Mechanical Ventilation in

Obstructive airway Diseases

Dr. Ankur Gupta

• 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.

• 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).

NIV – Inclusion criteria

• Primary diagnosis of COPD exacerbation

(known diagnosis / history and examination

consistent with diagnosis)

- Able to protect airway

- Conscious and cooperative.

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

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.

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.

NIV - MonitoringInclude 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.

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.

NIV - Monitoring

• Synchrony of ventilation should be checked

frequently.

• A clinical assessment of mask fit to include

skin condition and degree of leak.

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.

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.

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.

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).

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.

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.

• 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.

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).

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

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.

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)

Measurement of resistance

and compliance

Mechanical ventilation

• Prepare the machine and the area.

• Check connections.

• Intubate the patient.

• Drugs

– Sedatives, analgesics

– IV fluids and ionotrops / vasopressors

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 collapsibilitydue 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.

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

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.

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.

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.

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.

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.

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 ).

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 ventilatorydemand 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

Thank you