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1 Obrigada por ver esta apresentação Lembramos que esta apresentação é propriedade do autor É-lhe proporcionada pela Associação Portuguesa de Sono no contexto da Lufada 2016, para seu uso pessoal, tal como submetido pelo autor 2016 pelo autor

2 Noninvasive Ventilation Bringing Science to Clinical Care Teofilo Lee-Chiong MD Professor of Medicine National Jewish Health Professor of Medicine University of Colorado Chief Medical Liaison Philips Respironics

3 Disclosure Research funding: Philips Respironics Consulting: Elsevier, CareCore National Chief Medical Liaison: Philips Respironics Royalties: Oxford, Lippincott, Elsevier, Wiley, CreateSpace I will not be discussing off-label uses

4 Learning Objectives 1. Identify the causes of hypoventilation 2. Understand the mechanisms responsible for hypoventilation syndromes 3. Learn how to manage persons with hypoventilation syndromes and sleep disordered breathing

5 70, M, snoring and EDS Lifelong smoker, COPD Morbidly obese with OHS On opiates for chronic back pain

6 Overnight Oximetry Courtesy Jim Parish, MD

7 Upper airway closure Hypoventilation Hypoxia

8 Hypoventilation

9 Episodic nocturnal hypercapnia

10 Berger KI et al. Semin Respir CCM 2009

11 Berger KI et al. Semin Respir CCM 2009

12 Berger KI et al. Semin Respir CCM 2009

13 Episodic nocturnal hypercapnia Inadequate compensation (i.e., CO 2 unloading) during periods of ventilation

14 Pathophysiology VQ abnormalities Reduced chemosensitivity Altered lung mechanics Factors that can impair CO 2 elimination Suppression of respiratory drive leptin resistance

15 Lean mouse ob/ob mouse + Leptin - Leptin

16 Mokhlesi B. Respir Care 2009.

17 Episodic nocturnal hypercapnia Inadequate compensation (i.e., CO 2 unloading) during periods of ventilation Abnormal ventilatory control causes hypercapnia to persist into wakefulness

18 Elevation of bicarbonate due to chronic hypercapnia Blunts degree of acidosis from hypercapnia Reduces compensatory CO 2 ventilatory response

19 Berger KI et al. Semin Respir CCM 2009

20 Episodic nocturnal hypercapnia Inadequate compensation (i.e., CO 2 unloading) during periods of ventilation Abnormal ventilatory control causes hypercapnia to persist into wakefulness

21 Sleep-Related Hypoventilation In adults: PaCO 2, PetCO 2 or PtcCO 2 Exceeds 55 mmhg for 10 minutes, or Rises 10 mmhg above awake supine level to a value > 50 mmhg for 10 minutes during sleep

22 Sleep Related Hypoventilation Primary Idiopathic Central Alveolar Hypoventilation Congenital Central Alveolar Hypoventilation Syndrome Late-Onset with Hypothalamic Dysfunction Secondary Due to a Medication or Substance Due to a Medical Disorder Obesity Hypoventilation Syndrome

23 Demographics of OHS Population Reference Bariatric surgery px 8% Chau EHL. Anesthesiology 2012; 117: Hospitalized adult patients with a BMI> 35 kg/m2 31% Nowbar S. Am J Med 2004; 116:1-7. Patients with OSA 9% Akashiba T. Intern Med. 2006;45(20): Known OSA 11% Chau EHL. Anesthesiology 2012; 117: OSA px before CPAP tx 11% Laaban JP, et al. Chest Mar;127(3): OHS might be missed if CO 2 levels are not measured during PSG

24 42% of obese persons with OSA met criteria for OHS, and an elevated serum bicarbonate was a useful diagnostic feature. Bicarbonate threshold level of 27 mmol/l for the diagnosis of OHS Sensitivity of 76.6% Specificity of 74.6% Positive predictive value of 54.5% Negative predictive value of 88.9% Nadir SaO 2 threshold of < 80% for the diagnosis of OHS Sensitivity of 82.8% Specificity of 54.5% Positive predictive value of 56.9% Negative predictive value of 81.4% Clinical predictors of obesity hypoventilation syndrome in obese subjects with obstructive sleep apnea. Bingol Z, Pihtili A, Cagatay P, Okumus G, Kiyan E. Respir Care Jan 13.

25 Mokhlesi B. Respir Care 2009.

26 OHS Survival After Hospitalization Nowbar et al. Am J Med. 2004

27 Mokhlesi B. Respir Care 2009.

28 Upper airway closure Hypoventilation Hypoxia

29 Upper airway obstruction CPAP/EPAP Hypoventilation PS/Rate Volume Hypoxia EPAP/PS/Rate Volume

30 Pressure control Volume control

31 Pressure control CPAP Volume control

32 Pressure control CPAP BPAP S BPAP ST BPAP T Volume control

33 First generation CPAP / EPAP Manual Pressure support Manual Rate Manual

34 Sample setting EPAP 4 cmh2o IPAP 8 Rate 8-10 bpm PS = 4

35 Increase PS for low tidal volume, low SaO 2 or high PCO minutes 5-10 minutes BPAP 8/4 PS = 4 BPAP 10/4 PS = 6 BPAP 12/4 PS = 8

36 Change mode for hypoventilation 5-10 minutes 5-10 minutes BPAP 8/4 BPAP 8/4 BPAP 8/4 S mode S-T mode T mode

37 BPAP S Trilogy100 Clinical Manual 6/11/10

38 BIPAP ST Trilogy100 Clinical Manual 6/11/10

39 Pressure control CPAP BPAP S BPAP ST APC BPAP T Volume control

40 APC Trilogy100 Clinical Manual 6/11/10

41 BIPAP T Trilogy100 Clinical Manual 6/11/10

42 Pressure control CPAP BPAP S BPAP ST APC BPAP T VAPS Volume control

43 Second generation CPAP / EPAP Manual Pressure support Automated Rate Manual

44 Volume-assured pressure support Automatically adjusts PS between IPAPmin and IPAPmax To maintain target tidal volume

45 Sample setting EPAP 4 cmh2o IPAPmin 8 IPAPmax 25 Rate Tidal volume 8-10 bpm Formula; adjust to patient comfort to allow sleep onset PS = 4-21

46 Starting tidal volume Ideal body weight 8 ml/kg Patient comfort As suggested by physician

47 EPAP IPAP Tidal volume

48 During the night If upper airway closure persists Increase EPAP and IPAPmin (maintain PS) If hypoventilation persists Increase PS (IPAPmax) Increase rate If hypoxia persists Increase EPAP Increase PS Add O2

49 Pressure control CPAP BPAP S BPAP ST APC BPAP T VAPS VAPS-AE Volume control

50 Third generation CPAP / EPAP Automated Pressure support Automated Rate Automated

51 EPAP UA resistance IPAP Tidal volume

52 RR RR

53 RR Back-up rate

54 Pressure control CPAP BPAP S BPAP ST APC BPAP T VAPS VAPS-AE PC-SIMV Volume control

55 PC - SIMV Trilogy100 Clinical Manual 6/11/10

56 Pressure control Volume control CPAP BPAP S BPAP ST APC ACV BPAP T VAPS PC-SIMV

57 ACV Trilogy100 Clinical Manual 6/11/10

58 Pressure control Volume control CPAP BPAP S BPAP ST APC ACV BPAP T CV VAPS PC-SIMV

59 CV Trilogy100 Clinical Manual 6/11/10

60 Pressure control Volume control CPAP BPAP S BPAP ST APC ACV BPAP T CV VAPS PC-SIMV SIMV

61 SIMV Trilogy100 Clinical Manual 6/11/10

62 Pressure control Volume control CPAP BPAP S BPAP ST APC ACV BPAP T CV VAPS PC-SIMV SIMV

63 Trigger Features

64 Trilogy100 Clinical Manual 6/11/10

65 Trigger Features Automatic, volume, shape

66 Shape Trigger Trilogy100 Clinical Manual 6/11/10

67 Trigger Cycle Features Automatic, volume, shape

68 Trilogy100 Clinical Manual 6/11/10

69 Trigger Cycle Features Automatic, volume, shape Shape, flow reversal, maximum IPAP

70 Trigger Cycle Comfort Features Automatic, volume, shape Shape, flow reversal, maximum IPAP Flex, ramp, rise time, flow pattern

71 Ramp Trilogy100 Clinical Manual 6/11/10

72 Rise Time Trilogy100 Clinical Manual 6/11/10

73 Trigger Cycle Comfort Adaptability Features Automatic, volume, shape Shape, flow reversal, maximum IPAP Flex, ramp, rise time, flow pattern Dual prescription, sigh

74 Sigh Trilogy100 Clinical Manual 6/11/10

75 Trigger Cycle Comfort Adaptability Safety Features Automatic, volume, shape Shape, flow reversal, maximum IPAP Flex, ramp, rise time, flow pattern Dual prescription, sigh Alarms

76 Improvement in PCO 2 10 patients with OHS, failed CPAP Storre JH et al. CHEST 2006

77 Initial NIV increased and initial invasive mechanical ventilation decreased for COPD exacerbations over a 10-year period ( ) in the U.S. Any form of mechanical ventilation Annual change Increased by 4.4% 14.1% 20.3% Initial NIV Increased by 15.1% 5.9% 14.8% Initial IMV Declined by 3.2% 8.7% 5.9% Retrospective cohort study of 723,560 hospitalizations for exacerbation of COPD at 475 hospitals between 2001 and 2011; IMV: invasive mechanical ventilation Trends in mechanical ventilation among patients hospitalized with acute exacerbations of COPD in the United States, 2001 to Stefan MS, Shieh MS, Pekow PS, Hill N, Rothberg MB, Lindenauer PK. Chest Apr 1;147(4):

78 Significant declines in morality, length of stay and mechanical ventilation during hospital admissions for COPD exacerbation were seen from In-hospital all-cause mortality Mechanical ventilation % 4.7% 4.5% 4.2% P < % 5.7% 5.3% 5.4% P < NPPV 2.3% 2.9% 3.3% 3.5% P < Average hospital LOS (days) P < ,060,565 hospitalizations in patients with COPD exacerbation from : NPPV: noninvasive positive pressure ventilation; LOS: length of stay Trends in in-hospital outcomes among adults hospitalized with exacerbation of chronic obstructive pulmonary disease. Lima FV, Yen TY, Patel JK. COPD Aug 11.

79 In patients hospitalized for exacerbation of COPD, NIV was associated with comparable 30-day all-cause and COPD-specific readmission compared to IMV. NIV vs. IMV Odds ratio Lower risk of mortality 0.54 [95% CI, ] Lower risk of hospital-acquired pneumonia 0.53 [95% CI, ] Lower costs 0.68 [95% CI, ] Shorter length of stay 0.81 [95% CI, ] No difference in 30-day all-cause readmission 1.04 [95% CI, ] No difference in COPD-specific readmission 1.05 [95% CI, ] *25,628 patients hospitalized for COPD exacerbation; 17,978 patients were initially treated with NIV; IMV: invasive mechanical ventilation Outcomes associated with invasive and noninvasive ventilation among patients hospitalized with exacerbations of chronic obstructive pulmonary disease. Lindenauer PK, Stefan MS, Shieh MS, Pekow PS, Rothberg MB, Hill NS. JAMA Intern Med Oct 27.

80 Patients with acute COPD exacerbation initially treated with NIV had a 41% lower risk of death vs. treatment with IMV. Hospital mortality Treated with noninvasive ventilation - 7.4% Treated with invasive mechanical ventilation % Failed noninvasive ventilation % 3,520 patients; 27.7% received NIV and 45.5% received IMV; retrospective cohort study; NIV: noninvasive ventilation; IMV: invasive mechanical ventilation; NIV failure was recorded in 13.7% Comparative effectiveness of noninvasive and invasive ventilation in critically ill patients with acute exacerbation of chronic obstructive pulmonary disease. Stefan MS, Nathanson BH, Higgins TL, Steingrub JS, Lagu T, Rothberg MB, Lindenauer PK. Crit Care Med Jul;43(7):

81 Multicenter randomized controlled trial demonstrated that long-term NPPV targeted to reduce hypercapnia improved survival in patients with severe hypercapnic COPD. Mortality at 1-year NPPV group 12% Control group 33% Hazard ratio 0.24 (95% CI ; P = ); NPPV: non-invasive positive pressure ventilation; 195 subjects (102 given NPPV and 93 controls) with stable COPD (GOLD stage IV) and PaCO mmhg Non-invasive positive pressure ventilation for the treatment of severe stable chronic obstructive pulmonary disease: a prospective, multicentre, randomised, controlled clinical trial. Köhnlein T, Windisch W, Köhler D, Drabik A, Geiseler J, Hartl S, Karg O, Laier-Groeneveld G, Nava S, Schönhofer B, Schucher B, Wegscheider K, Criée CP, Welte T. Lancet Respir Med Jul 24.

82 A multifaceted therapeutic intervention, including use of AVAPS- AE, reduced hospital readmissions in COPD patients who had previously required frequent rehospitalizations. Year prior to initiation of intervention 100% Proportion of patients who were readmitted on two or more occasions Year of intervention 2.2% 397 patients; χ2 = 758; P < Retrospective assessment of home ventilation to reduce rehospitalization in chronic obstructive pulmonary disease. Coughlin S, Liang WE, Parthasarathy S. J Clin Sleep Med Jan 28.

83 Triple threat COPD OSA OHS Triple challenges UA obstruction Hypoventilation Hypoxia Triple solutions 1 st gen 2 nd gen 3 rd gen

84 Questions