4. Risk factors for fatal asthma
• Medical
– Previous attack with rapid/severe deterioration or
respiratory failure or seizure/loss of consciousness
• Psychosocial
– Denial ,non-compliance
• Family fear of inhalers
5. Lung Mechanics
• Hyperinflation
– Obstructed small airways cause premature airway
closure, leading to air trapping and hyperinflation.
• Hypoxemia
– Inhomogenous distribution of the affected areas
results in V/Q mismatch, mostly shunt.
6. Cardiopulmonary interactions
• Left ventricular load
– Spontaneously breathing children with severe asthma have
negative intrapleural pressure
as low as -35 cm H2O during almost the entire respiratory
cycle.
– Negative intrapleural pressure causes increased left
ventriculalr after load, resulting in risk for pulmonary edema
• Right ventricular load
– Hypoxic pulmonary vasoconstriction and lung hyperinflation
lead to increased right ventricular after load
7. Cardiopulmonary interactions
• Pulsus paradoxus
– It is the clinical correlate of cardiopulmonary
interaction during asthma. It is defined as exaggeration
of the normal respiratory drop in systolic BP:
• Normally <5 mm Hg, but >10mmHg in pulsus paradoxus
8. Pathophysiology
Severe air flow
obstruction
Incomplete exhalation Increased lung volume
Expanded small airwaysIncreased elastic recoil pressure
Increased expiratory flow Decreased expiratory resistance
Compenseted
Hyperinflation, normocapnia
Worsening airflow
obstruction
Decompenseted:
Severe hyperinflation, hypercapnia
11. Types of exacerbation
• Mild asthma exacerbation
– Dyspnea on exertion or tachypnea in young
children.
– PEF< 70% predicted
– Prompt relief with inhaled with short acting beta
agonist.
– Home management
12. Moderate asthma exacerbation
• Dyspnea usually limits activity
– PEF 40-69%
– Relief with frequent inhaled short acting beta
agonists
– Hospistal/clinic management
– Anticipate 1-2 days of symptoms after treatment
onset
13. Severe exacerbation
• Dyspnea at rest, limiting conversation
– PEF less than 40% predicted
– Only partial relief with inhaled short acting beta 2
agonists
– Emergency department management
• Hospitalization likely
• Systemic corticosteroids and ipratropium
• Anticipate > 3 days symptoms
14. Life threatening exacerbation
• Unable to speak, severe dyspnea with
associated diaphoresis
– PEF <25% of predicted
– Minimal relief with inhaled short acting beta
agonist
– Emergency stabilazation
• PICU admission
• Frequent or continuous salbutamol nebs
• Systemic Corticosteroid and ipratroprium
• ABC management.
15. Assessment: impending respiratory failure
• Altered level of consciousness
• Inability to speak
• Absent breath sounds
• Central cyanosis
• Diaphoresis
• Inability to lie down
• Marked pulsus paradoxus
18. Management
• Oxygen 100% warm, humidified
– Delver by non breather mask or high flow nasal canula
• Nebulized salbutamol with ipratroium continuously
to hourly
• Systemic corticosteriod
• Adrenergic agonists:
– Epinephrine
– Terbutaline ( alterntive)
• Two intravenous line
19. Further management
(Hypercarbia is a failure of ventilation not oxygenation)
• Hypotension
– Fluid bolus of normal saline
– Chest xray ? Tension pneumothorax
(SIADH may be common in severe asthma)
• Magnesium 40-75 mg/kg
• Consider ketamine
• Consider non invasive ventilation: CPAP
• Heliox (helium to oxygen60:40)
• Avoid aminophylline or theophylline
25. Case scenario 1
• A 6 yr male with previous history of hospital
admission for difficulty in breathing without fever
and treatment with salbutamol MDI. Re admitted
with severe respiratory distress. He is wheezing. RR
is 40/min, HR 145/min. He sits upright, leans
forward, has retractions and looks very anxious. He
correctly tells you his name and phone#, but has to
take breath after every few seconds.
• Discuss your initial therapeutic approach.
26. Case Scenario 1
• Which of the following are mandatory in this
child with severe asthma?
(you may choose none, more than one or all)
– Arterial blood gas analysis (to detect onset of
respiratory acidosis)
– Continuous pulse oxymetry
– Chest radiograph (to rule out
penumomediastinum/ thorax
– Frequent determination of PFR
– Blood count to assess need for anesthetics
27. Scenario 2
• When nebulizing drugs during status asthmaticus, the
following statement about gas flow rate is correct:
A. The higher is the gas flow rate through the nebulizer, the
more particles will be deposited in the patient’s alveolar
space.
B. Most devices require a gas flow rate of 10-12 L/min to
generate optimal particle size.
C. Gas flow rates above 5L/min should be avoided to
maintain laminar flow in the nebulizer output.
D. The nebulizer device should not be driven by 100%
oxygen.