This document discusses mechanical ventilation for patients with obstructive airway diseases like COPD. Some key points: - Non-invasive ventilation (NIV) should be considered within 60 minutes of hospital arrival for COPD patients with respiratory acidosis, as NIV can reduce intubation and mortality rates. - Invasive mechanical ventilation aims to rest respiratory muscles, avoid dynamic hyperinflation, and prevent overventilation. Dynamic hyperinflation can increase work of breathing and compromise cardiac function. - Ventilation strategies differ between asthma and COPD but generally use small tidal volumes, high inspiratory flows, and respiratory rates to minimize hyperinflation. Sedation and analgesia are also important to control distress and pain

1. Mechanical Ventilation in
Obstructive airway Diseases
Dr. Ankur Gupta

2. • Non-invasive ventilation (NIV), both within
ICU and the ward environment, has been
shown in RCTs and systematic reviews
Reduce intubation rate and mortality in COPD
patients with decompensated respiratory
acidosis.

3. • Therefore,it should be considered within the first
60 minutes of hospital arrival, in all patients with
an acute exacerbation of COPD in whom
respiratory acidosis persists despite maximum
standard medical treatment, which includes:
- Controlled oxygen to maintain SaO2 88–92%
- Nebulised Salbutamol 2.5–5 mg
- Nebulised Ipratroprium 500 μg
- Prednisolone 30 mg
- Antibiotic agent (when indicated).

4. NIV – Inclusion criteria
• Primary diagnosis of COPD exacerbation
(known diagnosis / history and examination
consistent with diagnosis)
- Able to protect airway
- Conscious and cooperative.

5. NIV – Exclusion criteria
• Life-threatening hypoxaemia
• Severe co-morbidity
• Confusion/agitation/severe cognitive impairment
• Facial burns/trauma/recent facial or upper airway surgery
• Vomiting
• Fixed upper airway obstruction
• Undrained pneumothorax
• Upper gastrointestinal surgery
• Inability to protect the airway
• Copious respiratory secretions
• Haemodynamically unstable requiring inotropes/pressors
(unless in a critical care unit)
• Patient moribund
• Bowel obstruction

6. NIV – Set - up
• Position - sitting or semi-recumbent position.
• A full-face mask should be used for the first 24
hours, followed by switching to a nasal mask if
preferred by the patient.
• An initial IPAP of 10 cm H2O and EPAP of 4–5
cm H2O should be used.
• IPAP should be increased by 2–5 cm increments,
at a rate of approximately 5 cm H2O every 10
minutes, with a usual pressure target of 20 cm
H2O or until a therapeutic response is achieved or
patient tolerability has been reached.

7. NIV – Set - up
• Oxygen, when required, should be entrained into
the circuit and the flow adjusted to achieve the
target saturation, usually 88–92%.
• Bronchodilators, although preferably
administered off NIV, should as necessary be
entrained between the expiration port and face
mask.

8. NIV - Monitoring
Include a mixture of physiological measures and
clinical parameters
1) Baseline observations:
– arterial blood gas (ABG)
– respiratory rate
– heart rate
2) Continuous pulse oximetry and electrocardiogram
(ECG) recording during the first 12 hours.
3) Repeat ABGs:
– After 1 hour of NIV therapy and 1 hour after
every subsequent change in settings.
– After 4 hours, or earlier in patients who are not
improving clinically.

9. NIV - Monitoring
4) Frequent clinical monitoring of acutely ill patients:
– Every 15 minutes in the first hour.
– Every 30 minutes in the 1- to 4-hour period.
– Hourly in the 4- to 12-hour period.
5) Observations including:
– Respiratory rate, heart rate.
– Level of consciousness, patient comfort.
– Chest wall movement, ventilator synchrony,
accessory muscle use.

10. NIV - Monitoring
• Synchrony of ventilation should be checked
frequently.
• A clinical assessment of mask fit to include
skin condition and degree of leak.

11. NIV - Duration of treatment
• Patients who benefit from NIV during the first 4 hours of
treatment should receive NIV for as long as possible (a
minimum of 6 hours) during the first 24 hours.
• Treatment should last until the acute cause has resolved,
commonly after about 3 days.
• In patients in whom NIV is successful (pH 7.35 achieved,
resolution of underlying cause and symptoms, respiratory rate
normalised) following the first 24 hours or longer, it is
appropriate to start a weaning plan:
• Gradual reduction of the duration of NIV should be
determined by clinical improvement
• The use of a proforma to chart physiological indices has
been shown to improve successful weaning from NIV.

12. NIV - Weaning
• Initially weaning should be during the day
with extended periods off the ventilator for
meals, physiotherapy, nebulised therapy etc.
• After successfully weaning during the day,
many patients will require an additional night
on NIV.
• The weaning strategy should be documented in
the medical and nursing records.

13. NIV - Weaning
• The following is recommended
- Continue NIV for 16 hours on day 2
- Continue NIV for 12 hours on day 3 including 6–
8 hours overnight use
- Discontinue NIV on day 4, unless continuation is
clinically indicated.
• Note that some patients may:
- Show at an earlier stage that they no longer
require NIV and self-wean
- Improve rapidly, prompting a clinical decision to
wean early
- Require long-term nocturnal support, indicated
following assessment by the respiratory team.

14. NIV - Escalation
• A management plan in the event of NIV failure
should be made at the outset.
• A decision to intubate should normally be
made within 4 hours of starting NIV or sooner.
Improvements in RR, HR and ABG parameters
are usually apparent within this time.
• Intubation rather than further NIV should be
considered in patients suffering 'late failure'
(defined as failure after 48 hours of NIV).

15. Mechanical ventilation
The three main goals of invasive mechanical
ventilation in patients who have acutely
exacerbated COPD or acute severe asthma are
to:
• rest the ventilatory muscles;
• avoid further dynamic hyperinflation;
• avoid overventilation and acute alkalemia.

16. Pathophysiologic Features Relevant
to Ventilator Support
• Deterioration of Respiratory Mechanics
–Increased Inspiratory Airway Resistance .
–Increased Expiratory Airway Resistance -
damage to the elastic scaffold
dynamic narrowing of the small airways.
–Dynamic Hyperinflation and Intrinsic
Positive End-Expiratory Pressure.

17. • Deterioration of Respiratory Muscle Function
–Respiratory Muscle Weakness.
–Respiratory Muscle Fatigue
• Deterioration of Gas Exchange- Abnormal
distribution of ventilation–perfusion ratios and
decreased mixed venous oxygen tension are
common causes of hypoxemia during
exacerbations.

18. Dynamic hyperinflation and iPEEP
• Dynamic hyperinflation: In the presence of
increased expiratory airflow resistance the
time available (expiratory time) to empty the
inspired volume may not be sufficient. The
next inspiration may start before the
completion of the expiration leading to air
trapping.
• The DHI results in positive alveolar pressure at
the end of expiration also referred to as auto-
PEEP (intrinsic PEEP).

19. auto-PEEP has many disadvantages:
• Increased work of breathing (WOB)
• Respiratory muscles, in particular the
diaphragm work at a considerable mechanical
disadvantage.
• Excessive PEEP can compromise cardiac
function.
• Predispose patients to barotrauma –
Pneumothorax, pneumomediastinum

22. In general, adapting the following measures can
reduce auto-PEEP:
• Provide the longest expiratory phase that is
possible.
• Reduce patient ventilatory demand and minute
ventilation.
• Reduce airflow resistance by bronchodilators
and steroids.

23. Measurement of resistance
and compliance
• Rapidly occluding the expiratory port at the
end of inspiration produces a rapid fall in peak
pressure and after 3–5 seconds the pressures at
the ventilator and alveoli equilibrates at which
point the pressure curve plateaus off.
• Peak pressure – plateau pressure (Pplat) = total
resistance of the respiratory tract.
Compliance = Tidal Volume/(Pplat – total PEEP)

24. Measurement of resistance
and compliance

25. Mechanical ventilation
• Prepare the machine and the area.
• Check connections.
• Intubate the patient.
• Drugs
– Sedatives, analgesics
– IV fluids and ionotrops / vasopressors

26. Lung Mechanics: Difference Between Asthma
and COPD
• Acute changes in lung mechanics from severe
bronchospasm due to asthma attacks are similar to
those in COPD exacerbations. However, the
pathophysiology of asthma differs substantially
from that of COPD.
• Advanced COPD - increased airway collapsibility
due to destruction of the lung parenchyma and
loss of lung elastic recoil
• Severe asthma – increased thickness of airway
walls (due to inflammation) and decreased
collapsibility, despite considerable reduction in
airway caliber.

27. Ventilation Strategy - Asthma
• Relatively small VT and higher inspiratory flow,
to preserve expiratory time and minimize
hyperinflation, barotrauma, and hypotension.
• Objective can be achieved with -
– an inspiratory flow of 80 –100 L/min,
– VT of 6 –10 mL/kg,
– Peak airway pressure 40 – 45 cm H2O,
– Alveolar plateau pressure not higher than 25–30 cm
H2O.
– Respiratory rate 8 –12 breaths/min, to achieve the least
possible hyperinflation

28. Ventilation Strategy - COPD
• Strategies are similar to those for asthma, but
patients with COPD often have less structural
airflow obstruction than patients with asthma.
• In most cases, patients can be rested adequately
with
– VT of 9 –10 mL/kg
– respiratory rate of 14 –16 breaths/min in
assisted/control mode.
• In both COPD and asthma, ventilator-trigger
sensitivity should be minimal.

29. Which MODE ?
• It is unknown whether one ventilator mode is superior
to another in patients with COPD
• In sedated patients, ACV and PCV over PSV is
preferred because Sedation can decrease respiratory
motor output and thus promote alveolar
hypoventilation.
• When using ACV inspiratory flow waveform may be
set in the square pattern to facilitate monitoring of
mechanics.
• Avoid controlled mechanical ventilation because it is
associated with the early development of respiratory
muscle atrophy and damage.

30. Sedation and Analgesia
• Sedation needs, vary widely in mechanically
ventilated patients, due to-
1) Anxiety is one of the most common indications
for sedation.
2) Dyspnea is common in ventilated patients and
may be a source of distress requiring sedation.
3) Amnesia is often cited as an indication for
sedation.

33. Analgesia
• Inadequate control of pain is unfortunately a
memory patients may have after ICU
management.
• Pain may cause many adverse effects, including
increased endogenous catecholamine activity,
myocardial ischemia, hypercoagulability,
hypermetabolic states, sleep deprivation, anxiety,
and delirium. Treating pain diminishes some of
these detrimental effects.

35. Weaning
• When to begin weaning is mostly dependent
on physician’s clinical judgment
• Weaning should begin once the cause of the
exacerbation is adequately treated and the
patient is hemodynamically stable
• PSV has not been shown to be superior to
SBT.

36. Weaning
• Physiologic parameters which can help in
predicting the patient’s ability to sustain
spontaneous ventilation are
– minute ventilation ( ≤ 15 L ),
– respiratory rate ( ≤ 30 ),
– Tidal volume (≥ 325 ml ),
– dynamic compliance ( ≥22 ), static compliance ( ≥
33 ),
– rapid shallow breathing index ( ≤ 105 ),
– maximum inspiratory pressure ( ≤–15 ).

37. Key points on ventilatory techniques
• The fundamental physiologic abnormality is worsening of
expiratory airflow limitation and consequent dynamic
hyperinflation.
• To reduce the DHI and auto-PEEP provide the longest
expiratory phase that is possible, reduce patient ventilatory
demand and minute ventilation and reduce airflow
resistance by bronchodilators and steroids.
• The minute volume should be adjusted to pH and not to the
PaCO2
• Keep the plateau pressure less than 30 cm water to
minimize barotrauma.
• Frequently monitor ventilatory waveforms and use
ventilatory maneuvers to check for DHI and auto-PEEP

38. Thank you