1/7/2021 Acute Severe Asthma SID • LITFL • CCC Respiratory

Acute Severe Asthma

Chris Nickson ● Feb 4, 2019

HOME CCC

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:
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 – 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

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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

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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

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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

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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:

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(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]

Chris Nickson
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne.
He is also the Innovation Lead for the Australian Centre for Health
Innovation at Alfred Health and Clinical Adjunct Associate Professor at
Monash University. He is a co-founder of the Australia and New Zealand
Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN
Clinician Educator Incubator programme. He is on the Board of Directors
for the Intensive Care Foundation and is a First Part Examiner for
the College of Intensive Care Medicine. He is an internationally
recognised Clinician Educator with a passion for helping clinicians learn
and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he

continued post-graduate training in New Zealand as well as Australia’s
Northern Territory, Perth and Melbourne. He has completed fellowship
training in both intensive care medicine and emergency medicine, as well
as post-graduate training in biochemistry, clinical toxicology, clinical
epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve

patient care and the design of processes and systems at Alfred Health. He
coordinates the Alfred ICU’s education and simulation programmes and
runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill
Airway’ course and teaches on numerous courses around the world. He is
one of the founders of the FOAM movement (Free Open-Access Medical
education) and is co-creator of litfl.com, the RAGE podcast,
the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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Related

CICM SAQ 2010.2 Q2 Noninvasive Ventilation and the Non-Invasive Ventilation (NIV)
critically ill

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