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