Ventilatory management in obstructive airway diseases

Ventilatory Management of
Obstructive Airway Diseases
DR. VITRAG SHAH
SECOND YEAR FNB RESIDENT,
DEPARTMENT OF CCEM,
SGRH, DELHI
MODERATOR
DR.VINOD SINGH
dr.vitrag@gmail.com -
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Obstructive airway diseases
• COPD
• Asthma
• Bronchiectasis
• Bronchiolitis
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Outline
• Respiratory physiology
• Respiratory mechanics in COPD
• DHI & AutoPEEP
• Ventilatory goal & strategy
• Indication & Contraindication of NIV
• NIV setup & optimizing NIV
• Indication of IMV
• Ventilator settings & it’s implications
• Weaning
• PSV, NAVA & PAV
• Approach to Patient-ventilator asynchrony
• Extubation
• Role of ECCO2R & Heliox
• Prognosis
• Key points
• References
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Respiratory Physiology
• In normal subjects, in the absence of respiratory effort,
the lung will come to lie at the point of the functional
residual capacity (FRC) or relaxation volume (Vrel). The
point at which this occurs is determined by a balance
between the inward elastic recoil of the lung and the
equal and opposite outward recoil of the respiratory
cage (mostly due to muscle tone). The intrapleural
pressure (Ppl) at this point is –3 to –5 cm water. To
generate a respiratory movement two factors must be
overcome:
Resistance
Compliance
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Resistance
• Resistance of the airways is described as
obstruction to airflow provided by the
conducting airways, resulting mainly from the
larger airways
• Airway resistance to flow is present during
both inspiration and expiration and the energy
required to overcome it represents the actual
work of breathing (WOB)
• R = PPeak – PPlat/Inspiratory Flow (L/sec)
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Compliance
• In a clinical setting, this refers to the combined
compliance of the lung and chest wall. It is the
volume change per unit pressure change.
• When compliance is low, more effort is
required to inflate the lungs. Compliance also
varies depending on the degree of inflation,
which is usually a sigmoid shaped curve in
normal subjects
• C = TV / (Pplat – PEEP)
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Respiratory mechanics in COPD
Airway
Obstruction
Resistance
Dynamic
Hyperinflation
Work Of
Breathing
Expiratory
Flow
Limitation
Intrinsic PEEP
COPD
Exacerbation
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DHI
V/Q Mismatch WOB* Barotrauma
Cardiac
Impaired
function
Decreased
venous return
Decreased LV
compliance
Increased RV
afterload
*In presence of DHI the lungs are operating at a higher than normal FRC. This
causes the inspiratory muscles to operate at shorter than normal lengths &
operates on flatter part of compliance curve.
*Diaphragm is lower in the chest wall during hyperinflation its ability to descend
further during inspiration is impaired.
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Airway resistance & DHI
• Expiratory flow limitation due to
– Peripheral airway narrowing due to mucosal swelling
– Peribronchial inflammation
– Loss of attachments which keep small airways open
via radial traction (Not in Asthma)
– Positive intrapleural pressure which further
compresses the airways
• This leads to prolonged expiration, increase in
FRC, dynamic hyperinflation which increases with
each breath and lead to intrinsic PEEP.
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DHI without airflow limitation
• Rapid respiratory rate
• High tidal volume
• Inspiratory time more than expiratory time
• Small bore endotracheal and ventilatory tubes
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Diagnosis of DHI
1. Slow filling of manual ventilator bag
2. Capnography trace not reaching plateau
3. Expiratory flow not reaching zero in
flow-time/volume graph
4. Measure intrinsic PEEP (PEEPi)
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AutoPEEP Mechanisms
1. Hyperinflation with dynamic airway collapse
(DAC) – e.g. COPD
2. Hyperinflation without DAC – e.g. Severe
Asthma exacerbation
3. Contraction of expiratory muscle which
increases Palv above Patm – e.g. During exercise
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AutoPEEP measurement
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Occult AutoPEEP
• Standard AutoPEEP measurement doesn’t
reflect pressure in lung areas behind
obstructed airways at end-expiration.
• Occult AutoPEEP is suspected when low
measured AutoPEEP but high Plateau pressure
& evidence of hyperinflation on Chest X-Ray.
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Ventilatory Goal
• Treatment principle is to support gas exchange and correct
lung mechanics
• Ventilatory Goal :
- To improve gas exchange
- Reduce dynamic hyperinflation
- Increase Expiratory Time , Increase Inspiratory Flow rate
- Decrease MV (TV, RR)
- Application of PEEP (Not in Asthma)
- Treat bronchospasm
- Rest to the respiratory muscles & decrease WOB
- Better patient ventilator synchrony
- Prevention of barotrauma
- Minimizing cardiovascular effects
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Ventilatory Strategy
• NIPPV is the first choice
• Assist control ventilation
• Target pH, not pCO2
• Optimize respiratory mechanics
• Optimum sedation
• Early weaning
• Extubation with NIPPV
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Mechanism of benefit in NIV
• Applied EPAP offsets PEEPi resulting from
expiratory airflow obstruction.
• IPAP augments tidal volume for any given
respiratory effort leading to unloading of
respiratory muscles, decreased WOB,
decreased RR, and improvements in alveolar
ventilation which improves gas exchange
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0
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Indication of NIV
• Patients with pH between 7.30 and 7.25
• Non-responders to medical therapy having PaO2 <50
mmHg, PaCO2 >80–90 mmHg, pH ≤7.2, with following:
 Sick but not moribund
 Able to protect airway
 Conscious and cooperative
 Haemodynamically stable
 No excessive respiratory secretions
 Few co-morbidities
• Patients who have declined intubation
• As a weaning facilitator & shorten IMV duration
• Post extubation respiratory failure
• Domiciliary NPPV for patients with recurrent
admissions. dr.vitrag@gmail.com -
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RECOMMENDED ALGORITHM
Noninvasive ventilation in acute exacerbations of COPD
M.W. Elliott, Eur Respir Rev 2005
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NIV Initiation
• S/T mode is most commonly used in BiPAP. Pressure
targeted mode are preffered, it also compensate for leak.
• Patient might be started on NIV with an IPAP of 15, this
should be progressively increased to reach an IPAP of 20–
30 within 10–30 min, the need for higher pressure and a
more rapid escalation being indicated by patient size and
more severe acidosis, respectively.
• In the presence of persisting hypoxaemia, that is thought
unrelated to sputum retention, the EPAP may need to be
increased in an attempt to recruit areas of poorly
ventilated lung. (It may also be appropriate if there is a
degree of upper airway obstruction).
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Optimizing NIV delivery
• Leak should always be minimised by mask
adjustment and/or by changing the mask type
• Head flexion is avoided, particularly in sleep.
• Patient–ventilator asynchrony may be caused by
mask leak, insufficient or excessive IPAP,
inappropriate setting of Ti or Te, high levels of
intrinsic PEEP or excessively sensitive triggers.
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Supplemental oxygen therapy with NIV
• The flow rate of supplemental oxygen may need
to be increased when ventilatory pressure is
increased to maintain the same SaO2 target.
• Mask leak and delayed triggering may be caused
by oxygen flow rates >4 L/min, which risks
promoting or exacerbating patient-ventilator
asynchrony.
• A ventilator with an integral oxygen blender is
recommended if oxygen at 4 L/min fails to
maintain SaO2 >88%.
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Humidification with NIV
• Humidification is not routinely required
• Heated humidification should be considered if
the patient reports mucosal dryness or if
respiratory secretions are thick and tenacious.
• HME increase dead space, resistance to
airflow & WOB, so can increase burden on
respiratory muscles and lead to failed
weaning.
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Sedation with NIV
• If intubation is not intended in NIV failure,
then sedation/anxiolysis is indicated for
symptom control in the distressed or agitated
patient
• In the agitated/distressed and/or tachypnoeic
individual on NIV, intravenous morphine 2.5–5
mg (± benzodiazepine) may provide symptom
relief and may improve tolerance of NIV.
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Duration of NIV in COPD
• Time on NIV should be maximised in the first
24 h depending on patient tolerance and/or
complications.
• NIV use during the day can be tapered in the
following 2–3 days, depending on pCO2 self-
ventilating, before being discontinued
overnight.
• NIV can be discontinued when there has been
normalisation of pH and pCO2 and a general
improvement in the patient’s condition
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Predictor of NIV failure
• Glasgow Coma Score <11
• Acute physiology and chronic health evaluation (APACHE) II
score ≥29,
• Respiratory rate ≥30
• pH <7.25
• After two hours of NIV, a pH <7.25 further increased the
likelihood of need for intubation from 70 to 90 percent
• A bedside scoring system, BAP-65 (elevated BUN, altered
mental status, pulse >109 beats/min, age >65 years), that
uses signs of respiratory distress, along with other risk
factors, has been found to predict the need for mechanical
ventilation in patients with acute exacerbations of COPD
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Indication of IMV
*pH<7.25 has been suggested as a level below which IMV should be considered and <7.15
as the level that IMV is indicated (following initial resuscitation and use of controlled
oxygen).
 These patients should be intubated based on the severity of respiratory distress rather
than any absolute value of PaCO2 or RR followed by 24 h of full ventilatory support to
rest the fatigued respiratory muscles.dr.vitrag@gmail.com -
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Intubation
• Anaesthesia can be provided using ketamine, propofol
or fentanyl with midazolam. Before induction, fluid
status has to be optimised in these patients as
haemodynamic collapse can occur due to increased DH
and PEEPi.
• If a patient becomes hypotensive after intubation that
is not responding to fluid, ventilator can be
disconnected and if the BP improves, a manual squeeze
of the thoracic cage can be performed to reduce DH
which can be appreciated on SpO2 tracings as huge
respiratory swings
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Ventilator initiation
• Ventilation should be adjusted based on the
degree of DH and Auto-PEEP and not PaCO2.
• There are only three factors that determine
auto-PEEP: (1) Minute ventilation, (2) I: E ratio &
expiratory time constants, (3) Expiratory flow
• Of these, minute ventilation is the most
important factor which causes DH. Hence, when
ventilating patients with COPD, a smaller VT, slow
RR, high peak flow should be used with an aim to
target normal pH and not PaCO2
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Initial settings
Mode ACV TV 6-8 ml/kg
RR 10-15
Target MV 115 ml/kg
I:E ratio 1:2-1:4
Flow 60-100 L/min
Square wave form
(Constant flow)
PEEP 50-80% of iPEEP
(Zero in Asthma)
<10- 12
FiO2 : To target SpO2
88-92%,
(>96% in Asthma)
PaO2 >60mmhg
Target pH : 7.2-7.4
Ppeak <40-45
Pplt <30
In PSV - Trigger
Flow (Preffered): 2L
Pressure : -1 to -2cm
Cycling : >35%
Controlled modes should be used as briefly as possible to avoid disuse atrophy of
respiratory muscles and unnecessary prolongation of the period of mechanical ventilation.
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Respiratory Rate
• During ACV, as a general rule, the VR is often set four breaths per
minute less than the RR (eg, VR is set at 16 when the patient's RR is
20 breaths per minute). However, the patient should be monitored
closely because a particularly high respiratory rate will decrease the
expiratory time. This can worsen dynamic hyperinflation and result
in inverse ratio ventilation, which is not desirable in COPD.
• During SIMV, the initial VR is typically set to ensure at least 80
percent of the patient's total minute ventilation (RR multiplied by
tidal volume) is delivered by the ventilator. For example, if the
patient's minute ventilation is recorded by the ventilator at 10
L/min with a set tidal volume of 0.4 L, then the rate would be set at
20 breaths per minute (20 x 0.4 = 8 L).
• The target rate is frequently adjusted to target a total minute
ventilation (tidal volume multiplied by rate) of 115 mL/kg.
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Measures to reduce DHI & AutoPEEP
• Reduce ventilatory demand and minute
ventilation (TV & RR), Optimum sedation and
analgesia
• Prolonged expiratory time
• Increase inspiratory flow rate
• Apply Extrinsic PEEP
• Adjust trigger sensitivity
• Reduce airflow resistance by bronchodilators and
steroids
Deep sedation should be used when required and N-M blockers should be avoided
as this patients are prone to difficult weaning and it contributes to CIN/CIMdr.vitrag@gmail.com -
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Expiratory time
• It is important to note that recent research
suggests that there is a plateau in expiratory
flow after a certain point, so increasing the
expiratory time above a certain value has
limited benefit. In general, after about 4
seconds of expiration there is nominal gain in
reducing hyperinflation.
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PEEP
Benefits of PEEP:
1. Decrease inspiratory threshold, so less WOB
2. Stenting collapsible airways, so increasing expiratory flow rates
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PEEP
• In contrast to COPD patients, applying PEEP during total
ventilatory support of a patient who has DH with fixed
airflow obstruction due to severe asthma and without
airway collapse may produce potentially dangerous
increases in lung volume, airway pressure and intrathoracic
pressure, causing circulatory compromise.
• Although some clinical studies have reported improved
airway function (without untoward effects) with continuous
positive airway pressure or with NIV and PEEP among
patients with acute asthma, the use of PEEP during total
ventilatory support of a patient with acute asthma is
controversial.
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Waterfall over dam concept in COPD
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When to wean
• Cause of exacerbation treated
• Hemodynamically stable
• Absense of major organ failure
• Optimum acid base & electrolyte balance
• MV <15 L
• RR <30
• TV >325ml
• Dynamic compliance >22
• Static compliance >33
• RSBI <105
• MIP > -15
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Daily SBT
<100
Mechanical Ventilation
RR > 35/min
Spo2 < 90%
HR > 140/min
Sustained 20% increase in HR
SBP > 180 mm Hg, DBP > 90 mm Hg
Anxiety
Diaphoresis
30-120 min
PaO2/FiO2 ≥ 200 mm Hg
PEEP ≤ 5 cm H2O
Intact airway reflexes
No need for continuous infusions of vasopressors or inotrops
RSBI
Extubation*
No
> 100
Rest 24 hrs
Yes
Stable Support Strategy
Assisted/PSV
24 hours
Low level CPAP (5 cm H2O),
Low levels of pressure support (5 to 7 cm H2O)
“T-piece” breathing
*If good sensorium, cough and swallowing presentdr.vitrag@gmail.com -
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Weaning
• Inability to wean is invariably associated with a worse
prognosis and prolonged ventilation.
• Marginal respiratory mechanics and continued presence
of auto-PEEP make weaning difficult in COPD patients.
• Factors that increase resistance such as size, secretions,
kinking of the tube and the presence of elbow-shaped
parts or a HME in the circuit have to be optimised to
promote early weaning.
• Patients of cor pulmonale may require small dose of
inotrope, diuretics and low fluid strategy during
weaning
• Role of tracheostomy is uncertain, but due to marginal
respiratory mechanics, it is also expected to help in
weaning
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Weaning Mode
• PSV, PAV, NAVA, Extubation f/b NIPPV
• Pressure support ventilation is the most common
mode used in weaning
• Key determinants of PSV
 Triggering of the ventilator
 Pressurization slope and
inspiratory flow,
 Level of PS
 Cycling
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Trigger
• Flow rather than pressure trigger preffered as it reduce
the incidence of asynchrony & WOB.
• Main determinants affecting workload associated with
triggering are :
– Magnitude of change required (Optimized by increasing
sensitivity & setting PEEP)
– Delay between onset of inspiratory effort & ventilator
response (Optimized by NAVA)
• During NIV, leak can cause autotrigger and asynchrony
• Highest possible sensitivity should be set, without
auto-triggering
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Rise time / Slope
• During PS, the slope of pressurization, that is, the
incremental increase in Paw per time unit, can be
adjusted on most ventilators . The steeper the
slope, the faster Paw will rise to its target value.
The steeper the slope the lower the WOB.
• But comfort is lowest at both the lowest and
highest pressurization rates.
• >100ms and, if a patient exhibits discomfort, to
increase the time up to 200 ms.
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Level of PS
• Avoid both insufficient support leading to
increased respiratory muscle load and excessive
support bearing the risk of worsening dynamic
hyperinflation and PEEPi by insufflation of high
tidal volume in obstructive patients
• A high level of PS can worsen the delayed cycling
phenomenon & increase in leak
• Empirically, PS can be titrated on the expiratory
tidal volume (approximately 8 to 10 ml/kg, the
lowest value being preferred in NIV) and the
patient’s respiratory rate, which should remain
below 30/minute.
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Cycling
• The transition from inspiration to expiration,
known as cycling, occurs when instantaneous
inspiratory flow (V′insp) decreases to a
predetermined fraction of peak inspiratory flow
(V′insp/V′peak), often referred to as an
‘expiratory trigger’ (ET)
• Delayed cycling has been shown to occur mostly
in patients with obstructive airways disease
• On many ventilators, the cutoff value of ET is pre-
determined, usually at a default setting of 0.25
• Higher the ET, decrease magnitude of delayed
cycling & better synchrony.
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Consequences of delayed cycling
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PAV & NAVA
• Both modes are designed to reduce patient effort
in response to changes in ventilatory demand.
• PAV generates respiratory support as a
proportion of the total pressure needed to inflate
the respiratory system.
• During PAV, the total pressure needed to inflate
the respiratory system is obtained by automatic
and repeated calculations of resistance and
compliance via short end-inspiratory occlusions.
This is why leaks impede proper PAV functioning.
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NAVA
• When NAVA is used, the inspiratory trigger does
not depend on airway flow detection; rather, gas
delivery starts when electrical activity in the
diaphragm is detected.
• The inspiration ends at a predetermined
percentage of peak EMG activity: 70% of the peak
if EADi values are higher than 1.5 μV. If EADi is
lower than 1.5 μV, then the inspiration ends at a
40% of the peak.
• Unlike PAV, the trigger mechanism in NAVA is not
affected by leaks or PEEPi.
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PAV & NAVA : Conclusion
• NAVA improved patient–ventilator synchrony
by reducing triggering and cycling delays in
comparison to PSV. In any case, despite the
theoretical promise of PAV and NAVA, data
published to date are insufficient to claim that
either mode is superior to conventional
modes such as PSV in terms of major clinical
outcomes (i.e., duration of MV, length of ICU
stay).
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NIV in Weaning
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Extubation
• Successful extubation is defined as the
absence of the need for ventilatory support
for 48 h.
• Patients receiving post-extubation NIV (see
below) are classified as ‘weaning in progress’.
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Role of ECCO2R
1. If, despite attempts to optimise IMV using
lung protective strategies, severe
hypercapnic acidosis (pH<7.15) persists
2. When ‘lung protective ventilation’ is needed
but hypercapnia is contraindicated, for
example, in patients with coexistent brain
injury (Grade D)
3. For IMV patients awaiting a lung transplant
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Role of Helium/Oxygen
• The percentage of oxygen in heliox should be at least
20% to prevent hypoxia, and no more than 40% for
heliox to show clinically significant effect
• As airway turbulence is dependent on density, heliox
having a lower density decreases the airway resistance
and, therefore, the WOB particularly in situations
associated with upper airway obstruction.
• Due to conflicting literature, Heliox should not be used
routinely in the management of AHRF (Grade B).
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Prognosis
• The mortality of patients with COPD who are
mechanically ventilated for acute respiratory
failure is high (37 to 64 percent). Factors that
portend a poor prognosis in this population
include failure to respond to noninvasive
ventilation, the presence of multiorgan failure
and the presence of virulent pathogens such
as Pseudomonas and Aspergillus species
cultured from airway secretions.
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Key points
• The overall goals of treatment should be to provide adequate gas
exchange while minimizing hyperinflation , unload respiratory load
and administering aggressive therapy to reduce airway
inflammation and bronchoconstriction.
• Primary cause of respiratory failure should be treated.
• NPPV is regarded as the first line of treatment while invasive
ventilation is reserved for life-threatening respiratory failure.
• The ventilatory graphics (flow, pressure and volume) of the most of
the modern ventilators becomes a valuable tool & assist in early
diagnosis and management of the patient’s condition before it
becomes clinically overt.
• MV should be adjusted to pH , not pCO2.
• Weaning from MV is typically difficult in these patients, and factors
amenable to pharmacological correction (such as increased
bronchial resistance, tracheobronchial infections, and heart failure)
are to be systematically searched and treated.
• In selected patients, early use of NIV may hasten the whole process
of weaning. dr.vitrag@gmail.com -
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1. Davidson AC, Banham S, Elliott M, et al. Thorax 2016;71:ii1–ii35 - BTS/ICS
guideline for the ventilatory management of acute hypercapnic respiratory failure
in adults
2. Ahmed SM, Athar M. Mechanical ventilation in patients with chronic obstructive
pulmonary disease and bronchial asthma. Indian J Anaesth 2015;59:589-98
3. Jolliet, Philippe, and Didier Tassaux. "Clinical review: patient-ventilator interaction
in chronic obstructive pulmonary disease." Critical Care 10.6 (2006): 1-6.
4. Parrilla, Francisco José, et al. "Ventilatory strategies in obstructive lung disease."
Seminars in respiratory and critical care medicine. Vol. 35. No. 4. 2014.
5. Reddy, Raghu M., and Kalpalatha K. Guntupalli. "Review of ventilatory techniques
to optimize mechanical ventilation in acute exacerbation of chronic obstructive
pulmonary disease." International journal of chronic obstructive pulmonary
disease 2.4 (2007): 441
6. Medoff, Benjamin D. "Invasive and noninvasive ventilation in patients with
asthma." Respiratory care 53.6 (2008): 740-750
7. Gilman B Allen, MD et al “Invasive mechanical ventilation in acute respiratory
failure complicating chronic obstructive pulmonary disease” UpToDatedr.vitrag@gmail.com -
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Ventilatory management in obstructive airway diseases

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