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
Deterioration
Exacerbations

End of Life
Time

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

1.0 • Group A
• Patients with no acute
exacerbations
Probability of surviving

0.8
A
p<0.0002 • Group B
0.6
• Patients with 1–2 acute
B p<0.0001
exacerbations of COPD
0.4 requiring hospital management
p=0.069
C
0.2 • Group C
• Patients with ≥3 acute
exacerbations of COPD
0 1 2 3 4 5 6 requiring hospital management
0 0 0 0 0 0
Time (months)

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

 Combined Assessment of COPD
Predictions for Exacerbations
(GOLD Classification of Airflow Limitation)

Patient is now in one of

four categories:

(Exacerbation history)
(C) (D) >2
A: Less symptoms, low risk

Risk
Risk

B: More symptoms, low risk

(A) (B) <2 C: Less symptoms, high risk

D: More symptoms, high risk

mMRC 0-1 mMRC > 2
CAT < 10 CAT > 10

Symptoms
Consequences of COPD exacerbation

O’Donnell DE, Parker CM. COPD Exacerbation. Pathophysiology. Thorax 2006; 61: 354-361
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
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 RBSI > 105

(n= 83) (n= 18)

Requiring 26 patients 10 patients

intubation (31%) (55%)

In-hospital 7 patients 6 patients

mortality (8.4%) (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
COPD Exacerbation
Invasive mechanical ventilation
• 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
COPD Exacerbation
Invasive mechanical ventilation

• 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 High Peak Pressures

Low Plateau 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

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

Byrd RP, et al. Mechanical Ventilation. Medscape

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
 Ventilator Associate Lung Injury (VALI)

• 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 “tidal overdistension”
preferentially to these open
still compliant parts
Ventilator Associate Lung Injury (VALI)

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

Byrd RP, et al. Mechanical Ventilation. Medscape
Byrd RP, et al. Mechanical Ventilation. Medscape
Pulmonary Injury
• 2 injury zones during
mechanical ventilation
use
– Low lung volumes
tears adhesive
surfaces
– High volumes cause
barotrauma
Upper inflection point
• 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
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)
Upper inflection point
• Allows maximal alveolar
recruitment

• Decrease injury by repeated

opening and closing of small
Lower inflection point
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
Pneumothorax in COPD

• 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
 Pneumothorax in COPD

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

?
Cryptogenic hemoptysis in COPD
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
 Cryptogenic hemoptysis in COPD
• 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
 Cryptogenic hemoptysis in COPD

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