Fatal & Near-Fatal Asthma

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Transcript Fatal & Near-Fatal Asthma

Rising to the challenge
Robert Donovan MD FACEP
Medical Director PHI California
Chief of Staff Doctors Medical Center
Asthma in Ancient Times
Maimonides
 “No magic cure for asthma”
 “Asthma often starts with a
common cold during the rainy
season”
 “The air pollution in Cairo may in
part be responsible”
C a i r o
Cairo is here!
Pathophysiology of Asthma
Inflammatory cells in asthma
 Mast cells
 Eosinophils
 Macrophages
 Activated T lymphocytes
Autopsy Findings in Fatal Asthma
 smooth muscle
wall thickness
inflammation
Severe Asthma
 5% to 10% of asthmatics
 Pts. are particularly hard to manage
 Still poorly understood
Severe Asthma
Severe
Asthmatics
Female gender
Poor management skills
Smoking/drugs/alcohol
Prior severe attacks
Age > 40
Ability to sense & respond
to airway stimulus
Precipitants of Near Fatal Asthma
 Air pollution
 Viral URIs
 Non-compliance
 Emotional stress
 Weather changes
 Heavy allergen exposure
How Near-Fatal Asthma presents
10% Quickly
-
90% S l o w l y …
-
Physical Exam
 Dyspneic, scared, and diaphoretic
 Sitting upright or tripod, tachycardic and tachypneic,
and using accessory muscles.
 Auscultation reveals diffuse wheezing or, worse, no
breath sounds at all.
Measure Peak Flow?
 FEV1 usually low, often
can’t be measured
 Although it might be
helpful, ill patients won’t
even try
 Failure to FEV1 – not
good!
Lab Findings
 WBC might be 
In allergic patients, the % eosinophils might be 
 Serum K+ is often low
  lactate is common
 ? high-dose catecholamine therapy
 ? increased production by respiratory muscles and
decreased clearance due to circulatory failure
? ABG ?
 Blood gas might help
 Supplemental O2 generally will correct
hypoxia
 CO2 might be  or 
 A steadily rising PaCO2  impending
respiratory collapse
 Changes in the pH might be the most help
Management
IV, O2, monitoring
Bronchodilators
Corticosteroids
Plan for ICU Admission
Adjunctive and Experimental Therapy
Albuterol
 Mainstay Bronchodilator
 MDI’s don’t work
 Side effects are tolerable
Atrovent (ipratropium)
 Atrovent (with high-dose albuterol) may improve
bronchodilation
 Dose of 0.5 mg delivered by nebulization q 1 hour
 In our ED, routinely added to full-strength Albuterol
nebulizer
Corticosteroids in Near-Fatal Asthma
 Essential Treatment
 Effects may be within 1-2
hours although a response
may not be apparent for
days
 Possible role for inhaled
corticosteroids in addition
Magnesium
 Interferes with calcium-mediated smooth muscle
contraction
 Decreases acetylcholine release from parasympathetic
nerve endings
 Can cause hypotension and loss of
deep tendon reflexes.
 2 grams IV over 20 minutes
BiPAP?
 Might be worth a trial
 Some supporters
 If you can get the patient
to keep it on…..
Ketamine Case Presentation
 47 yo male: Hx Asthma, Smoker, Depression, COPD
 Began with productive cough  yellow/green sputum
 Treated in ER; released
 Returned 1 hour later – much worse
 Tripod, tachypneic, 87% sats.
 Initial ABG pH 7.42 pCO2 46 PO2 96% (with o2)
 Worsened despite treatment; intubated
 Got even worse
 difficult to ventilate
 high peak airway pressures >80 cmH2O
 pH 7.04; pCO2 91; pO2 86% on 100% FiO2.
Other Possibilities
 Theophylline
 Heliox (70% Helium 30% Oxygen)
 IV montelukast
 IV terbutaline
 Cardio-Pulmonary Bypass
What if things worsen?
Intubation
 100% O2
 Get back-up airways out
 Best person does it
 Do full RSI
 Decompress the stomach
 Keep them paralyzed
 DON’T put them on a ventilator! (at first)
 You take over the initial bagging of the patient
Premature
Ventilator = Death
Normal Lung
Dynamics
Dynamic Hyperinflation
Dynamic Hyperinflation
 Barotrauma
 Hemodynamic compromise from 
intrathoracic pressure



Decreased venous return
 Pulmonary vascular resistance
Decreased cardiac output
Ways to identify
Dynamic Hyperinflation
 High Peak airway pressure
 Presence of Intrinsic positive end-expiratory pressure
(autoPEEP)
 High Plateau Pressure
 Clinical
If BP and  Airway Pressure
 Think tension pneumothorax or DHI stacking
 Immediately disconnect pt. from vent and slowly bag, or
not at all
 If due to DHI, BP should quickly
 If no change, needle both sides of the chest – now!
How to Minimize DHI
 Do what it takes to ensure enough time to exhale
 Ways to increase expiratory phase include:
 Increasing the inspiratory flow rate in order to
decrease inspiratory time - good
 Decreasing the Tidal Volume. -
better
 Decreasing the respiratory rate -
best
Tidal Volume: 1 liter
Resp. Rate : 10
Insp. Flow : 60 Liters/min
Insp/Exp. Ratio = 1:5
Tidal Volume: 1 liter
Resp. Rate : 10
Insp. Flow : 120 Liters/min
Insp/Exp. Ratio = 1:11

Tidal Volume: 1 liter
Resp. Rate : 10
Insp. Flow : 60 Liters/min
Insp/Exp. Ratio = 1:5
Tidal Volume: 1 liter
Resp. Rate : 6
Insp. Flow : 60 Liters/min
Insp/Exp. Ratio = 1:9

Goal - Avoid Hypoxia
 Aim for SaO2 >90% - 95%
 For the short term– keep the patient sedated and
paralyzed
 PEEP is generally not useful
 Be aware of theoretical concerns of too much oxygen
promotes free radicals
How I determine a respiratory rate
 Use your Stethoscope !!
 Don’t be surprised with rates of 6-10 breaths per
minute at first
 Start the ventilator at this rate, use stethoscope to
determine increases in rate
Goal – Minimize Volu-trauma
 Aim for Tidal Volume 0f 8 to 10 ml/kg.min
 Aim for rate of 10 – 12 breaths per minute
Fatal & Near Fatal Asthma
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