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COPD Management in the ICU

December 2, 2011
Disclosures
I am on the Speakers 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 Petos 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

ODonnell DE, Parker CM. COPD Exacerbation. Pathophysiology. Thorax 2006; 61: 354-361
Classification of COPD severity and
exacerbations

Severity FEV1 % pred

Mild Stage I 80

Moderate Stage II 5080

Severe Stage III 3050

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 12 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-Catalua 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

ODonnell 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 31
intubated (74%)
43 NIPPV rx group 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 ventilationeither 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


ODonnell 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

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