Mechanical ventilation of bronchial asthma, is it a real dilemma

DR.MOHAMED ABOSAMAKLecturer of anesthesia and ICU

Consultant of critical care medicine in SFH

Ventilatotion OF Bronchial Asthma

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.

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 evidenceIntravenous beta-agonist bronchodilators for refractory bronchospasmMethylxanthinesNebulised adrenalineMagnesium sulfateHelium-oxygen mixtureThird-tier therapies without any supporting evidenceKetamineVolatile anaestheticsECMO in asthma

The nurse asks you about the O2 flow by face mask, how much you need high or low?

Humidified oxygen titrated to SpO2 90-92%

Hyperoxia is harmful in asthmatics

ABGPH 7.44, Po2 80,Pco2 31, Hco3 17

BiPAP

The patient tired

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

Things which increase intrinsic PEEP are things which Impair elastic recoil

Emphysema Increase expiratory resistance

BronchospasmAirway collapse at the equal-pressure point (where intrathoracic pressure equals intrabronchial pressure)

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

Should we try BIPAP firstHalf of the life-threatening complications occur at or around the time of intubation

BiPAP fails and the patient is successfully intubated.

Soon after intubation

Before intubation

Disconnect the endotracheal tube from the ventilator circuit.

What is your plan ?

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.

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.

The most important causes of hypotension following the intubation of a patient with asthma are

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.

What is your immediate assessment after intubation?

Never intubate an asthmatic… unless you absolutely have to!

•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.

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.

Correct hypoxaemia.Reduce dynamic hyperinflation and to buy

time for medical treatment.Decrease work of breathing.

What are the initial goals of mechanical ventilation

Initial ventilator settings in the intubated asthmatic

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

Use heavy sedation.Use neuromuscular blockade.

Atracurium is associated with histamine release.

Rocuronium or pancuronium is the agents of choice.

Ketamine +/- propofol +/- analgesiaPreferentially 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.

Expect that

 Monitoring for dynamic hyperinflation (DHI). 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.

Intrinsic or Auto PEEP (PEEPi) 

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.

Plateau pressure is measured with the inspiratory hold maneuver 2s pause

The high pressure at the plateau ensures all the little airways are splinted openThis 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.

Plateau Pressure

Peak pressure Plateau pressure

Following intubation

Airway pressure started alarming

Ventilatorinappropriate settingsventilator malfunction

What are the possible causes of high airway pressures in the intubated and ventilated patient?

Circuit kinking pooling of condensed water vapour wet filters causing increased

resistanceEndotracheal tube

displacement, e.g. endobronchial intubation

kinking obstruction with foreign materia

consider the machine:

 Man Bronchospasm (e.g. asthma) Decreased compliancelung  (e.g. collapse, consolidation, pulmonary edema) Pleural  (e.g. pneumothorax,

pleural effusion) Chest wall (e.g. abdominal

distention, kyhposcoliosis, obesity) Patient-ventilator dysynchrony,

coughing

Order CXR to check no PTX post PPV 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

Auscultate bilateral air entry.

Airway pressure = flow x resistance + alveolar pressure

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.

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

Alveolar pressure = (volume/ compliance) + PEEP

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.

Next day you stopped sedation but patient started to fight the ventilator

What changes would you make to the ventilator settings?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

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 mlRespiratory rate        16 breaths/min Inspiratory flow         20 litres per min PEEP                         5 cmH2OHe 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%.What additional measurements would you take to assist ventilator management?

Peak pressure, plateau pressure and total PEEP

What change in ventilator settings you would make ?

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 highRate should be immediately reduced to 10 or fewer. I:E of 1:1.5. I:E should be 1:3

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.

 Peak inspiratory pressure approx. 40 cmH2O and plateau pressure less than 20 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 ?

What changes would you make to the ventilator settings?Reduce rateReduce T inspReduce VT(Check intrinsic PEEP)

Expiratory flow scooped out/Increased expiratory resistance

Incomplete emptying/potential for gas trapping

Patient lung mechanics improving and you decided weaning off ventilator

What do the variables A, B, C & D indicate?

A- PEEP, B- PIP, C- Plateau pressure, D- Auto PEEP

What will determine the slope of the pressure curve between points A and B?

Inspiratory flow patternInspiratory flow rate

What are the factors which determine variable B?Resistance, compliance, tidal volume, PEEP, insp flow rate and flow patternIf the delivered tidal volume was 600 ml, what is the calculated static compliance?

30 ml/cm water  [TV/(Plateau-PEEP)]

 List the change(s) you would make to the ventilator settings to treat an increase in the value of variable D. Increase expiratory time Decrease I:E ratio, decrease RR, reducing MV

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.

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

What is your initial management?

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.

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