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Acute Severe Asthma
By: Kane Guthrie
Objectives
• Pathophysiology of ASA• Assessing the patient with ASA• Emergency department management• NIV vs Mechanical Ventilation in ASA
Case Study
Case Study PMHx: Medications:
HT Ramipril
DM Type 2 Glicazide, Metformin
Asthma Seritide, Ventolin PRN
Obesity
Smoker
Vital Signs
Epidemiology of Asthma
• Over 2.2 million Aussie’s have asthma• Over 400 hundred die each year• Highest risk of death >70years• Severe acute asthma is a life threatening
condition.
Pathophysiology
Acute Severe Asthma
2 distinct phenotypes of ASA identified:
Type 1•Most common, responsible for 80-85% mortality•Characterised by esinophilic inflammation•Gradual deterioration over days-weeks•Occurs in patients with poorly controlled asthmaType 2•Characterised by neutrophilic inflammation•Presents with rapid onset•Responds quickly to therapy
Differential Dx:• Upper airway obstruction
• Foreign-body aspiration
• Vocal cord dysfunction syndrome
• APO
• Acute Ex of COPD
• Hysterical conversion syndrome
• Munchausen syndrome
AssessmentAirway Breathing Circulation Disability Exposure
•Cyanosis•Tracheal tug
•Using accessory muscles•Talking in words•Silent chest•Tripod position
•Hypotension•Tachycardia > bradycardia
•Confusion•Agitation•Coma
•Diaphoresis
Assessing Severity
Severe (Require Admit) Critical (Require ICU)
•PEFM >33-55% predicted best • PEFM 33% of predicted best
• Unable to complete sentences •Silent chest, Cyanosis
• RR >25bpm • Bradycardia, hypotension
•HR >120bpm •Exhaustion, confusion, coma
Investigations
• Diagnostic test generally provide limited information, compared to clinical assessment
CXR
• Limited Use• Hyperinflation 5-10%• Infiltrates 5%• PTX <1%• Pnemomediastinum <1%
Blood Gas
• Respiratory alkalosis typical• Inaccurate predictor of outcome• Seldom alters treatment plan• Clinical assessment gives better information• Painful
Pulse Oximetry
• Simple, less invasive and painful, compared to blo0d gas.
• Provides continuous o2 measurement• Aim >Spo2 94%
PEFM
• Objective measurement of lung function• Useful to assess response to treatment• Limited role in ASA
PEFM Measurements (predicted best)
<25% severe
25-50% moderate
50-70% MILD
>70% D/C goal
Complications of ASARespiratory Cardiac Electrolytes Other
• Pneumothorax•Pnemomediastinum•Pneumopericardium
• Arrhythmias•Ischaemia•Infarction
• Low K•Low Mg•Low Phosphate
• Lactic acidosis•Hyperglycemia
ED Management
The sick and dying asthmatic!!!
Nursing Care
• Apply o2/neb (humidified)• Monitor BP,HR,RR, Spo2, EtCo2, Temp, GCS• IVC x2• Monitor electrolytes/arrhythmias closely• ECG• FBC• IDC
o2
• Asthmatic die from hypoxia• Keep Sp02 > 94%• A slight ∧ in Pco2 may occur, (not clinically
significant)
Bronchodilators
• Salbutamol• First line therapy • Nebulizer (back to back nebs)• Dose?• Not improving consider IV (back door)• Monitor K• Salbutamol toxicity= ∧Lactic acidosis
Anticholinergics
• Ipratropium bromide• Blocks muscarinic receptors in smooth muscle,
resulting in bronchodilation• Dose: 500mcg• Can give up to 3 dose’s initially then ever 4/24
Mg
• Controversial• Best evidence is in the sick/dying asthmatic• Cause smooth relaxation, inhibits histamine &
acetylcholine release from nerve endings• Indicated when bronchodilators are failing• Dose: 2-4mg over 30-60mins
Steroids
• Prednisolone vs Hydrocortisone• Given within 1st hour greatly reduces hospital
admission• Target airway oedema and secretions via anti-
inflammatory role• Dose: Pred 50mg PO, Hydrocort 100-200mg IV
Adrenaline
• Given via Neb or IV• Alpha effects target ∨ airway oedema• Beta effect target ∨bronchodilation• Used as a rescue therapy in the hypotensive,
poor responding asthmatic• Dose: Neb 1-6mg in 3ml Nacl• Dose: IV 6mg in 100mls 5% dextrose (1-
15mls/Hr), “also push dose’s 0.10-0.50mcg”.
AB’s
• Not routinely indicatedGive• Underlying pneumonia/bacterial cause• Preventing VAP
Airway Management
NIV
• Becoming more popular, (research, case reports)
• Unloads resp muscles, augments alveolar ventilation until asthma resolves.
• CPAP vs BiPAP• Start with low IPAP & EPAP• Good indicator which patients need intubating
What the literature says on NIV.
Clinical Evidence:• Decreases airway resistance
• Re-expands atelectic lung
• Offsets intrinsic PEEP
• Delivers aerosolized medication
• Delivers Heliox
Mechanical VentilationIndications
Clinical Indicators Laboratory Indicators
•Cardiac or respiratory arrest •Severe hypoxia despite maximal o2
•Altered mental status •Failure to reverse Resp acidosis
•Progressive exhaustion • pH7.2, Co2 ∧5mmHg/hr or greater the 55-70mmHg,
Intubating
• Ketamine for bronchodilator effects• Use rapid sequence intubation• Fluid bolus before (pre-load)• Allow permissive hypercapnea
Challenges of Mechanical Ventilation
• Effective pre-oxygenation difficult• No margin for error or delay• Need to be intubated by most senior person
available• Develop high Intrathoracic pressure after RSI• Intubation causes higher mortality via= lung
hyperinflation, VILI, cardiovascular collapse.
The BIG issue
• Asthmatics require prolonged expiratory times• Severe asthma pt initiates inspir before expir ceases• Results in increase lung volume, auto-peep and
hyperinflation• Minimizing hyperinflation and avoiding excessive
airway pressures are the goals• Use low RR and prolonged exhalation times• Allow Co2 to rise, but keep pH .7.15 • Monitor (P plat) >30 cm H20 against expir time
Initial Ventilator Settings
• Assist control mode• Tidal volume 7-8mL/kg (use ideal body weight)• RR 10-12bpm• Fi02: 100%• PEEP: 0cm H20• Patients require deep sedation to tolerate the
Vent.
Crashing Ventilated Asthmatic
• D.O.P.E.S.
• Displaced ETT
• Obstructed ETT
• Pneumothorax
• Equipment failure
• Stacked breaths
Take Home Points
• Assessment skills are paramount• Maximizing therapy to prevent MV is the
GOAL!!!• Mg works in the sick asthmatic• NIV works• Experience makes a big difference• These patients will challenge you
Questions
Thank-you