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Management of Severe Obstructive Lung Disease

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1 Management of Severe Obstructive Lung Disease
Craig Rackley, MD Assistant Professor of Medicine Duke University Medical Center

2 Faculty Disclosures None
Faculty notes: Please list on this slide any potential conflicts of interest (COI) you reported to the ACCP when agreeing to speak for this course or any new, previously not disclosed, potential COIs that you have . OR Simply type in “no potential conflicts of interest to disclose.”

3 Objectives Understand the anatomy of COPD
Understand GOLD classification of COPD Understand basic pharmacologic treatment targets and goals Understand when to use non-invasive ventilation for acute exacerbations of COPD/Asthma Understand how to manage a patient with COPD or asthma requiring invasive ventilation

4 Clinical case 69 yo man with a 90 pk-yr smoking history, FEV1/FVC ratio of .48 and an FEV1 of 26% predicted comes in for an initial evaluation in pulmonary clinic.

5 Anatomy of obstructive lung disease

6 Causes of Airflow Obstruction
Increased resistance and narrowing of airways due to Airway smooth muscle hypertrophy and contraction Mucous cell hypertrophy, increased mucous production and impaction Airway inflammation Airway fibrosis External compression from hyper-inflated alveoli

7 Hyperinflation and Air Trapping

8 Treatment goals Decrease resistance and narrowing of airways by reversing Airway smooth muscle hypertrophy and contraction Inhaled beta agonists, anticholinergics, Magnesium, theophylline Mucous cell hypertrophy, mucous production and impaction Inhaled anticholinergics, corticosteroids Airway inflammation Corticosteroids, antibiotics if indicated Airway fibrosis Irreversible External compression from hyper-inflated alveoli Allow for effective exhalation

9 Airway response to therapy

10 What do we use to guide therapy?

11 GOLD classification of severity of airflow limitation in COPD
Global Initiative for Chronic Obstructive Lung Disease

12 Combined Assessment of COPD
FEV1≥50% FEV1<50% Global Initiative for Chronic Obstructive Lung Disease

13 Clinical case cont. He had an FEV1/FVC ratio of .48 and an FEV1 of 26% predicted. He had 2 exacerbations last year, one required hospitalization, and he is short of breath with minimal activity. He is on no medications other than prn albuterol, which he uses 5+ times/day..

14 GOLD recommended first choice therapy
Global Initiative for Chronic Obstructive Lung Disease

15 Clinical case cont. Patient is started on an ICS + LABA and a LAMA with recommendation to use albuterol as needed. He has a walk in clinic that demonstrates he needs 2 LPM oxygen via nasal cannula with exertion, he is given appropriate immunizations, and he is referred to pulmonary rehab.

16 Clinic template Chronic Obstructive Pulmonary Disease:
Based on the Global Initiative for Chronic Obstructive Lung Disease Combined Assessment of COPD, the patient is in risk category: A: FEV1 >/= 50% and </=1 exacerbation/yr and minimal/no symptoms or dyspnea B: FEV1 >/= 50% and </=1 exacerbation/yr and moderate/severe symptoms or dyspnea C: FEV1 <50% or >1 exacerbation/yr and minimal/no symptoms or dyspnea D: FEV1 <50% or >1 exacerbation/yr and moderate/severe symptoms or dyspnea Recommendation: -Tobacco dependence: -No longer smoking. Encouraged continued abstinence. -Currently smoking. Extensively discussed need for smoking cessation. Provided information on Quit Now. Offered nicotine replacement and pharmacotherapy. We will *** -Pulmonary rehab/exercise: -Patient currently in rehab or exercising regularly. Encouraged continued lifelong exercise. -Patient currently not exercising adequately. We discussed options for exercise and pulmonary rehab. We will *** -Oxygen: -Patient has an oxygen sat >/=88% on RA at rest and with walking. Therefore, supplemental oxygen is not indicated. -Patient has an oxygen sat <88% on RA at rest and/or with walking. Therefore, supplemental oxygen is required at *** LPM at rest, *** LPM with sleep, and *** LPM with exertion. -Pharmacotherapy: -GOLD A: Short acting bronchodilator as needed -GOLD B: Long acting bronchodilator -GOLD C: ICS + long acting bronchodilator -GOLD D: ICS + long acting beta agonist and/or long acting anticholinergic

17 Clinical case cont. He does well over the next 6 months until he gets an upper respiratory infection. This leads to significant increase in his shortness of breath and cough. His symptoms progress to where he is so short of breath he calls EMS and is taken to the ED.

18 Clinical case cont. On initial evaluation he has a temp of 38.2 C, HR of 108, BP of 95/60, RR of 26, and O2 sat on RA of 87%. He is alert and oriented, but speaking in 2-3 word sentences. He is using accessory muscles to breath and has very poor air movement. ABG on RA: pH: 7.30 pCO2: 64 pO2: 53

19 When to consider ventilatory support
Evidence of respiratory muscle fatigue (clinical work of breathing, serum lactate) Hypercarbia Respiratory acidosis

20 What is the “best” way to provide ventilatory support?

21 NIV reduces need for intubation in COPD exacerbations
Cochrane Database Syst Rev. 2004;(3):CD

22 NIV reduces mortality in COPD exacerbations
Cochrane Database Syst Rev. 2004;(3):CD

23 NIV for life‐threatening asthma attacks
Diagram showing management of patients experiencing severe attacks of asthma. NIV, non‐invasive ventilation. © IF THIS IMAGE HAS BEEN PROVIDED BY OR IS OWNED BY A THIRD PARTY, AS INDICATED IN THE CAPTION LINE, THEN FURTHER PERMISSION MAY BE NEEDED BEFORE ANY FURTHER USE. PLEASE CONTACT WILEY'S PERMISSIONS DEPARTMENT ON OR USE THE RIGHTSLINK SERVICE BY CLICKING ON THE 'REQUEST PERMISSION' LINK ACCOMPANYING THIS ARTICLE. WILEY OR AUTHOR OWNED IMAGES MAY BE USED FOR NON-COMMERCIAL PURPOSES, SUBJECT TO PROPER CITATION OF THE ARTICLE, AUTHOR, AND PUBLISHER. 18% 4% Respirology May;15(4):

24 NIV for life‐threatening asthma attacks
Diagram showing management of patients experiencing severe attacks of asthma. NIV, non‐invasive ventilation. © IF THIS IMAGE HAS BEEN PROVIDED BY OR IS OWNED BY A THIRD PARTY, AS INDICATED IN THE CAPTION LINE, THEN FURTHER PERMISSION MAY BE NEEDED BEFORE ANY FURTHER USE. PLEASE CONTACT WILEY'S PERMISSIONS DEPARTMENT ON OR USE THE RIGHTSLINK SERVICE BY CLICKING ON THE 'REQUEST PERMISSION' LINK ACCOMPANYING THIS ARTICLE. WILEY OR AUTHOR OWNED IMAGES MAY BE USED FOR NON-COMMERCIAL PURPOSES, SUBJECT TO PROPER CITATION OF THE ARTICLE, AUTHOR, AND PUBLISHER. Respirology May;15(4):

25 How to initiate NPPV Initiate with oronasal facemask. If patients cannot tolerate then consider full face mask. Settings are adjusted to Achieve adequate oxygenation Reduce work of breathing Maintain “adequate” pH Provide tolerable pressure that does not lead to worsened hyperinflation Maximize patient-ventilator synchrony

26 Clinical case cont. ABG on RA: pH: 7.22 pCO2: 74 pO2: 65
The patient is placed on bipap 12/5 and 40% FiO2. His RR decreased to 20 and his work of breathing improved. However, over the next several hours his work of breathing increased, and he became less alert despite adjustments to his bipap settings. A repeat ABG was sent. ABG on RA: pH: 7.22 pCO2: 74 pO2: 65

27 Indications for intubation
Respiratory arrest Altered level of consciousness Extreme exhaustion Inability to adequately ventilate with NPPV

28 After the tube goes in…

29 Success vs failure

30 Remember the problems

31 Remember the problems Normal COPD

32 How to initiate mechanical ventilation
Respiratory rate: adjusted to a rate that allows expiratory flow to reach zero prior to next breath Tidal Volume: approximately 6-8 cc/Kg ideal body weight Inspiratory time(PAC): adjusted to allow for adequate volume and to continue delivering breath with patient effort (i.e. inspiratory flow does not stop while patient is still wanting more air.) Inspiratory flow rate(VAC): adjusted to give adequate flow and allow for adequate exhalation (I:E ratio) PEEP: adjusted to the lowest level needed to ensure patient is able to trigger all breaths Plateau pressure: <30 cm H2O Appropriate level of sedation is key to ensure adequate patient-ventilator synchrony

33 Clinical case cont. He is sedated, paralyzed, and placed on mechanical ventilation: VAC with a Vt of 6 cc/kg, RR of 24, PEEP of 5, and an FiO2 of 40 %. After 20 min his HR is 120, BP is 80/45, and his sat is 90%. You send a stat ABG. ABG: pH: 7.18 pCO2: 82 pO2: 58

34 Our Patient’s Waveforms
Pressure Flow Volume Time

35 Dynamic Hyperinflation
Chest. 2015;147(6):

36 Air Trapping

37 Consequences of hyperinflation or air trapping
Barotrauma/volutrauma Decreased venous return, preload, and cardiac output

38 How to reduce hyperinflation or air trapping
Reduce respiratory rate Reduce tidal volume Increase expiratory time Increase inspiratory flow rate (VAC) Decrease inspiratory time (PAC) Tolerate increased PCO2

39 Clinical case cont. The patient’s RR is decreased to 16. His new settings are VAC with a Vt of 6 cc/kg, RR of 16, PEEP of 5, and an FiO2 of 40 %. After 30 min his HR is 80, BP is 110/65, and his sat is 98%. You send a repeat ABG. ABG: pH: 7.32 pCO2: 56 pO2: 84

40 Our patient after the vent changes
Pressure Flow Volume Time

41 Clinical case cont. He remains stable overnight, so the paralytics are discontinued and his sedation is lightened. When you come back the next morning he is awake, alert, and following commands, but just doesn’t quite look comfortable.

42 Pressure Flow Volume Time

43 Information from an end expiratory pause
“Clamp” circuit PEEPi = 10 Flow (L/s) Airway pressure (cm H2O) Volume (L)

44 Intrinsic PEEP is end expiratory alveolar pressure

45 PEEP can be increased until all patient efforts trigger the ventilator in assisted modes
Hyperinflation will lead to increased Pplat in VAC or reduced tidal volumes with PAC

46 Why not increase extrinsic PEEP to match intrinsic PEEP?

47 Regional effects of positive pressure ventilation in obstructive lung disease
Regional over-distention can lead to worsened V/Q matching, increased dead space ventilation, and increased lung injury.

48 Clinical case cont. His PEEP is increased to 8 cm H2O, and he is successfully triggering all breaths. Over the next 24 hours his sedation is further reduced, and the next morning he passes an SBT, but at the end of 30 min he appears to have a slight increase in his work of breathing. He is alert, cooperative and following all commands. What do you do??

49 NIV decreases extubation failure in COPD
Patients RR for extubation failure 95% CI COPD 0.33 Mixed MICU population 0.66 Diagram showing management of patients experiencing severe attacks of asthma. NIV, non‐invasive ventilation. © IF THIS IMAGE HAS BEEN PROVIDED BY OR IS OWNED BY A THIRD PARTY, AS INDICATED IN THE CAPTION LINE, THEN FURTHER PERMISSION MAY BE NEEDED BEFORE ANY FURTHER USE. PLEASE CONTACT WILEY'S PERMISSIONS DEPARTMENT ON OR USE THE RIGHTSLINK SERVICE BY CLICKING ON THE 'REQUEST PERMISSION' LINK ACCOMPANYING THIS ARTICLE. WILEY OR AUTHOR OWNED IMAGES MAY BE USED FOR NON-COMMERCIAL PURPOSES, SUBJECT TO PROPER CITATION OF THE ARTICLE, AUTHOR, AND PUBLISHER. Heart Lung Mar-Apr;44(2):150-7.

50 Clinical case cont. He is extubated directly to bipap, does well for 6 hours, and is successfully weaned from bipap with improved work of breathing. He transfers out of the ICU the next morning.

51 Summary Airflow obstruction has multiple components that should be adequately treated pharmacologically NPPV reduced mortality and reduces need for intubation in patients with COPD exacerbations Understanding intrinsic PEEP and allowing for adequate exhalation are key to mechanical ventilation in obstructive lung disease Extubation to NIV may reduce risk of re-intubation

52 Questions? PowerPoint tip: End your presentation with a simple question slide to: Invite your audience to ask questions. Provide a visual aid during question period. Avoid ending a presentation abruptly.

53 Information from an end inspiratory pause
Peak and Plateau similar Large difference between Peak and Plateau Flow stops prior to next breath Flow does not reach zero prior to next breath Inhaled volume = exhaled volume Inhaled volume > exhaled volume No obstruction Obstruction


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