OVERVIEW
- increased prevalence worldwide
- significant morbidity and mortality -> related to underestimation of severity
- improved outpatient management + more inhaled corticosteroids have meant less serious presentations
- aetiology: ?’hygiene hypothesis’, IgE dependent inflammatory response:
Characteristics:
- reversible obstruction
- inflammation
- mucous formation
Resulting in:
- increased WOB – increased airway resistance and decreased pulmonary compliance -> hypercapnic respiratory failure
- V/Q mismatch – from airway narrowing and closure -> impaired gas exchange and increase WOB to compensate
- adverse cardiorespiratory interactions – increase 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<3h
- 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
EXAMINATION
- RR
- SpO2
- suprasternal retraction
- 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 CONSIDER
- LVF
- anaphylaxis
- aspiration
- upper airway obstruction (vocal cord dysfunction, tracheal stenosis)
- inhaled foreign body
- PE
- hyperventilation syndrome
- pneumothorax
- parodoxical motion of the vocal cords
MANAGEMENT
Established Treatments
- O2 – titrated to SpO2 92%
- Beta-agonists – salbutamol nebulised/MDI/IV – bolus 250mcg (5-10mcg/kg) -> 1-20mcg/min
- Anticholinergics – ipratropium bromide 500mcg Q2-6 hourly nebulized
- 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
RAPID SEQUENCE INTUBATION
- induction agent: — ketamine preferred due to bronchodilation — propofol is an alternative, but beware hypotension
- consider a ‘delayed sequence intubation’ approach using ketamine and non-invasive ventilation for pre-oxygenation if experienced
- avoid drugs that cause histamine release and may worsen
- intubated asthma patients are prone to post-intubation hypotension due to dynamic hyperinflation (‘stacking’), hypovolaemia, induction drugs and tension pneumothorax (SH!T)
- initially provide gentle BVM post-intubation then transition to mechanical ventilation with appropriate settings (see below) when stable
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:
- 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
- dyssynchrony
- increased expiratory work and hyperinflation
Management
- test patients response by starting with CPAP of 5cmH2O and then titrate IPAP and EPAP to patients comfort.
- 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 of 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
COMPLICATIONS
HYPOTENSION -> PEA ARREST
- causes:
(1) sedation (2) DHI (3) pneumothorax with tension (4) arrhythmias (5) hypovolaemia (rare) (6) endobronchial intubation (7) myocardial depression from prolonged hypoxia (8) 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 to avoid!
References and Links
Journal articles
- Holley AD, Boots RJ. Review article: management of acute severe and near-fatal asthma. Emerg Med Australas. 2009 Aug;21(4):259-68. doi: 10.1111/j.1742-6723.2009.01195.x. Review. PubMed PMID: 19682010. [Free Full Text]
- Stanley D, Tunnicliffe. Management of life-threatening asthma in adults. Contin Educ Anaesth Crit Care Pain (2008) 8 (3): 95-99. doi: 10.1093/bjaceaccp/mkn012 [Free Full Text]
- Wener RR, Bel EH. Severe refractory asthma: an update. Eur Respir Rev. 2013 Sep 1;22(129):227-35. doi: 10.1183/09059180.00001913. Review. PubMed PMID: 23997049. [Free Full Text]
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