asthma and its ventilation management

1. NIV
Asthma
.
Critical Care Seminar
Nigussie S.
January 2019
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2. NIV
People say life can not exist without air, but it does under
water, in fact it started in the sea.
---Richard Feynman
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3. Introduction
 Non-invasive ventilation (NIV) is A method of providing ventilatory
support for respiratory failure without the need for tracheal intubation.
TYPE I : Hypoxemic Respiratory Failure is characterized by a
PaO2 < 60 mmHg with a normal or low PaCO2.
 type 2: Hypercapnia respiratory failure is characterized by a
PaCO2 of > 50 mmHg
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4. HOW DOES NIV WORK?
 Reduction in inspiratory muscle work and avoidance of respiratory muscle
fatigue
• Augments tidal volume
• Improves compliance by reversing microatelectasis
• Overcome intrinsic PEEP
• Enhanced cardiovascular function (afterload reduction)
• Stent the airway
• Reduce CO2 production

5. NIV FOR HYPOXEMIC RESPIRATORY
FAILURE
 Increased FIO2
• PEEP
• Alveolar recruitment
• Increased V/Q
• Decreased Shunt
• Increased FRC
• Decreased RR and WOB

6. NIV FOR HYPERCAPNIC RESPIRATORY FAILURE
 Offsets auto-PEEP
• Reduce airway resistance
• Improve VT, VE, PaCO2

7. Advantage of NIV
Symptomatic relief of
dyspnea
Correction of gas
exchange
Improve lung mechanics
Facilitate sleep
Correct mental status
Pre-oxygenate for
intubation
Prevent ETI
Avoid complications of ETI
 VAP
 Sepsis/shock
 Tracheostomy
 GI bleed/DVT
Decrease mortality associated with respiratory
failure
Use NIV in the place of IMV

8. Disadvantage of NIV
 System
• Slower correction of gas exchange abnormalities
• Time commitment/attention
• Gastric distention
• Interface
• Leaks
• Skin necrosis/rash
• Eye/ear irritation
• Sinus pressure
• Airway
• Aspiration
• Limited secretion clearance

9. Suitable Clinical Conditions for NIV
Most patients with :
COPD/Cardiogenic pulmonary edema
Selected patients with :
CAP + COPD
Asthma / CF
Decompensated OSA/ cor pulmonale
ARDS
Immunocompromised state / mild PCP
Neuromuscular respiratory failure
Post extubation COPD / post –op respiratory failure

10. C/I to the use of NIV
 Non-compliant patient
 unconscious patient / unable to protect airway.
 facial fractures-
 Excessive secretions—risk of aspiration
 Following oesophagectomy (risk of anastomatic breakdown
due to increased pharyngeal/oesophageal/intracranial
pressures)
 Haemodynamic instability –hypotension
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11. Complications
Kelly, C et al. NEJM 2015; 372: e30

12. The Different Modes of NIV
 methods Includes :
– continuous positive airway pressure (CPAP)
– bi-level positive airway pressure (BiPAP),
– pressure support ventilation (PSV) and
– non-invasive intermittent positive-pressure ventilation (NIPPV)
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13. Protocol for Non Invasive Ventilation
Procedure for patient setup
 Explain to the patient what you are doing and what to
expect
 Keep the head of the patient's bed at >45 degree
angle
 Choose the correct interface
 Turn on the ventilator and dial in the settings

14.  Hold the mask gently over the patient's face until the patient
becomes comfortable with it. Strap the face mask on using the
rubber head strap and minimize air leak without discomfort.
 Connect humidification system.
 Monitor- respiratory rate, heart rate, level of dyspnoea, O2
saturation, blood pressure, minute ventilation, exhaled tidal volume,
abdominal distension and ABG
Protocol for Non Invasive Ventilation
Procedure for patient setup

15. CPAP
 The provision of positive airway pressure throughout all
phases of spontaneous ventilation.
– · This increases the FRC of the lungs by holding airways open
and preventing collapse.
– The application of CPAP also causes the patient to breathe at
higher lung volumes, making the lungs more compliant.
– CPAP is particularly useful for improving oxygenation in type
1 respiratory failure.
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16. CPAP
 CPAP by nasal mask provides pneumatic splint which holds the upper
airway open in patients with nocturnal hypoxemia due to episodes of
obstructive sleep apnea.
 CPAP reduces left ventricular transmural pressure therefore increases
cardiac output. Thus it is effective for treatment of pulmonary edema.
 Pressures are usually limited to 5-12 cm of H2O, since higher pressure
tends to result in gastric distension requiring continual aspiration through
nasogastric tube

17. Bi-level positive airway pressure (BiPAP)
 BiPAP Achieves ventilation by cycling the PAW b/n high and low values in
synchrony with the patient’s own breathing. results in reduced work of
breathing and an improvement in VT and CO2 removal;
 particularly useful in the treatment of type 2 respiratory failure.
 Inspiratory positive airway pressure (IPAP): pressure on inspiration to increase tidal volume size. This
will ensure sufficient removal of carbon dioxide. This inspiratory support also helps to alleviate the
sensation of breathlessness
 Expiratory positive airway pressure (EPAP): splints airways open during expiration to overcome
obstruction/ airway collapse. Maintaining a positive pressure in the airways at the end of expiration
will improve the compliance of the alveoli, making expansion during inspiration easier.
 Pressure Support: the difference between the IPAP and EPAP. It is the amount of ‘help’ which the
ventilator will give on inspiration
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18. Initial Ventilatory Settings
 Initial ventilator setting should be IPAP of 10 cm H2O, and EPAP of 5 cmH2O
 Increase EPAP by 1-2 cm increments till the patient triggers the ventilator in
all his inspiratory efforts.
 Increase IPAP in small increments, keeping it 5cmH2O above EPAP, to a
maximum pressure, which the patient can tolerate without discomfort and
major leaks.
 Titrate pressure to achieve a respiratory rate of <25 breaths/min and Vt
>7ml/kg
 Increase FiO2 to improve O2 saturation to 92%

19. PSV

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PSV Non-invasive PSV can be administered with standard critical care
ventilator or bilevel portable devices.
PSV mode has unique ability to vary inspiratory time breath by
breath, permitting close matching with the patient's spontaneous
breathing pattern
Drawbacks of PSV:
(a) Patient-ventilator asynchrony in COPD patients having rapid
respiratory rate and exacerbation of asynchrony in presence of air
leaks.
(b) Breathing discomfort as inspiratory force is required to trigger the
ventilator.

20. How to monitor the patient’s response to NIV?
– The most useful indicator is how the patient feels.
– They should be able to tell you if they feel better or worse.
– Where available ABG are useful to assess changes in
oxygenation and CO2 clearance.
– Physiologic response-If the patient is getting increasingly
tired, or their ABG deteriorating despite optimal settings,-
needs intubation
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21. Acute severe Asthma
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22. Introduction
 Asthma is an episodic disease with acute exacerbations
interposed with symptom-free periods
 it is a disease of predominantly reversible airway obstruction
characterized by a triad of
– bronchial smooth muscle constriction-insp/exp. wheeze
– airway inflammation, and
– increased secretions.
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23. Pathophysiology of life threatening asthma
 gas trapping with dynamic hyperinflation and the generation of
intrinsic (PEEPi).
 Disproportionate increases in resistance to expiratory gas flow, rapid
RR
 changes in pulmonary elastic recoil, and asynchronous respiratory
muscle activity
– Impaired gas exchange reduced Co2 elimination
– Increased work of breathing.
– V/Q mismatch
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24. What define a severe acute attack?
Status asthmaticus: is defined as life-threatening
bronchospasm that persists despite treatment
 Disturbance in level of consciousness
 Inability to speak and/or feed
 Severely diminished or absent breath sounds
 Central cyanosis.
 Use of accessory muscles while breathing.
 Increased respiratory and cardiac rate
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25.  Non-invasive objective measures, which aid in the assessment of the
patient with acute asthma include:
– peak expiratory flow rate (PEFR)
– pulse oximetry
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What define a severe acute attack?...

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27. Management of life-threatening asthma
 A rapid ABC assessment
– Many patients will be hypoxaemic, hypovolaemic, acidotic, and hypokalemic.
 Controller’ treatment
– Aims on preventing and controlling bronchial inflammation
– inhaled and systemic corticosteroids, theophylline, and antileukotrienes
 Reliever’ treatment
– Rescue agents for acute bronchospasm
– Short-acting β-adrenergic agonists, Intravenous magnesium sulphate, Epinephrine‘ and
Anticholinergic drugs
• Oxygen support
– High FIO2 (≥0.60) to maintain SpO2≥95%.
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29. Mechanical ventilation
Indications for mechanical ventilation
Absolute indications
– coma, respiratory or cardiac arrest and severe refractory hypoxaemia
Relative indications
– adverse response to initial management-fatigue-cardiovascular
compromise, and the development of a pneumothorax.
In life-threatening asthma, the induction of anaesthesia, tracheal
intubation, and initial ventilation are all extremely hazardous
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30. Technique of intubation and ventilation
 RSI with diligent preoxygenation “breathing down” with IAAs –if
possible
 Preloading and consider vasopressor
 care should be taken to avoid excess air trapping, high airway pressures
and high tidal volumes.
– consideration disconnection of ETT and with the addition of
pressure on the chest wall to assist expiratory flow when
development of profound hypotension
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31. What are the initial goals of MV and how are
they achieved?
 to correct hypoxaemia, reduce dynamic hyperinflation and to buy
time for medical management to work.
– Adequate sedation is vital with fentanyl, and midazolam/propofol
with ketamine.
– Initial ventilator settings should adopt relatively low rates(5-10bpm) ,
VT of 4–8 ml /kg and Fio2 of to maintain saturations > 92%
– relatively long expiratory times (I:E 1:4) and little or no PEEP (5 cm
H2O).
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32.  If using VCV appropriate goals would be to
– achieve a P plat <35 cm H2O with pH > 7.2.
– Plateau airway and end-expiratory pressures generally
reflect the degree of gas trapping in severe asthma
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What are the initial goals of MV and how are they
achieved?

33. Maintenance of ventilatory management
 The use of neuromuscular blockade and deep sedation should be avoided
– Administer muscle relaxants for a minimum 2–4h, until severe
bronchospasm has subsided and gas exchange improved.
– Volatile inhalational anaesthetic---to maintain
 Adequate rehydration
 Generous humidification and Physiotherapy to loosen mucus plugs
 Normalize ventilator setting
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34. Weaning
 Bronchospasm may increase on lightening sedation due to awareness of
endotracheal tube and increased coughing.
 May need trial of extubation while still on high FIO2
 Consider extubation under inhalational or short-acting IV sedation.
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35. References
 Global Strategy for the Diagnosis, Management, and
Prevention of COPD Updated 2017
 e-SAFE –Safe Anaesthesia From Education
 Simon Wharton & Roslyn Purcell Respiratory support
.Critical Care Journal
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