Mechanical ventilation of asthmatic patient is really challenging that needs a planned strategy.

1. DR.MOHAMED ABOSAMAK
Lecturer of anesthesia and ICU
Consultant of critical care medicine in SFH

2.  You are called to review a 29-year-old male with
confirmed asthma in the Emergency Department.
He has been unwell for 2 days with increasing
cough, wheeze and shortness of breath.

3.  Humidified oxygen titrated to SpO2 90-92%
 Nebulised beta-agonist bronchodilators
 Nebulised anticholinergic drugs
 Steroids: IV hydrocortisone or oral prednisone
First-tier therapies with strong supporting evidence
Second-tier therapies with weak supporting evidence
Intravenous beta-agonist bronchodilators for refractory bronchospasm
Methylxanthines
Nebulised adrenaline
Magnesium sulfate
Helium-oxygen mixture
Third-tier therapies without any supporting evidence
Ketamine
Volatile anaesthetics
ECMO in asthma

4.  Humidified oxygen titrated to SpO2 90-92%
 Hyperoxia is harmful in asthmatics

5. BiPAP
The patient tired

6. Application of extrinsic PEEP minimises this
difference and reduces WOB. IPAP reduces the
WOB associated with resistance.

7. Things which increase intrinsic PEEP are things which
 Impair elastic recoil
Emphysema
 Increase expiratory resistance
Bronchospasm
Airway collapse at the equal-pressure point (where intrathoracic pressure
equals intrabronchial pressure)

8. Markers of deterioration of asthmatic patient
Rising carbon dioxide levels (including
normalization in a previously hypocapnic
patient).
Exhaustion.
 Mental status depression.
 Haemodynamic instability .
 Refractory hypoxaemia

9. Half of the life-threatening complications occur at or around the
time of intubation

10. Soon after intubation
Before intubation

11. Disconnect the endotracheal tube from the
ventilator circuit.
In asthmatics, this may be life-saving. If the cause is dynamic hyperinflation (‘gas
trapping’) blood pressure will rise over 10-30 seconds as the gas is released.

12.  Dynamic hyperinflation (gas-trapping) due to
excessive ventilation — especially in the patient with
bronchospasm.
 Hypovolemia exacerbated by decreased venous
return due to positive intrathoracic pressure.
 Vasodilation and myocardial depression due to the
induction drugs used for rapid sequence intubation
(e.g. thiopentone, propofol).
 Tension pneumothorax due to positive-pressure
ventilation.

13.  Movement of the chest during ventilation —is it
absent or is movement only on one side? Is the chest
hyper-expanded?
 Arterial saturation (SpO2) and PaO2 —obtain an ABG
sample
 Skin colour of the patient (is he turning blue or
pinking up?) —the SpO2 monitor lags behind the true
oxygen saturation of the patient.
 Hemodynamic stability.

14. •Dynamic hyperinflation.
— Hypotension
— Barotrauma and pneumothoraces
— PEA arrest due to dynamic hyperinflation.
•Aggravation of bronchospasm.
•Risk of myopathy from the combination of corticosteroids
and neuromuscular blockade required to facilitate
mechanical ventilation.

15. Absolute indications for intubation of a patient with
severe asthma are:
•Cardiac or respiratory arrest
•Severe hypoxia (e.g. hypoxic seizure)
•Deteriorating level of consciousness
Relative indications for intubation are:
•Patient fatigue
•Hypercapnea
Use the largest tube possible.

16. Correct hypoxaemia.
Reduce dynamic hyperinflation and to buy time for
medical treatment.
Decrease work of breathing.

17. There is no clear evidence for the superiority of one ventilation
mode over another (i.e. volume-controlled versus pressure-
controlled).
Initial ventilator settings (volume-controlled ventilation):
Tidal volume 6-8 mL/kg
Respiratory rate LOW 8-10/min
Inspiratory flow rate (80-100L/min) to allow longer expiratory times
PEEP 0 cmH2O (some experts like a bit of PEEP)
FiO2 Titrated to keep SaO2 >93%
With I:E ratio 1:3 or 1:4
Reset the pressure limits (i.e. ignore high peak airway pressures).
PEEP splints airways open and reduces airflow obstruction

18.  Use heavy sedation.
 Use neuromuscular blockade.
Atracurium is associated with histamine release.
Rocuronium or pancuronium is the agents of choice.
Ketamine +/- propofol +/- analgesia
Preferentially use non histamine releasing analgesia – fentanyl
High peak inspiratory pressures (PIP) — don’t worry this does not necessarily
correlate with lung barotrauma.
Respiratory acidosis due to a low target minute ventilation — sedation and
neuromuscular blockade may be required to suppress spontaneous ventilation.

19. Peak airway Pressure (Ppk)
Represents the sum of pressures required to overcome the elastic recoil pressure of
the inflated respiratory system and to overcome resistance in the airway.
Not useful for assessing DHI.

20. At expiration many of the smaller airways end up closed (particularly in
bronchospasm)
Only the most "open" (least bronchospastic) lung units will reveal their
intrinsic PEEP by the end-expiratory pause method, and the really spastic lung
units with the highest intrinsic PEEP will not be observed.
Not useful for assessing DHI.

21. Plateau pressure is measured with the inspiratory hold maneuver 2s pause
The high pressure at the plateau ensures all the little airways are splinted open
This allows the intrinsic PEEP to equlibrate across the entire respiratory circuit.
Need for a paralysed patient, and a circuit without significant leak
The ideal pressure is as usual, under 25-30 cmH2O.
Peak pressure Plateau pressure

26. Ventilator
inappropriate settings
ventilator malfunction
Circuit
 kinking
 pooling of condensed water vapour
 wet filters causing increased resistance
Endotracheal tube
 displacement, e.g. endobronchial intubation
 kinking
 obstruction with foreign materia
consider the machine:
Man
 Bronchospasm (e.g. asthma)
 Decreased compliance
lung (e.g. collapse, consolidation,
pulmonary edema)
 Pleural (e.g. pneumothorax, pleural
effusion)
 Chest wall (e.g. abdominal distention,
kyhposcoliosis, obesity)
 Patient-ventilator dysynchrony, coughing

27.  Increasing salbutamol
 Deepen sedation
 Adding adrenalin/ aminophylline/ ketamine/ Mg ( no evidence) – doses
required by candidate
 Volatile anaesthesia
 Paralysis- Train of four essential .
 ? Bronchoscopy
 Measurement of iPEEP

28. Thus if flow or resistance is markedly altered, a change in airway pressure
will not be indicative of a change in the alveolar pressure.
Airway pressure is more conveniently measured than alveolar pressure. Peak inspiratory pressure
(PIP) is displayed on most ventilators.
A maximum acceptable PIP of <35 cmH20 is widely used.
How can alveolar pressure be estimated?
Alveolar pressure is estimated by determining the inspiratory pause
pressure, which corresponds to the plateau pressure.

29. High alveolar pressures can be due to excessive tidal
volume, gas trapping, PEEP or low compliance

30. High airway pressures do not correlate with lung barotrauma.
Airway pressure itself is not particularly deleterious unless it reflects
excessive alveloar pressure.
Inadequate ventilation can occur because many ventilators are set to terminate the
inspiratory flow if the upper pressure limit setting is reached. When this occurs
inspiratory volumes are markedly reduced, resulting in low tidal volumes and
minute ventilation.

31. Reduce auto-PEEP by
 Reducing inspiratory time/increasing expiratory time
 Increase peak inspiratory flow rate – 100 lpm
 Decrease respiratory rate (use IMV without PSV) – rate of 12 usually is good
 Decrease tidal volume to 8 cc per kg IBW

32. A 20-year-old, 80 kg man presents to the ED with acute
severe asthma. In ED he has a respiratory arrest and is
intubated. He is then transferred to your ICU with the
following ventilator settings:
 Mode SIMV
 FiO2 1.0
 Vt 500 ml
 Respiratory rate 16 breaths/min
 Inspiratory flow 20 litres per min
 PEEP 5 cmH2O
 He has a tachycardia 130 bpm and a BP of 80/60.
Arterial blood gas analysis shows pH 7.1, PCO2 93
mmHg, PO2 69 mmHg , HCO3 28 mmol/L SaO2 90%.
Peak pressure, plateau pressure and total PEEP

33. SIMV No benefit for PCV, and risks of
hyperinflation with rapid changes in
resistance. Will need sedation and probably
paralysis to tolerate.
FiO2 leave
Vt Increase Vt if necessary to help control pCO2
High PCO2 most probably relates to gas trapping and is
best controlled by changes in flow rate and respiratory
rate.
Rate Too high
Rate should be immediately reduced to 10 or fewer.
I:E of 1:1.5. I:E should be 1:3

34. Inspiratory flow 20 L/min is too low, causing prolonged inspiratory time (1.5
sec for Vt 500 ml).
Flow should be adjusted up to minimise inspiratory time. Peak
pressure will rise, but this should be tolerated so long as plateau
pressure is safe.
PEEP Extrinsic PEEP in this situation is controversial.
Hypotension suggests significant dynamic hyperinflation.

35.  Prolonged expiration
 Expiratory flow not returned to baseline at end of expiration indicating auto-
PEEP / gas trapping / dynamic hyperinflation
What can you see in this ventilator wave form ?

36.  Reduce rate
 Reduce T insp
 Reduce VT
 (Check intrinsic PEEP)

37. Expiratory flow scooped out/Increased expiratory resistance
Incomplete emptying/potential for gas trapping

41.  What do the variables A, B, C & D indicate?
A- PEEP, B- PIP, C- Plateau pressure, D- Auto PEEP

42.  Inspiratory flow pattern
 Inspiratory flow rate
What are the factors which determine variable B?
Resistance, compliance, tidal volume, PEEP, insp flow rate and flow pattern
If the delivered tidal volume was 600 ml, what is the calculated static
compliance?
30 ml/cm water [TV/(Plateau-PEEP)]
 Increase expiratory time
 Decrease I:E ratio, decrease RR, reducing MV

43.  36 year old female is brought into Emergency
Department with acute shortness of breath. She is
unable to provide any history due to her tachypnoea.
 She has a respiratory rate of 30 breaths per minute,
has a GCS of 15, is afebrile and has a BP of
90/60mmHg. She is using accessory muscles. On
auscultation.
 she has widespread expiratory wheeze spread
throughout both lung fields.

44.  You decided to intubate her, intubation was
uneventful, then connected to ventilator.

45. Vocal Cord Dysfunction (VCD)
Vocal Cord Dysfunction (VCD) occurs when the vocal cords (voice box) do not
open correctly.
VCD is sometimes confused with asthma because some of the symptoms are similar.
In asthma, the airways (bronchial tubes) tighten, making breathing difficult. With
VCD, the vocal cord muscles tighten, which also makes breathing difficult.
Many people with asthma also have VCD.
laryngoscopy Vocal cords should be open when taking in a breath. In some
people with VCD, the vocal cords actually close instead of opening.

46.  Extrathoracic causes
 Anaphylaxis
 Vocal cord paralysis
 Laryngeal stenosis
 Goiter with thoracic inlet obstruction
 Anxiety with hyperventilation
 Intrathoracic central airway causes
 Tracheal stenosis
 Mediastinal tumours
 Hyperdynamic airway collapse due to tracehomalacia
 Mucus plugs
 Thoracic aortic aneurysm
 Foreign body inhalation
 Intrathoracic lower airway causes
 Bronchitis or bronchiolitis
 COPD
 Pulmonary oedema - "cardiac asthma"
 Airway distortion due to mechanical causes, eg. bronchial mass, bronchiectasis,
pneumothorax
 Exposure to inhaled irritant or corrosive agent, and this includes the aspiration of
gastric contents