ICU Management of COPD & Asthma 2
ICU Management of COPD & Asthma 2
ICU Management of COPD & Asthma 2
Bronchial Asthma
COPD
• Airflow limitation that is not fully reversible
(Global initiative for chronic obstructive
lung disease or GOLD)
• Persistent & progressive
• Risk factors
Smoking
Poor lung function in childhood
LBW
Bronchial hyper responsiveness
Precipitating factor
• Infection
• Atmospheric pollution
• Temperature change
• Intercurrent illnesses like cardiac failure,
Pulmonary embolism, pneumonia
• Postoperative
• Excessive use of sedatives & O2
• Trauma
Clinical features
• Increase in dyspnea, cough
• Sputum volume & purulence
• Fever, tachycardia, bounding pulse
• Tachypnea, cyanosis
• Pursed lip breathing
• Accessory muscle use
• Hypotension
• Flapping tremor
• Impaired level of consciousness
Diagnosis
• Spirometery
• FV loop
• Chest Xray
• CTscan
• ECG
• ABG
Therapeutic Goals
• Improvement in gas exchange
• Reduction of lung volume & increase in
expiratory flow
• Reduction of pulmonary inflammation
• Treatment of precipitating factor
Improvement in gas exchange
• Controlled oxygen therapy
• Achieve SpO2>90%
• Risk of hypercarbia
• Monitor ABG
• For nebulisation use air with nasal prongs
Reduction of lung volume &
increase in expiratory flow
Bronchodilators
• ß2-agonists
• Ipratropium bromide
• Methylxanthines
Treatment of precipitating factor
• Antibiotics
• Antiviral agent
• Analgesia
• Heparin
Reduction of pulmonary
inflammation
• Corticosteroids
• Mediator antagonists
• Antioxidants
• Retinoic acid
Mechanical ventilation
Support the gas exchange & fatigued resp
muscles
• Non- invasive ventilation
• Invasive mechanical ventilation
NIV
Status asthmaticus
Mortality-1-3%
Upto 40% when mechanical ventilation is used
Risk factors for SAE
Pt related factors
• Poor compliance
• Accustomed to disability
• Unable to gauge the severity of an attack
• Underuse of peak flowmeters
Doctor related factor
• Underestimate the severity of the attack
• Under use of ß2 –agonist & steroids
• Overuse of ß2-agonist
• Injudicious use of sedatives
• Theophylline levels not monitored
Pathophysiology of SAE
• Sudden onset (3-6hr) <15%, responds to bronchodialator
• Slower onset-Airway wall inflammation, bronchospasm &
accum of mucus
• Pt with SAE shows critical airflow obstruction leads to
DHI
• DHI places diaphragm at mech disad
• Incomplete exhalation elevates alveolar vol & P
• Auto PEEP increases work of breathing-Vent Failure
• V-Q mismatch
• Adverse cardipulmonary interaction
Clinical features
• Dyspnea at rest
• Upright posture
• Inability to complete the sentence in one
breath
• Disturbance in level of consciousness
• RR>30/min, HR>120
• Silent chest
• Pulsus paradox
Features of imminent resp arrest
• Altered mental status
• Paradoxical respiration
• Bradycardia, cyanosis
• Quiet chest
• Absence of pulsus paradoxus
Clinical assessment
• Medical history
• Physical examination
• D/D
Cardiac asthma
Airway obstruction
Pulm embolism
Angioneurotic edema
Laryngeal spasm
Foreign body
Factitious asthma
Monitoring
• Measures of airflow obstruction-PFR
• SpO2
• ABG
• Chest-X ray
• Hematology
• Sputum analysis
• Electrolytes
Treatment
• O2 therapy-Improve O2 delivery, reverses HPV, stimulate
bronchodilation
• Humidified, low flow, SpO2 >90%
• Nebulized ß2-agonist or MDI with spacer
• Salbutamol 2.5 mg in 2-3 ml NS every 20 min
• Salmetrol addition after 48 hrs improves FEV1
• In long term long acting ß-agonist with steroids lessens SAE
• SC epineph or terbutaline used in altered mental status &
near arrest situations
• IV ß2- agonist- rapid onset but more side effects
• Ipratropium Bromide –In combination improve
FEV1, PEFR
• Steroids- prednisolone/Methylpred 120-180mg in
divided doses for 48 hrs & then 60-80 mg/day
until PEFR>70% predicted
• Inhaled steroids(flunisolide) also showed benefit
in combination therapy
• Theophylline-controversial
• MgSo4- conflicting results
• Heliox-80-20% mixture –conflicting results
• Anaesthetic agents
• Leukotrien modifiers
Zafirlukast 160mgor Montelukast
10mg
• Less hospital stay, relapses, decrease dose
of ß2-agonists & steroid use
• Antibiotics -not recommonded
• Bronchoalveolar lavage
• Mechanical ventilation
NIV
• NIPPV or NINPV
• NIPPV help in overcoming inspiratory
threshold created by auto- PEEP
• Face mask or nasal mask
• CPAP of 5 or 7.5 cm of H2O
• BiPAP
• Complications
• Discomfort ,dyspnea,air leak,gastric
distension,pressure sores
Indications of Invasive ventilation
•Fatigue or impending resp failure
•Deteriorating consciousness
•Refractory hypoxia
•Failure of secretion clearance
•Respiratory arrest
Oral ETT
Post intubation hypotension & pneumothorax
Assessment of ventilation
• Plateau P
• PEEPi
Adjuvants
• Use of sedation & Paralysis
• Use of mucolytics & expectorants
• Inhalational agent
• Chest physiotherapy
•
Weaning & Extubation
• No validated criteria's
• Spontaneous breathing trial
Paco2 normalises
Airway resistance <20 cm of H2O
• Pt follows commands
• No neuromuscular weakness
Conclusion
• Any asthmatic can develop SAE
• General appearance gives imp clues
• 1st line Tt- ß2-agonist, sys corticosteroids, low flow O2
• Alternate Tt-ipratropium bromide, MgSo4, leukotrien
modifiers, heliox & NIV
• Hypotension after intubation, trial of apnea or hypopnea is
diagnostic
• Permissive hypercapnia limit hyperinflation
• Avoid prolong use of muscle relaxant
• Education, environmental control measures & anti-
inflammatory drugs for future