messages It is not always iRDS that causes hypoxemia in the preterm infant If you don’t know what to do next with your ventilator settings reduce your airway pressures first Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator

50. Pressure – Flow – Time - Volume Time constant:  = Crs x Rrs To short Ti and/or Te will lead to inefficient alveolar ventilation and risk of intrinsic PEEP Adapt your respirator rate (Ti and/or Te) to the stage and mechanical characteristics of lung disease The saying “ we ventilate at 60/min” is a testimony of no understanding

51. Take home messages In pulmonary disease lung volumes (functional for gas exchange) are usually reduced – the “need” for smaller VT than physiological VT is a logical consequence of this If you don’t know what to do next with your ventilator settings reduce your airway pressures first Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator When you try to recruit a lung you need to have appropriate monitoring (CO 2 !)

52. In situations of difficult ventilation an analytical approach is required 3) Which bedside method (monitoring) might be helpful during a PEEP trial? 2) Is the problem “physician”-induced? 1) What are the characteristics of airway or lung disease? - type (etiology) of disease - stage of disease, history - mechanical behaviour