COPD Management in the ICU

COPD Management in the ICU December 2, 2011

Disclosures

• I am on the Speaker’s Bureau for the following companies: – Grifols, CSL Behring, Genentech

• There is no conflict of interest as it pertains to

this presentation

Objectives

• Discuss the risks and management of COPD exacerbation

• Review methods to monitor waveforms on the invasive and non-invasive mech ventilator

• Discuss Pneumothorax management • Cryptogenic hemoptysis in COPD

Case Presentation • 57 y/o Caucasian F with COPD/Emphysema phenotype Spirometry: FVC 2.67L, 53% predicted FEV1 0.87L, 24% predicted FEV1/FVC 33 FEF25-75% 0.23L, 7% predicted F/V loops show a severe obstructive defect • Complains of a 2 day worsening of dyspnea, increased sputum

production and thicker consistency. No hemoptysis. Sputum color is green

Case Presentation • Height: 179cm. Weight: 95kg (BMI 29.6kg/m2), Blood pressure

140/93, HR 105, RR 29, Temp 36.8C, SpO2 96% on 2L/min

• LUNGS: Chest wall is symmetrical and equal with respirations. Diminished breath sounds bilaterally bases, noted to have wheezing in the anterior segments, 4 word conversational dyspnea

• CARDIAC: sinus tachy, positive S/S2 without murmur, rub, gallop. No RV heave or thrills, pulses are 3+/regular

Case Presentation

• Current medications for COPD management – Prednisone 20 mg po q day – Advair 250/50 micrograms 1

puff BID (LABA/ICS) – ProAir HFA 90 mcg INH p.r.n. – Nebulizer machine with

albuterol 2.5 mg q.i.d. (SABA)

• He has had 3 exacerbations in the last 12 months

Question

• Individuals who have acute exacerbations of COPD, as compared with individuals with COPD who do not have exacerbations, will have an increased risk of:

a. Rapid decline in lung function b. Reduced quality of life c. Increased risk of death d. All of the above

Definition of COPD

• Chronic obstructive pulmonary disease (COPD) is a disease state characterized by persistent blockage of airflow from the lungs

• The airflow limitation is

usually progressive Underwhelming definition?

Classifying COPD

• Should the classification be based on – Imaging? – FEV1? – Symptoms?

• What are the pulmonary complications related to

COPD that we face in the ICU? – Review gap in knowledge – Practical approach

Classifying COPD

CXR Differences

Emphysema CXR Normal CXR

COPD/Emphysema

Normal CT Chest Upper lobe involvement

COPD/Emphysema

Normal CT Chest Lower lobe involvement

Modified version of Fletcher and Peto’s graph showing the decline in FEV1

Trajectory of a Patient with COPD Which is the most important part?

Symptoms, FEV1, 6 min walk, BODE index

Exacerbations

Exacerbations

Exacerbations Deterioration

End of Life

Donaldson GC, et al. Relationship between exacerbation frequency and lung function decline in chronic obstructive pulmonary disease. Thorax 2002;57:847-852

Time

COPD Exacerbation

• Expiratory flow limitation, as a consequence of airway inflammation, is the pathophysiological hallmark of COPD

O’Donnell DE, Parker CM. COPD Exacerbation. Pathophysiology. Thorax 2006; 61: 354-361

Classification of COPD severity and exacerbations

Severity FEV1 % pred

Mild Stage I ³80

Moderate Stage II 50–80

Severe Stage III 30–50

Very severe Stage IV <30

Hurst JR, et al. Susceptibility to exacerbation in COPD. N Engl J Med 2010;363:1128-1138

COPD complications requiring ICU admission - Acute Exacerbation of COPD - Respiratory Failure (NIV, IV) - Pneumothorax - Hemoptysis

Acute Exacerbation of COPD (AECOPD)

COPD Exacerbation Definition

An acute change in the a patients baseline dyspnea, cough and/or sputum beyond day-to-day variability sufficient to warrant a change in therapy Causes of exacerbations can be both infectious and non-infectious

Worse Prognosis in Frequent Exacerbators

• ≥3 acute exacerbations requiring hospitalisation is associated with a risk of death 4.30 times greater than for those patients not requiring hospitalization

Time (months)

0 10

20

30

40

50

60

0.2

0.4

0.6

0.8

1.0

Prob

abili

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f sur

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p<0.0001

A

B

C p=0.069

p<0.0002

• Group A • Patients with no acute

exacerbations

• Group B • Patients with 1–2 acute

exacerbations of COPD requiring hospital management

• Group C • Patients with ≥3 acute

exacerbations of COPD requiring hospital management

Soler-Cataluña et al. Thorax 2005; 60:925-931

Combined Assessment of COPD Predictions for Exacerbations

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mMRC 0-1 CAT < 10

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Symptoms

Patient is now in one of four categories:

A: Less symptoms, low risk B: More symptoms, low risk C: Less symptoms, high risk D: More symptoms, high risk

Consequences of COPD exacerbation


COPD exacerbations

• Occlusion of the bronchiolar lumen by mucus, cells, thickened/contracted smooth muscle, bronchial wall inflammation and edema

• Leads to: – Increased WOB – Low V/Q ratio – Dynamic hyperinflation

COPD exacerbations

Classification 3-6% of AECOPD patients require hospitalization - Mortality ranges from 3-10% - If the ICU is required, mortality rate approaches

30% in patients older than 65 years

MacIntyre N, Huang YC. Acute exacerbations and respiratory failure in COPD. Proc Am Thor Soc 2008;5:530-535

Messer B, et al. The prognostic variables of mortality in patients with an exacerbation of COPD admitted to the ICU: an integrative review. QJM 2012; 105: 115-126

Mohan A, et al. Clinical presentation and predictors of outcome in patients with severe acute exacerbation of COPD requiring admission to intensive care unit. BMC Pulmonary 2006;6:27

COPD Exacerbation Therapeutic Options

• Supplamental oxygen, goal 88-92% • Bronchodilators

– Aerosolized albuterol – Ipratropium?

• Corticosteroids • Antibiotics • Management of Respiratory Failure

– Non-invasive mechanical ventilation – Invasive Mechanical ventilation

COPD Exacerbation Antibiotics

• Indications – Increased dyspnea, sputum quantity and quality

(purulence) – Mechanical ventilation

• Organisms – Spneumoniae, H Influenza, M catarrhalis

• Risk factors for PsA – Frequent antibiotics – Severe COPD exacerbations – Prior PsA – Recent health care visit

Patients treated in the ICU for AECOPD

Ai-Ping C, et al. Patients treated in the ICU for acute exacerbation of COPD. Chest 2005; 128:518-524

• Median ICU days 3 d • Median hospital stay 9 d • In-hospital mortality 24.5% • Of the survivors who were

discharged – Most required readmission

for exacerbation – Median time to the next

exacerbation: 5 months – Those who required a

second ICU admission had a mortlality rate of 39% at 6 months, 42.7% at 1 year, 61.2% at 3 years

Ai-Ping C, et al. Patients treated in the ICU for acute exacerbation of COPD. Chest 2005; 128:518-524

Respiratory Failure

COPD Exacerbation Respiratory Failure

• Type I: Hypoxemic respiratory failure is characterized by pO2 < 60 mmHg with a normal or low pCO2

• Type II: Hypercapnic respiratory failure is characterized by pCO2 > 50 mmHg (unless having a chronic feature) – Acute form develops within minutes to hours;

therefore, pH <7.3

Non-invasive Mechanical Ventilation

Case Presentation

• You receive a page from the ER. • The patient was placed on BiPAP and feels

”better” • Vent settings are: FiO2 100%, IPAP 8/EPAP 4 • Is there anything else you want to know? • When do you want to check up on her

COPD Exacerbation Non-invasive mechanical ventilation

• Indications – Accessory muscle use, short of respiratory

failure/agonal breathing – Patient cooperative (exclused agitation, belligerent,

coma) – Showing signs of retaining pCO2

• Assess the pCO2 with the respiratory rate, not what a normal value is (pH 7.1-7.3)

• RR> 25

– Hypoxemia; P/F ratio < 200

COPD Exacerbation Contraindications to NIV

• Cardiovascular instability • Inability to protect airway

– Impaired mental status (GCS <8) – Aspiration risks, recent facial surgery or injury – Poor clearance of secretions

• Potential for upper airway obstruction – Angioedema – Extrinsic compression of the trachea (eg. tumor,

hematoma)

Benefits of NIV

• Symptomatic relief of dyspnea • Correction of gas exchange • Improve lung mechanics • Decrease mortality associated with resp failure • Prevent intubation and associated

complications: – Tracheal stenosis, VAP, tracheostomy need, GI

bleed, DVT, mopathy

Benefits of NIV

• Unload respiratory muscle inspiratory cycle: – Hyperinflation >> resp muscle shortening – Decrease compliance of respiratory system

• Overcome intrinsic PEEP • Stent open lower airway expiratory cycle

– Overcome the dynamic airway collapse in the expiratory phase and coughing episodes

• Stent open upper airway – Associated OSA

Non-invasive ventilation for acute exacerbation of COPD INCLUSION CRITERIA COPD with exacerbation of dyspnea > two days and at least two of the following:

RR>30 PaO2 < 45 mm Hg pH < 7.35 after > 10 min on RA

EXCLUSION CRITERIA RR< 12 breaths, sedative drugs within the previous 12 hours CNS disorder unrelated to hypercapnic encephalopathy or hypoxemia Cardiac arrest (within the previous five days) Cardiogenic pulmonary edema Asthma

Brochard et al. NEJM 1995, supportive ventilation RCT

Non-invasive ventilation for acute exacerbation of COPD EXCLUSION CRITERIA • kyphoscoliosis as the cause of chronic respiratory failure • neuromuscular disorder as the cause of chronic

respiratory failure • Upper airway obstruction, facial deformity, tracheotomy • need for immediate intubation = a clear cause of

decompensation requiring specific treatment (e.g., peritonitis, septic shock, AMI)

• pulmonary thromboembolism • pneumothorax, hemoptysis • severe pneumonia • recent surgery or trauma

Non-invasive ventilation for acute exacerbation of COPD

• Primary Outcome: Need for intubation • Secondary outcomes:

– hospital LOS – Complications – Length on mechanical ventilation – In hospital mortality

Non-invasive ventilation for acute exacerbation of COPD • Standard treatment arm

– O2 via nasal canula up to 5L for target SpO2 > 90% – Antibiotics, bronchodilators, iv steroids or

aminophylline

• NIV treatment arm – Standard treatment above + : – BIPAP for at least 6 hours/day, nasal cannula for at

least 2 hours/day – IPAP=20, EPAP=0, flow cycled

Non-invasive ventilation for acute exacerbation of COPD Major Criteria for intubation:

–respiratory arrest, pauses with LOC, gasping, requiring sedation, HR<50 with lethargy, SPB<70

Minor Criteria for intubation: –RR> 35 and > on admission, pH < 7.3 and < admission, PaO2<45 despite O2, worsening MS

One Major Criteria or 2 Minor Criteria after one hour of RX would be indication for intubation. In the NIPPV group if 2 minor criteria met off NIV, they can be placed back on it. But if problem persisted then intubation performed

Non-invasive ventilation for acute exacerbation of COPD

•85 patients total –42 standard rx (ST) group à 31 intubated (74%) –43 NIPPV rx group à 11 intubated (26%) –ARR = 48%, NNT= 2

• Major criteria for intubation met by 10/31 (ST) and 8/11 (NIPPV) • At 1 hour:

–NIPPV group: •improved encephalopathy, rr, PaO2, pH

– Standard group: •worsening enceph, PaCO2, pH

Encephalopathy score 1= mild asterixis, 2= marked asterixis, mild confusion, sleepy during the day 3= major confusion with daytime sleepiness or agitation

Recommended algorithm

Noninvasive ventilation in acute exacerbations of COPD M.W. Elliott, Eur Respir Rev 2005

Rapid Shallow Breathing index

• RBSI = respiratory frequency/Vt

RBSI < 105 (n= 83)

RBSI > 105 (n= 18)

Requiring intubation

26 patients (31%)

10 patients (55%)

In-hospital mortality

7 patients (8.4%)

6 patients (33%)

Berg KM, et al. The rapid shallow breathing index as a predictor of failure on non-invasive ventilation

Invasive Mechanical Ventilation

COPD Exacerbation Invasive mechanical ventilation

• Indications – Accessory muscle use – Showing signs of retaining pCO2

• Assess the pCO2 with the respiratory rate, not what a normal value is

• Does not meet criteria for NIPPV • RR> 35

Case Presentation

• You receive a page from the ER. • The patient was intubated • Vent settings are: FiO2 100%, Vt 500cc, RR 18, PEEP 5

• You are asked, “Is there anything else you need

to know?”

COPD Respiratory Failure Invasive mechanical ventilation

• Mechanical ventilation principles are to balance out airway pressures with gas exchange

• Additional information you need to know are: – PIP, plateau, expiratory Vt, I:E time – waveforms – ABG

COPD Respiratory Failure Invasive mechanical ventilation

• Ventilator mode – Volume ventilation in the AC or SIMV mode – Or pressure ventilation—either PRVC or PC

• Tidal volume and respiratory rate

– Good starting point: 10 ml/kg and 10 to 12 bpm – A small tidal volume (5-8 ml/kg) and 8 to 10 bpm with

increased flow rates to allow adequate expiratory time


• Flow rate – 60 L/min

• I:E ratio – 1:2 or 1:3

• General goals and/or concerns – Air-trapping and auto-PEEP can occur when

expiratory time is too short – ↑ Expiratory time to offset auto-PEEP – May ↑ inspiratory flow up to 100 L/min to ↑ expiratory time – May ↓ VT or rate to ↑ expiratory time – Do not overventilate COPD patients with chronically

high PaCO2 levels


• Vent settings: – Use a slow respiratory rate to reduce the risk of air-

trapping – Auto-PEEP: consider matching extrinsic PEEP if the

patient appears to have difficulty triggering the ventilator

Mechanical Ventilation • Vent settings:

– Mode A/C, PC – FiO2 21%-100% – Vt (6-10cc/kg) or Pressure setting (15-20 cmH2O) – RR (10-30/min) – PEEP 0-24 cmH2O

• Patient monitors:

– Difference between inspiratory and expiratory Vt • leaks

– PIP, Plateau, I:E ratio – Waveforms

Byrd RP, et al. Mechanical Ventilation. Medscape

Airway Pressures Resistance vs. Compliance

• Peak Pressures – Airway resistance AND compliance – Keep below 40-45 cm H2O

• Plateau Pressures (EIP) – Lung and chest wall compliance – Keep below 30 cm H2O

• Normal difference between PIP and plateau

pressure is up to 10 cmH2O

Compliance

• Lung compliance is the ability of the lung to stretch during a change in volume relative to an applied change in pressure

• Compliance is greatest at moderate lung volumes, and much lower at volumes which are very low or very high – LIP and UIP are good guidelines

• Low compliance indicates a stiff lung and extra work may be required to bring it in a normal volume

Trouble Shooting the Ventilator

High Peak Pressures

Low Plateau Pressures

High Peak Pressures

High Plateau Pressures

Mucus Plug ARDS

Bronchospasm Pulmonary Edema

ET tube blockage Pneumothorax

Biting ET tube migration to a single bronchus

Effusion

*** Compliance can also be viewed on the waveforms

Resistance vs. Compliance


Considerations in providing invasive PPV for COPD patients

• Regional over-distention injury applies to COPD

patients just as it does to ARDS patients

• Hence, strategies should be similar to protecting healthy lung units in other forms of respiratory failure

Ventilator Associate Lung Injury (VALI)

Mechanical over-distension or shearing


• The propensity to injury is related partly to the inhomogeneity in distensibility of injured lungs

• The open and thus relatively healthy lung parts will be prone to overinflation, while the injured lung areas will not be inflated

• When this lung is inflated, even with small Vts, air will go preferentially to these open still compliant parts

“tidal overdistension”

These forces include repetitive (cyclic) strain (stretch) from overdistension and interdependence and shear stress to the epithelial cells as lung units collapse and reopen, atelectrauma


Methods of recruitment

• Vt • RR • PEEP • I:E

Problem of this heterogeneity

• Finding the right balance of Vt, RR and PEEP to keep the lungs open without generating high pressure is the goal

• This may be a challenge when these are at a constant setting without a dynamic response to the lungs signals being provided – e.g. waveforms, compliance trends

Upper inflection point

Lower inflection point

Pulmonary Injury

• 2 injury zones during mechanical ventilation use – Low lung volumes

tears adhesive surfaces

– High volumes cause barotrauma


• It is predicted that a transpulmonary pressure of 30 cm H2O could result in shear forces of 140 cm H2O

• Shear forces, the frequency and end-inspiratory overstretching may all place a role in epithelial disruption and loss of barrier function of the alveolar epithelium

Physiology of PEEP Opens up collapsed alveoli and prevents alveolar collapse during exhalation PEEP Decreases alveolar distending pressure Increases FRC by alveolar recruitment Improves ventilation Increases V/Q, improves oxygenation, decreases work of breathing

Over distention

• An increase in airway pressure at the end of inspiration without a significant increase in delivery of tidal volume – ‘beaking’ at the end of inspiration


Lower inflection point

Optimal PEEP • PEEP should be high enough to shift the end-expiratory pressure above the lower inflection point by 2-3 cm H2O (usually 12-15 cm H2O) • Allows maximal alveolar recruitment • Decrease injury by repeated opening and closing of small airways

Intrinsic PEEP/Air trapping

• Determined by – Minute ventilation

(frequency x Vt) – I:E ratio

• To fix it,

– Decrease minute vent (either frequency or Vt)

– Prolong I:E

Complications associated with PEEP

• Barotrauma • Regional hypoperfusion • Paradoxical hypoxemia • Hypercapnea and respiratory acidosis • Diminished cardiac output • Augmentation of ICP • Pulmonary edema

High PEEP • In rats ventilated with PEEP

10 and a peak Pressure 45, no injury was present

• Rats with PEEP 0 and a peak Pressure 45, severe pulmonary edema was present within 20 minutes

• Subsequent study showed a preservation of the structure of the alveolar epithelium by using PEEP 10, which was accompanied by the lack of alveolar flooding

Pneumothorax associated with COPD

Case Presentation

• Your patient had developed a Pneumothorax during the night. A heimlich valve was placed.

• You are told that there was an air leak.

• You ask yourself, the following 2 questions: 1. “Are all air leaks the same?” 2. “Does this impact mortality?”

Pneumothorax in COPD

• Incidence: 4-15% in mechanically vented patients

– Tension PTX more – Mortality rate: 46-77%

• High airway pressures are required to overcome severe bronchial obstruction. However, because of a variability of obstruction in the different airways, there is a mal-distribution of mechanical tidal volume, which promotes gas trapping and non-uniform alveolar distention

Hsu CW, Sun SF. Iatrogenic pneumothorax related to mechanical ventilation. World J Crit Care Med 2014; 3: 8-14


• Defined as a spontaneous secondary PTX – More severe than primary spontaneous PTX – Rapidly progressive – Mortality rate 16%

• Cause of death: sudden death before chest tube insertion, respiratory failure within the first 24 hours, massive gastrointestinal bleeding

• Most COPD patients developing a spontaneous secondary pneumothorax: – Age older than 50 years – FEV1 < 1.0L

Algorithm to PTX related to mech vent

To achieve this goal, ACCP Recommendation for secondary PTX; use a 16 French catheter or larger

Treatment Goals with the Chest Tube 1. Evacuate air from the

pleural space 2. Achieve pleural-pleural

apposition 3. Decrease likelihood of

recurrence • The median time to

resolve air leaks in COPD patient is longer than primary spont PTX – In 20% of COPD patients;

median day is 15 days – 44% recurrence rate

Shen KR, Cerfolio RJ. Decision making in the management of secondary spontaneous pneumothorax In patients with severe emphysema. Thorac Surg Clin 2009; 19:233-238


Cerfolio RJ. Advances in thoracostomy tube management. Surg Clin N Am 2002; 82:833-848

Bullae vs PTX

?

?

Cryptogenic hemoptysis in COPD


• Mild = blood tinged sputum or < 30 cc/24 hours • Moderate = 30-100 cc/24 hours • Severe (massive) = > 100 cc/24 hours


• 39 patients ( 36 men, 3 women) – Average time of COPD dx to hemoptysis: 4.7 + 5.4 yr

• Mean age 51.3 years (24-80) • All patients were active smokers

– Duration 17.2 + 4 years – Mean total 31.7 + 15 packs

• 15 pts (38%) had cardiovascular conditions • 21 pts (54%) had predisposition for bleding

– 5 with thrombocytopenia, 5 with prolonged PTT – 11 taking medications known to cause bleeding

Delage A, et al. cryptogenic hemoptysis in COPD: Characteristics and Outcome. Respiration 2010: 80:387-392


• No difference between CT and bronch to determine the site of bleed

• Arterial embolization succeeded in controlling bleeding in all patients who underwent the procedure

• 34 pts followed for 5 yrs; only 2 had recurrent hemoptysis. None died


Important fact about the lungs • The lungs are heterogeous in nature • Non-physiological ventilation in healthy lungs

induce lung injury

Summary

• Pulmonary complications related to COPD can portend poor outcomes

• The need to identify “responders” to a particular therapeutic intervention is crucial – “Devil is in the detail”

COPD Management in the ICU

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