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Published byDana Ponton Modified over 9 years ago
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Rising to the challenge Robert Donovan MD FACEP Medical Director PHI California Chief of Staff Doctors Medical Center
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Asthma in Ancient Times Ebers Papyrus
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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”
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Insert obligatory vacation photo here Cairo is here! Cairo
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Pathophysiology of Asthma
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Inflammatory cells in asthma Mast cells Eosinophils Macrophages Activated T lymphocytes
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Autopsy Findings in Fatal Asthma smooth muscle wall thickness inflammation smooth muscle wall thickness inflammation
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Severe Asthma 5% to 10% of asthmatics Pts. are particularly hard to manage Still poorly understood
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Severe Asthma
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Severe Asthmatics
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Female gender Poor management skills Smoking/drugs/alcohol Prior severe attacks Age > 40 Ability to sense & respond to airway stimulus
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Is it truly asthma?
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Precipitants of Near Fatal Asthma Air pollution Viral URIs Non-compliance Emotional stress Weather changes Heavy allergen exposure
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How Near-Fatal Asthma presents 90% - Slowly… 10% - Quickly
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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.
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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!
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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
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? 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
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Management IV, O2, monitoring Bronchodilators Corticosteroids Plan for ICU Admission Adjunctive and Experimental Therapy Anticipate bad things happening
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Albuterol Mainstay Bronchodilator MDI’s don’t work Side effects are tolerable
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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
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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
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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
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BiPAP? Might be worth a trial Some supporters If you can get the patient to keep it on…..
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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 pCO 2 46 PO 2 96% (with o2) Worsened despite treatment; intubated Got even worse difficult to ventilate high peak airway pressures >80 cmH 2 O pH 7.04; pCO 2 91; pO 2 86% on 100% FiO 2.
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Ketamine Started
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Other Possibilities Theophylline Heliox (70% Helium 30% Oxygen) IV montelukast IV terbutaline Cardio-Pulmonary Bypass
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What if things worsen?
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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
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Premature Ventilator = Death
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Normal Lung Dynamics
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Dynamic Hyperinflation
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Barotrauma Hemodynamic compromise from intrathoracic pressure Decreased venous return Pulmonary vascular resistance Decreased cardiac output
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Ways to identify Dynamic Hyperinflation High Peak airway pressure Presence of Intrinsic positive end-expiratory pressure (autoPEEP) High Plateau Pressure Clinical
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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!
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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
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Tidal Volume: 1 liter Resp. Rate : 10 Insp. Flow : 60 Liters/min Insp/Exp. Ratio = 1:5 Expiration time : 5 seconds Tidal Volume: 1 liter Resp. Rate : 10 Insp. Flow : 120 Liters/min Insp/Exp. Ratio = 1:11 E x p i r a t i o n t i m e : 5. 5 s e c o n d s
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Tidal Volume: 1 liter Resp. Rate : 10 Insp. Flow : 60 Liters/min Insp/Exp. Ratio = 1:5 Expiration time : 5 seconds Tidal Volume: 1 liter Resp. Rate : 6 Insp. Flow : 60 Liters/min Insp/Exp. Ratio = 1:9 E x p i r a t i o n t i m e : 9 s e c o n d s
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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
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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
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Goal – Minimize Volu-trauma Aim for Tidal Volume 0f 8 to 10 ml/kg. min Aim for rate of 10 – 12 breaths per minute
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Oxygen B-2 Agonists IV Steroids/MgSO4 “Extras” Be watchful If intubated: Slow & Low Add ketamine
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Fatal & Near Fatal Asthma doctor@donovans.com
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