Transcript Management of Obstructive Lung Disease

MANAGEMENT OF SEVERE OBSTRUCTIVE
LUNG DISEASE
Craig Rackley, MD
Assistant Professor of Medicine
Duke University Medical Center
Faculty Disclosures
•None
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
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.
Anatomy of obstructive lung disease
www.nhlbi.nih.gov
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
Hyperinflation and Air Trapping
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
Airway response to therapy
What do we use to guide therapy?
GOLD classification of severity of
airflow limitation in COPD
Global Initiative for Chronic Obstructive Lung Disease
FEV1≥50%
FEV1<50%
Combined Assessment of COPD
Global Initiative for Chronic Obstructive Lung Disease
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..
GOLD recommended first choice therapy
Global Initiative for Chronic Obstructive Lung Disease
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.
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 1-800Quit 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
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.
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
When to consider ventilatory support
• Evidence of respiratory muscle fatigue
(clinical work of breathing, serum lactate)
• Hypercarbia
• Respiratory acidosis
What is the “best” way to provide
ventilatory support?
or
NIV reduces need for intubation in
COPD exacerbations
Cochrane Database Syst Rev. 2004;(3):CD004104.
NIV reduces mortality in COPD
exacerbations
Cochrane Database Syst Rev. 2004;(3):CD004104.
NIV for life‐threatening asthma attacks
18%
Respirology. 2010 May;15(4):714-20.
4%
NIV for life‐threatening asthma attacks
Respirology. 2010 May;15(4):714-20.
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
Clinical case cont.
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
Indications for intubation
•
•
•
•
Respiratory arrest
Altered level of consciousness
Extreme exhaustion
Inability to adequately ventilate with
NPPV
After the tube goes in…
Success vs failure
Remember the problems
Remember the problems
Normal
COPD
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
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
Our Patient’s Waveforms
Pressure
Flow
Volume
Time
Dynamic Hyperinflation
Chest. 2015;147(6):1671-1680.
Air Trapping
Consequences of hyperinflation or air
trapping
• Barotrauma/volutrauma
• Decreased venous return, preload, and cardiac
output
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
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
Our patient after the vent changes
Pressure
Flow
Volume
Time
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.
Pressure
Flow
Volume
Time
Information from an end expiratory pause
Flow (L/s)
Volume (L)
Airway pressure (cm H2O)
PEEPi = 10
“Clamp” circuit
Intrinsic PEEP is end expiratory
alveolar pressure
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
Why not increase extrinsic PEEP to match
intrinsic PEEP?
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.
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??
NIV decreases extubation failure in COPD
Patients
RR for extubation failure
95% CI
COPD
0.33
0.16-0.69
Mixed MICU population
0.66
0.25-1.73
Heart Lung. 2015 Mar-Apr;44(2):150-7.
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.
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 reintubation
Questions?
Information from an end inspiratory pause
Peak and Plateau
similar
No obstruction
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
Obstruction