Acute Severe Asthma
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PY Mindmaps
OH
- increased prevalence worldwide
- significant morbidity and mortality -> related to underestimation of severity
- improved outpatient management + more inhaled corticosteroids have meant less serious
presentations
- characteristics: (1) reversible obstruction, (2) inflammation, (3) mucous formation
- aetiology: ?’hygiene hypothesis’, IgE dependent inflammatory response
- producers:
(1) increased WOB – increased airway resistance and decreased pulmonary compliance ->
hypercapnic respiratory failure
(2) V/Q mismatch – from airway narrowing and closure -> impaired gas exchange and
increase WOB to compensate
(3) adverse cardiorespiratory interactions – increased venous return because of high
intrapleural pressures, but also increased afterload -> pulsus paradoxus
HISTORY
-
SOB
cough
wheeze
chest tightness
status asthmaticus = anyone failing to respond to nebulised bronchodilators
acute severe asthma (90%) – chronic presentation with previous poor control
hyperacute, fulminating asthma (10%) – onset over <3 hours
-
previous intubations
previous control
multiple admissions
poor psychological circumstances
poor response to treatments
Triggers
- specific: URTI, housemite, pollen, animal, aspirin, beta-blockers
- non-specific: cold air, exercise, atmospheric pollutants, stress, emotion
Jeremy Fernando (2011)
EXAMINATION
-
RR
SpO2
suprasternal retraciton
upright posture
sweating
Markers of severe episode
-
accessory muscle use
pulsus paradoxus > 25mmHg
HR >110
RR > 25-30
phrases and words
PEFR < 50%, < 100L/min
SpO2 < 92%
Markers of imminent respiratory arrest
-
altered mental status
paradoxical respiration
bradycardia
quiet chest
absence of pulsus paradoxus
INVESTIGATIONS
- ABG: initially respiratory alkalosis -> with tiring CO2 rises -> metabolic lactic acidosis from
salbutamol/adrenaline (beta adrenergic stimulation -> increases glycolysis and increased
pyruvate+lactate production)
- CXR: perform in severe asthma, LRTI or barotrauma expected
- monitor K+
- Mg2+
DIFFERENTIALS TO ENTERTAIN
-
LVF
anaphylaxis
aspiration
upper airway obstruction (vocal cord dysfunction, tracheal stenosis)
inhaled foreign body
PE
hyperventilation syndrome
MANAGEMENT
Established Treatments
O2 – titrated to SpO2 92%
Beta-agonists – salbutamol nebulised/MDI/IV – bolus 250mcg (5-10mcg/kg) -> 120mcg/min
Anticholinergics – ipratropium bromide 500mcg Q2-6 hourly nebulized
Jeremy Fernando (2011)
Corticosteroids – hydrocortisone 200mg Q6hrly -> prednisone 0.5mg/kg/day
Aminophylline – 6mg/kg load -> 0.5mg/kg/hr (check levels daily, aim 30-80micromol/L)
Non-established Treatments
Adrenaline – nebulised 5mg, SC 0.5mg, IV – load with 1mg -> 1-20mcg/min
MgSO4 – 5-10mmol over 20min (up to 80mmol have been given)
Heliox – reduces turbulent air flow, 70:30 (He:O2)
Ketamine – 0.5-2mg/kg/hr
Inhalational agents – sevoflurane, anaesthetic machine or custom fitted ventilator required
Leukotriene anatagonists – some benefit in chronic asthma
BAL – can clear mucous plugging but transiently worsens bronchospasm
Ventilation
Dynamic Hyperinflation
- slow expiratory airflow -> incomplete exhalation of gas during normal expiratory times ->
gas trapping
Dynamic Hyperinflation on controlled MV
- the gas trapping = dynamic hyperinflation
- this continues until an equilibrium point is reached where the exhaled volume matches
inspired volume to:
(1) increases small-airway calibre
(2) increases lung elastic recoil pressure
-> improvement in expiratory airflow
-> allows inspired tidal volume to be exhaled in the available expiratory time available
Assessing DHI in the Mechanically Ventilated
- plateau airway pressure (Pplat) = airway pressure after transient expiratory occlusion at the
end of inspiration
- inspiratory hold function on ventilator
- this pressure is directly proportional to degree of DHI
- should be maintained at < 25cmH2O
Other techniques:
Jeremy Fernando (2011)
- end-inspiratory lung volume – not routinely used but is good predictor of complications
during MV
- assessment of change in BP and CVP during ventilator disconnection – disconnect for 1-2
min or decrease rate to 4/min -> increase in MAP and CVP if DHI present
Auto-PEEP or PEEPi
- the gas trapped at the end of expiration exerts a positive pressure on the alveoli (intrinsic
positive end-expiratory pressure – PEEPi or auto-PEEP)
- during expiration sequential closure of the most severely obstructed airway occurs with only
the less obstructed airway remaining in communication with the airway -> measured PEEPi
underestimates the true magnitude of PEEPi.
-> the only way to infer whether the patient has occult Auto PEEP is the presence of a
elevated Pplat and low Auto PEEP -> there must be occult Auto PEEP that is not
accounted for when measuring the end-expiratory pressure from gas trapping.
Assessing PEEPi in the Mechanically Ventilated
= this is the airway pressure during occlusion of expiratory flow at the end of expiration
- end-expiratory hold function on ventilator
- this measurement is known to underestimated PEEPi as a consequence of small airway
closure during expiration (occult PEEPi) -> thus this measurement can only be used to show
the presence of DHI but not to regulate mechanical ventilation.)
- ideally should be < 12cmH2O but exact safe level unknown.
Non-invasive Ventilation
Advantages
- helps overcome PEEPi from gas trapping -> reduces inspiratory WOB
- augmentation of inspiration -> decreases WOB, increases TV and minute ventilation
- can decrease expiratory work by opposing dynamic airway compression and allowing more
expiration with less gas trapping and hyperinflation
- reduce V/Q mismatch
- decreased hospitalisation rate
- significant increase in FEV1
- significant decrease in hospital admission rates
- titrate to patient comfort and decrease in WOB
Disadvantages
-
claustrophobia
agitation
gastric distension
dys-synchrony
increased expiratory work and hyperinflation
Management
- test patients response by starting with CPAP of 5cmH2O and then titrate IPAP and EPAP to
patients comfort.
Jeremy Fernando (2011)
- there is no role for NIV in patients with respiratory or cardiac arrest or those who are
uncooperative or can’t protect their airway
Invasive Ventilation
- life saving but associated with major mortality and morbidity
Indications
-
arrest
severe hypoxia
altered mental state
failure to respond to treatment
Procedure
-
load with IVF and have inotropes ready to go
large ETT
RSI with ketamine/propofol
slow hand ventilation
attention to possible complications
Ventilator settings
- goals: avoid DHI and hypoventilation
- MV 100mL/kg/min (<8L/min in adult)
- TV 6mL/kg
- RR 10
- short inspiratory time (flow rate 80-100L/min) -> high peak airway pressure but low plateau
pressure -> decreased barotrauma
- I:E of 1:>4
- hypercapnia will result -> sedation and often paralysis initially
- PEEP – traditionally no PEEP was used out of fear of exacerbating Auto PEEP -> but it is
now known that PEEP should be set at 60-80% of Auto-PEEP to augment distal airway
emptying through splinting airways open
Adjustment of Ventilation
- adjust ventilation to degree f DHI (not PaCO2 or pH)
- if Pplat > 25cmH2O or cardiovascular suppression -> reduce rate
- if Pplat < 25cmH2O -> ventilation can be liberalised with increase in RR and reduction in
sedation
- hypercapnia is well tolerated but can consider bicarbonate if pH < 7.1
Jeremy Fernando (2011)
Complications
HYPOTENSION -> PEA ARREST
- causes:
(1)
(2)
(3)
(4)
(5)
(6)
(7)
(8)
sedation
DHI
pneumothorax with tension
arrhythmias
hypovolaemia (rare)
endobronchial intubation
myocardial depression from prolonged hypoxia
reversal of pleural pressures impairing venous return
->
->
->
->
->
->
->
->
->
disconnect from ventilator
slow RR and load with fluid
auscultate the chest
check ETCO2 and ECG
urgent CXR
treat cause
fluids + inotropes
heliox
ECMO
PNEUMOTHORAX
-> decrease ventilation to protect other lung
-> if hypotensive -> decompress
-> if not hypotensive -> urgent CXR as signs not reliable
ACUTE NECROTISING MYOPATHY
- caused by prolonged, deep sedation, steroids +/- paralysis
- results in prolonged weakness and rehabilitation
-> try and avoid
Jeremy Fernando (2011)