PS201 Week 6 Cue Cards - Chronic Lung Conditions and Oxygen Therapy
Chronic respiratory diseases: overview and obstructive vs restrictive
Global terminology: chronic lung conditions = chronic respiratory diseases (World Health Organization); sometimes called chronic respiratory conditions. Broad categories include obstructive and restrictive lung diseases.
Global burden and demographics:
Self-reported data (Australia, 2022): around 34% of Australians live with a chronic lung condition.
Global burden is disproportionately higher in low- and middle-income countries.
Example death rates from respiratory disease (higher is darker):
India: 133 deaths per 100,000 people
PNG: 204 deaths per 100,000 people
Australia: 23 deaths per 100,000 people
Contributing factors: remoteness, lower socioeconomic status, exposure to air pollution, occupational hazards, environmental challenges.
Session focus:
Obstructive lung diseases (airflow limitation, especially on exhalation).
Asthma and chronic obstructive pulmonary disease (COPD) are key examples.
Restrictive lung diseases are covered in the second podcast with additional examples.
Obstructive vs restrictive: key physiologic distinction
Obstructive: airflow limitation due to airway/airspace abnormalities, typically worse during expiration.
Restrictive: reduced lung expansion capacity leading to smaller lung volumes; not primarily due to airway narrowing.
Obstructive lung diseases: COPD and asthma
Definition and general pathophysiology
COPD: persistent, progressive airflow limitation due to airway and alveolar abnormalities; largely preventable and treatable.
Asthma: airflow limitation that is variable and may be reversible with medication.
Core COPD aetiology: significant exposure to noxious particles or gases; gene–environment lifetime interactions influence development.
Airway mechanisms of obstruction (illustrative mechanisms):
Lumen narrowing due to secretions and mucus plugging.
Thickening of the airway wall (potentially reversible in some asthma).
Destruction of lung tissue and loss of elasticity (emphysema) leading to airway collapse and gas trapping.
In obstruction, expiratory flow is reduced as airways close prematurely during expiration.
COPD diagnosis workflow
Symptom reporting + history of exposure to risk factors (tobacco, indoor/outdoor pollution, occupational hazards).
Confirmed by spirometry: measure volumes and flows; key metric is FEV1 (Forced Expiratory Volume in 1 second) and FVC (Forced Vital Capacity).
Diagnostic criterion (guideline-based):
fracFEV1FVC < 0.70;(or below lower limit of normal, LLN)LLN consideration: fixed 0.70 cut-point can over/under diagnose at age extremes; LLN values vary by age.
Spirometry interpretation and normal vs obstructed traces
Normal: rapid FEV1 decline after first second; high FEV1/FVC ratio with adequate total exhaled volume.
Obstructive trace: slower exhalation; FEV1 reduced relative to FVC; lower ratio (< 0.70 or LLN).
Clinical manifestations of COPD
Breathlessness (often progressive; worse with exercise).
Sputum production varies; chronic cough and chest tightness common; fatigue.
Exacerbations: flare-ups requiring treatment changes; can be mild, moderate, or severe.
Quality of life reduction and exercise intolerance.
Gender and ethnicity: COPD affects men and women; Indigenous Australians have higher risk (~2.5x compared with non-Indigenous).
Symptom and function assessment tools
COPD Assessment Test (CAT): self-rating of cough, phlegm, chest tightness, exercise tolerance, confidence in getting about, sleep, energy.
Breathlessness assessment: multiple domains—severity, unpleasantness, qualitative qualities, emotional distress, functional impact.
Exacerbation definitions and management implications:
Mild: short-acting bronchodilators only.
Moderate: plus steroids and antibiotics.
Severe: hospitalization required.
Prognosis and prognosis-related considerations: hospitalisation associated with poorer outcomes.
Comorbidities and systemic effects
Very common comorbidity: cardiovascular disease.
Frailty: five components—weakness, slowness, exhaustion, low physical activity, unintentional weight loss.
Skeletal muscle dysfunction and systemic inflammation may worsen activity limitations.
Mental health: depression and anxiety common; cognitive impairment possible with prolonged hypoxemia.
Screening for lung cancer remains important in COPD patients.
Pathophysiology of COPD and emphysema (structure–function changes)
COPD inflammatory changes affect airways, parenchyma, and pulmonary vessels due to chronic irritants.
Structural changes include tissue breakdown (emphysema) and airway remodelling; potential progression to fibrosis in airways.
Emerging evidence links lung-gut microbiota with COPD progression.
Emphysema and gas trapping/hyperinflation
Emphysema: enlargement of air spaces due to destruction of alveolar walls; gas exchange becomes inefficient.
Gas trapping: obstruction leads to incomplete alveolar emptying; increased residual volume (RV).
Dynamic hyperinflation: during exercise, air trapping worsens; diaphragmatic flattening reduces respiratory pump efficiency; increased work of breathing.
Barrel-shaped chest (increased anterior–posterior diameter) reflects chronic hyperinflation.
Gas exchange and ventilation–perfusion mismatch
COPD causes V/Q mismatch and hypoxemia; may contribute to dyspnoea and exercise limitation.
Arterial blood gas (ABG) testing can reveal PaO2, PaCO2, and acid–base status in advanced disease or when oximetry is unreliable.
The COPD cycle and physiotherapy role
Breathlessness leads to activity restriction, social isolation, and mood changes; inactivity reduces respiratory muscle strength and overall exercise tolerance.
Physiotherapy intervention aims to break the cycle via breathlessness management and progressive exercise (pulmonary rehabilitation).
Airways clearance and chronic mucus production
Some COPD patients have mucus hypersecretion (chronic bronchitis phenotype), inflammatory responses damage cilia, impairing mucus clearance.
Increased mucus retention perpetuates inflammation and airway obstruction.
Silent mucus plugs can occur (CT-detected) even without prominent cough/sputum; associated with worse outcomes (lower 6-minute walk distance, more exacerbations).
Guidelines and care standards
Australian guidelines for management of COPD (updated regularly).
Pharmacologic and non-pharmacologic interventions: inhaled bronchodilators, anti-inflammatory agents, vaccination, infection control, and pulmonary rehabilitation.
Australian Clinical Care Standards (2024): emphasis on education/self-management, nonpharmacological breathlessness management, airway clearance, and pulmonary rehabilitation.
Quality indicators: timely referral to pulmonary rehabilitation; access to rehab within four weeks post-hospitalization for COPD exacerbation.
Acute COPD exacerbation management evidence
Evidence supports early mobilization and certain breathing strategies during acute exacerbations.
Moderate-intensity rehabilitation is generally more appropriate after the acute phase rather than during an acute exacerbation.
Principles of assessment and management approach
Biopsychosocial approach: assess physical, psychological, and social factors limiting exercise and breathlessness.
Evidence-based physiotherapy interventions are central to improving function and quality of life in COPD.
Strong therapeutic alliance and patient education are critical; pulmonary rehabilitation has robust evidence base.
Interstitial lung disease (ILD) and idiopathic pulmonary fibrosis (IPF)
Prevalence and common forms
ILD prevalence: about 70--100 per 100,000 population; increasing in some settings.
Idiopathic pulmonary fibrosis (IPF) accounts for roughly one-third of ILD cases.
ILD associations: connective tissue diseases (e.g., rheumatoid arthritis, systemic sclerosis), environmental/occupational exposures (e.g., silicosis, asbestosis), drugs, radiation, infections, and post-COVID ILD.
Pathophysiology and clinical features
Fibrosis leads to reduced lung compliance and low lung volumes; alveolar walls thicken and gas exchange is impaired.
Ventilation–perfusion mismatch is common; hypoxemia during exercise is typical; PaCO2 can be preserved early.
Pulmonary hypertension risk rises with advanced disease due to increased pulmonary vascular resistance.
Quality of life is often severely affected; breathlessness, fatigue, persistent dry cough, and sleep disturbances are common; high dyspnoea burden and low exercise tolerance.
Prognosis
IPF five-year survival around 46% (2022 data), highlighting heavy disease burden.
Management principles
Pharmacologic strategies have evolved with the introduction of antifibrotic drugs, but IPF generally remains progressive.
Nonpharmacologic care includes pulmonary rehabilitation referral, comorbidity management, and often long-term oxygen therapy.
Lung transplantation consideration and palliative care involvement are common in IPF.
Pulmonary rehabilitation in ILD/IPF
Randomized trials show benefits similar to COPD: reduced breathlessness, improved health-related quality of life, and enhanced exercise capacity.
Exercise prescriptions often require interval training due to serious dyspnoea; oxygen supplementation is commonly used during rehab.
Education and psychological support are key components; symptom control for breathlessness and fatigue is important.
Pleural and neuromuscular restrictive conditions
Pleural disease
Pleural effusion: abnormal pleural fluid accumulation that can restrict lung expansion.
Restricted lung expansion and diaphragmatic movement can be improved or managed with physiotherapy and targeted rehab strategies.
Recurrent pneumothorax can worsen restriction and promote inflammation.
Neuromuscular and thoracic cage restrictive conditions
Neuromuscular diseases (e.g., Guillain–Barré syndrome, muscular dystrophies like Duchenne, spinal muscular atrophy) disrupt respiratory pump function.
Thoracic cage deformities (e.g., kyphoscoliosis) contribute to restrictive physiology.
Physiotherapy goals in restrictive disease
Improve exercise capacity and quality of life.
Use pulmonary rehabilitation principles tailored to reduced lung volumes and dyspnoea.
Address comorbidities and optimise symptom control and mobility.
Summary: role of physiotherapy in chronic lung conditions
Core aim: address reduced exercise capacity and troublesome breathlessness to improve quality of life.
Approach: biopsychosocial assessment to identify impairments amenable to physiotherapy and tailor pulmonary rehabilitation-based programs.
Typical physiotherapy interventions across chronic lung conditions
Breathlessness management strategies (pacing, exertion supervision, energy conservation).
Aerobic and resistance training components of pulmonary rehabilitation.
Airway clearance techniques when mucus retention is an issue (especially in COPD with mucus hypersecretion).
Management of comorbidities (frailty, anxiety, depression, sleep disturbance, cognitive concerns).
Neuromuscular and musculoskeletal considerations (flexibility and strength training, posture optimisation).
Critical evidence and guidelines
Pulmonary rehabilitation is strongly supported for COPD and ILD/IPF with improvements in dyspnoea, exercise capacity, and QoL.
Guidelines emphasise early referral and access to pulmonary rehabilitation; nonpharmacological management is a key component of care.
Monitoring attachments and pain relief (clinical attachments frequently seen in acutely unwell patients)
Common monitoring and attachments
Naso-oxygen delivery: nasal cannula/specs for low-flow oxygen.
Pulse oximeter: non-invasive SpO2 monitoring; oxygenation tracking is a vital sign alongside HR, BP, temperature.
Arterial line (A-line): invasive arterial blood pressure monitoring and ABG sampling; flush system to maintain patency.
Example bedside monitor displays include HR, arterial BP, mean arterial pressure (MAP), CVP, respiratory rate, SpO2, and non-invasive BP.
Central venous catheter (CVC): accessed via IJ, subclavian, or femoral vein; used for CVP monitoring, drug/fluids/nutrition delivery; chest X-ray confirmation required post-insertion; avoid dislodgement.
Other common attachments in acutely unwell patients
Intravenous therapy (IV): IV fluids/medications; IV lines often in dorsum of the hand or cubital fossa; gel/catheter management.
Indwelling urethral catheter (IDC): urinary drainage; indications include urinary retention or precise urine output monitoring; normal output sim 30 ml/hour; ensure secure taping and avoid bag tipping during mobilisation.
Nasogastric tube (NGT): enteral nutrition and/or gastric content aspiration; avoid dislodgement; confirm position with chest X-ray before mobilising.
Patient-controlled analgesia (PCA): patient-activated analgesia pump; allows rapid relief of pain; may cause drowsiness or reduced respiratory drive; often requires supplemental oxygen when used.
Epidural analgesia: continuous infusion via epidural catheter; provides pain relief without depressing respiratory drive as much as systemic opioids, but can cause lower limb sensory/motor reduction, reduced gastric motility, and hypotension; mobilise with caution and assess lower limb sensation and strength.
Pain relief and physiotherapy timing
Do not prescribe medications; rather, coordinate care and time PT with pain relief when appropriate (e.g., bronchodilator timing with airway clearance manoeuvres).
Consider how analgesia affects breathing, coughing, and ability to participate in airway clearance techniques or incremental mobilisation.
Ensure patient safety by recognising potential respiratory depressant effects of analgesics (e.g., PCA usage and oxygen therapy needs).
Practical considerations for physiotherapists
Do not tug on or dislodge lines/tubes; confirm securement and position before movement.
When planning mobilisation or airway clearance, consider all attachments (PCA, NIV/ETT, airway devices) and coordinate with the care team.
Know common medications and routes (oral, IV, subcutaneous, regional blocks) and how they might interact with physiotherapy techniques.
Oxygen therapy: indications, delivery, monitoring, and safety
Oxygen is a medicine
Indication: used for acute respiratory failure, hypoxemia, increased metabolic demand (trauma, sepsis), post-operative prophylaxis.
Hypoxemia definition in this con: PaO2 < 80 mmHg; in many settings, hypoxemia is reflected by SpO2 below target ranges.
Precautions, particularly in COPD
COPD patients on high-dose oxygen may have reduced respiratory drive due to loss of hypoxic drive; require careful titration and monitoring.
Oxygen terminology
FiO2: fraction of inspired oxygen; fraction of inspired oxygen value for room air is FiO2=0.21 (21%).
SpO2: peripheral oxygen saturation; normal range typically 95%--98% in healthy individuals without supplemental oxygen.
PaO2: arterial oxygen partial pressure; measured via ABG when invasive measurement is needed.
Delivery systems and their typical FiO2 ranges
Nasal cannula (nasal specs): low-flow delivery; typically 1–4 L/min; approximate FiO2:
1 L/min ~24%
4 L/min ~36%
Simple face mask (CIG/Hudson mask): higher FiO2; flow rates around 5–10 L/min; must not be used if patient cannot tolerate no eating/drinking; claustrophobic for some.
Non-rebreathing mask: closes system to prevent room air entry; can achieve FiO2 up to about 90% under appropriate conditions.
High-flow nasal cannula (HFNC): delivers heated/humidified gas up to about 40 L/min; can deliver near-ambient FiO2 up to sim 100%; allows eating/drinking while on oxygen due to higher flow and humidity.
Non-invasive ventilation (NIV): sealed mask delivering positive airway pressure to support ventilation (e.g., CPAP/BiPAP).
Invasive mechanical ventilation: endotracheal or tracheostomy tube with ventilator support; used when NIV is insufficient or contraindicated.
Monitoring and targets
SpO2 monitoring via pulse oximetry; normal SpO2 typically 95%--98%; targets vary by condition:
Acute medical conditions: target SpO2 generally 92%-96% (practical interpretation from guidelines).
COPD or chronic respiratory failure: target often lower to avoid hypercapnia risks; specific targets individualised.
ABG (arterial blood gas) as the gold standard for arterial oxygenation and ventilation status; provides PaO2, PaCO2, SaO2, acid–base status; used when oximetry is unreliable or when hypercapnia risk exists.
When to escalate oxygen therapy or refer
If high-flow requirements (>4–6 L/min nasal flow or FiO2 targets persist), consider review by senior clinician/ICU.
For persistent desaturation on supplemental oxygen, ABG analysis or invasive monitoring may be warranted.
Practical considerations for physiotherapists
Know patient’s oxygen delivery method and target ranges before initiating mobilisation or airway clearance.
Watch for signs of oxygen-related risks (fire hazards, increased humidity issues, skin breakdown from devices).
Coordinate with the team to time airway clearance and other respiratory therapies with oxygen adjustments.
Common pitfalls and accuracy issues with SpO2
Pulse oximetry accuracy can be affected by
Low perfusion or cold extremities, dark or pigmented skin, movements, nail polish (blue/black), CO poisoning, severe anaemia, or very high PaO2.
SpO2 reflects SaO2 noninvasively but does not provide direct acid–base information.
Summary takeaways for oxygen therapy in physiotherapy practice
Confirm indications, target SpO2, and oxygen delivery method; monitor continuously.
Be aware of COPD patients’ possible reduced hypoxic drive and adjust targets accordingly.
Use ABG selectively when invasive information is needed or O2 delivery does not correct desaturation.
Always consider safety: avoid smoking around oxygen, manage equipment, and ensure humidification when using high-flow systems.
Key numerical references and concepts to remember
COPD diagnostic threshold (spirometry): fracFEV1FVC < 0.70
Alternative: use lower limit of normal (LLN) to reduce misclassification at age extremes.
Common prevalence and risk figures mentioned in the lecture:
Australians with chronic lung condition (2022): ~34%
Global death rate variety by country (respiratory disease): India 133/100,000, PNG 204/100,000, Australia 23/100,000
COPD in Australians 40+ years: about 1/13approx 7.7%
Indigenous Australians with COPD risk: ~2.5x non-Indigenous risk
IPF five-year survival (2022): 46%
Pathophysiology terms to recall
Gas trapping and dynamic hyperinflation: due to expiratory flow limitation and premature airway closure
Barrel chest appearance: increased AP diameter due to hyperinflation
V/Q mismatch leading to hypoxemia
Emphysema: alveolar wall destruction; enlarged air spaces
Oxygen therapy targets and values
Room air: FiO2=0.21 (21%)
Nasal cannula: 1–4 L/min to ~FiO2approx 0.24-0.36
Simple mask: higher FiO2 (often up to around 60% depending on flow)
Non-rebreather: FiO2 up to near 0.9-1.0 under appropriate setup
HFNC: up to 40L/min with humidification; FiO2 up to nearly 1.0
Normal SpO2 range: 95%--98%; LLN varies by age (e.g., 18-year-old LLN sim 96%, 70-year-old LLN sim 94%)
Practical clinical care standards cited
Pulmonary rehabilitation is a cornerstone intervention with strong evidence across COPD and ILD/IPF
Time to referral to rehab and re-access after hospitalisation are monitored care indicators in healthcare standards.
Practical cues for exam-style understanding
Distinguish obstructive vs restrictive by spirometry patterns and clinical features:
Obstructive: reduced FEV1, reduced FEV1/FVC, hyperinflation signs; examples include COPD and asthma.
Restrictive: reduced lung volumes with relatively preserved or high FEV1/FVC; examples include ILD/IPF, pleural diseases, neuromuscular restrictions.
Understand the role of pulmonary rehabilitation as a non-pharmacological mainstay for improving dyspnoea and exercise tolerance in both COPD and ILD/IPF, with evidence-based exercise components and education.
Recognise that oxygen therapy is a medication with specific indications, delivery methods, target ranges, and safety considerations, particularly in COPD and acute respiratory illness; know the basic delivery systems and typical FiO2 ranges for common devices.
Be able to discuss how attachments and devices in acutely unwell patients influence physiotherapy management, including timing with analgesia, risk of line dislodgement, and safe mobilisation practices.