Respiratory Failure & NIV: Prior to session read & think about the case in the next 10 slides

1. Respiratory Failure & NIV: Prior to session read & think about the case in the next 10 slides Ken Whyte, Respiratory Physician

2. 67 yr old male smoker: July 2001 • Forklift driver, heavy smoker (60 pack years) with exertional dyspnoea for 3+yrs • Heavy alcohol intake (6+ cans of beer/day) • No relevant past medical history • Only regular medication: Combivent inhaler

3. 67 yr old male smoker: July 2001 • 3/52 history of cough (initial response to antibiotic) then increasing SOB for 1/52. On Examination: • cyanosed, respiratory rate 30/min, SpO2:85%; • in respiratory distress with widespread wheeze and scattered crackles, tired ++. • Clinically hyperinflated; ABG on 2l/min O2: PaO2-7.6kPa (58mmHg); PaCO2-11.5kPa (87mmHg); HCO3--34; pH-7.22

4. CXR on admission

5. 67 yr old male smoker:July 2001 • Commenced on nebulised ipratropium and IV beta agonist + aminophylline; oral prednisone and antibiotic; • Repeat blood gas marginally better but still acidotic (pH - 7.27) and respiratory rate remains >30/min. Tired++ • Commenced on mask ventilation at 2+hrs;

6. Date Time pH PaCO2 PaO2 Comment 21/07 19:40 7.27 11.3 9.5 NIV started 21/07 21:55 7.32 9.6 6.9 IPAP  22/07 03:45 7.35 7.5 9.6 No change 23/07 20:30 7.40 6.2 10.4  weaning 27/07 08:50 7.33 9.7 5.6 Off NIV+O2 27/07 10:15 7.35 9.0 8.0 On O2 Sequential blood gas measurements

7. 67 yr old male smoker: July 2001 • Mask ventilation weaned off over first 48hrs; • Mobilised in ward, smoking cessation; • Discharged home after 9 days, weaning off oral steroids; • Continued to smoke & returned to work

8. 67 yr old male smoker: August • Readmitted 31/8/01: increasing dyspnoea for ?3/52 and sputum darker (grey/green): • pyrexial; respiratory rate 26/min, not distressed; • widespread wheeze; • pH: 7.35; PaO2:7.4kPa; PaCO2:8.5;HCO3-:35; • Rx: low flow oxygen, antibiotics, nebulisers and increased prednisone, PaCO2:7.4kPa. • Discharged at 8 days, FEV1: 0.86l (27%);

9. 67 yr old male smoker: October • Admitted on 20/10/01: • 24 hr history of increasing SOB with purulent sputum; • respiratory distress, respiratory rate 36/min; • cyanosed on O2 (24%); SpO2:55%; • IV aminophylline, nebulised ipratropium & β2 ; • after 4-5 hrs deteriorating and transferred to DCCM for CPAP;

10. 67 yr old male smoker: October • CPAP not tolerated; • pH: 7.1-7.2; PaCO2: 11-14kPa; • IV salbutamol added; [theophylline] normal; • trial of bi-level pressure support ventilation via mask: struggled to cope: abandoned; • sedated with boluses of IV morphine (5mg in total) - increasingly comatose but PaCO2 fell!

11. 67 yr old male smoker • Transferred to Respiratory Medicine: Day 3 • re-commenced on mask ventilation; increased inspiratory pressure and changed to nasal mask; • other therapy continued; • respiratory rate fell from 40/min to 32/min; • well oxygenated on 4l/min; • gradual improvement; • NIV only at night on day 6, home at day 10;

12. Respiratory Failure & NIV Ken Whyte, Respiratory Physician Greenlane Respiratory Service

13. Oxygen cascade

14. Oxygen Delivery depends on intact cardiorespiratory system Pulmonary failure Heart failure Hypoxia versus Hypoxemia DaO2 = CaO2 x CO SaO2 x Hb x 1.34 SV x HR

15. Oxygen content equation CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2) ie: normal blood carries between 160-220mls per litre e.g. Hb: 150 then CaO2: 200mls/litre Hb: 100 then CaO2: 133mls/litre

18. 63 yr old male: ex-smoker • Known severe lower lobe bronchiectasis +/- CORD (uses inhalers) • Recently returned from living in Australia • Found “in extremis” by daughter – no clear history available • On Exam: • hypotensive and shutdown • Respiratory distress • GCS 12/15 • No wheeze or crackles

19. 63 yr old male: ex-smoker • Cyanosed: SpO2: 73% on air • Respiratory rate 40/min • HR: 140/min, sinus, BP 90/55 • No urine on catheterisation • CXR: extensive bilateral lower lobe change & hyperinflation What test next?

20. Arterial blood gas on admission • PaO2: 6.2kPa (47mmHg) • PaCO2: 11.1kPa (83mmHg) • pH 7.13 • HCO3(-) 25 What type of respiratory failure is this?

21. Types of respiratory failure

22. Respiratory Failure Definitions: Type I Respiratory Failure: PaO2 < 8.0kPa; PaCO2 <6.0kPa Type II Respiratory Failure: PaO2 < 8.0KPa; Pa CO2 > 6.0kPa

24. The Respiratory System Lungs Respiratory pump • Pulmonary Failure • PaO2 • PaCO2 N/ • Ventilatory Failure • PaO2 • PaCO2 Hypoxic Respiratory Failure Hypercapnic Respiratory Failure

25. Types of respiratory failure

26. Arterial blood gas on admission • PaO2: 6.2kPa (47mmHg) • PaCO2: 11.1kPa (83mmHg) • pH 7.13 • HCO3(-) 25 Hypercapnic hypoxic respiratory failure What is his A-aO2 gradient? What other tests would you order based on these results?

27. On Admission

28. Further investigation? • Lactate: 10 mmol/L • Creatinine: 245 • Mixed acidosis: • Renal failure (?dehydration) • Poor tissue oxygenation – lactic acidosis • ?all acute respiratory acidosis or acute on chronic respiratory acidosis? Not possible to determine with certainty but if this was pure acute respiratory acidosis plus metabolic acidosis he should be even more acidotic?

29. On Admission ?starting point

30. Is it important to distinguish? • Essential to have an aim of therapy? • Does he have a normal CO2drive? • If not then ventilating him down to normocapnia will not be wise! • If he is normally hypoxic then restoring normoxia with active therapy may not be wise!

31. Effect of chronic hypercapnia on CO2 drive

32. Ventilatory response to CO2: effect of hypoxia

33. Ventilatory response to hypoxia Raised Pa CO2

34. Is it important to distinguish? • Essential to have an aim of therapy? • Does he have a normal CO2drive? • If not then ventilating him down to normocapnia will not be wise! • If he is normally hypoxic then restoring normoxia with active therapy may not be wise! What is your next step in writing down an action plan in this man?

35. Hypoxia versus hypercapnia

36. What is the mechanism of hypercapnia in airways disease?

37. 50 45 PaCO2 40 35 30 Determinants of PaCO2 PaCO2 = k V’CO2 / V’A CO2output (V’CO2) Alveolar Ventilation (V’A)

38. Determinants of alveolar ventilation Alveolar Ventilation Respiratory muscles Work of breathing Activation Neural drive NM transmission Muscle function Strength Efficiency Loads Elastic Resistive Energy supply Blood flow Arterial O2 Nutrition

39. Acute and acute-on-chronic respiratory failure in COPD Airway infection  expiratory flow limitation • Raw and EL,dyn V’/Q’ inequality  TTOT, TI, and TE  FB  work of breathing  PEEPi  O2 cost of breathing Dynamic hyperinflation Respiratory muscle fatigue  respiratory muscle efficiency Roussos & Koutsoukou ERJ 2003

40. Work of breathing • To maintain a normal V’A and PaCO2, respiratory muscles must maintain a power output (work rate) to overcome respiratory loads. • Work of breathing es in proportion to • V’E • Inspiratory pressure • Inspiratory duration • Inspiratory flow • High work of breathing  • respiratory muscle fiber injury (membrane damage and sarcomere disruption) (Zhu et al. AJRCCM 1997; Orozco-Levi et al. AJRCCM 2001). • fatigue (“reversible weakness”): peripheral or central Tension time index (TTI)

41. END-EXPIRATION NORMAL COPD Airway P = 0 P = +3cmH2O Alveolus Increased elastic loads in COPD • Intrinsic PEEP • >50% of the  in WOB in COPD (Coussa et al. JAP 1993) • Reduced compliance at high lung volumes

42. Respiratory failure in COPD: effect of hyperinflation on resp. muscles Emphysema Healthy •  muscle length • distorted geometry of diaphragm  mechanical disadvantage:  conversion of tension to pressure (Laplace law) and displacement;  action on lower rib cage. •  energy supply during sustained muscle contractions •  predisposition to respiratory muscle fatigue.

43. Consequences of reduced respiratory muscle length in COPD

44. Altering deadspace: work of breathing

45. Respiratory muscle fatigue Diaphragm fatigues at • PI > 60% max at FRC and • PI > 30% max during hyperinflation ( FRC + 50% IC) Diaphragm fatigues at tension time index (TTI) > 0.15 Roussos et al. JAP 1979 Bellemare & Grassino JAP 1982

46. Effect of fatiguing respiratory loads on pattern of breathing • Rapid shallow breathing •  FB, VT, constant or slightly V’E. • May be a behavioural response to  dyspnoea • es load on muscle by •  PI developed and • respiratory muscles work at a more optimal length • may postpone or prevent fatigue. • But inefficient in terms of gas exchange •  VD/VT leading to  PaCO2.

47. Ventilatory failure in COPD/emphysema Alveolar Ventilation  Work of breathing  Resp. muscle reserve Activation Neural drive  NM transmission Muscle function Strength  (steroids, fatigue) Efficiency  (reduced length, mechanical disadvantage) • Elastic  • PEEPi • Hyperinflation • Resistive  Energy supply Blood flow  (sustained forceful contractions) Arterial O2  Nutrition

48. Hypercapnic respiratory failure in COPD: Aims of therapy • Not to restore either “normal” PaO2 or PaCO2: • avoid death by either hypoxia or acute on chronic respiratory acidosis; • Stop the slide into increasing acidosis and support the pump whilst “standard” medical therapy restores the status quo (i.e. chronic respiratory failure); Aim: pH>7.35 and SpO2>88-92% (>85% acceptable?)

49. Treatment of Respiratory Failure • Maximise remaining respiratory function; • Minimise work of breathing; • Monitor closely: Oximetry is not enough! Repeated ABGs are essential!

50. Effect of alveolar ventilation on alveolar gas tensions Lumb 2000