PS201 - Week 5 Cue Cards - Acute Lung Conditions and Secretion Clearance
Overview and session objectives
This lecture introduces physiotherapy in acute lung conditions as a continuation of prior modules on respiratory physiology, pathophysiology, and secretion clearance, and as a companion to chronic lung condition physiotherapy.
Objectives: provide an overview of common acute lung conditions, outline the pathophysiological problems they cause, and discuss how physiotherapy might address these problems (and when it may not). Future sessions will cover more detail on pneumonia, asthma, and other conditions.
Emphasis on the importance of understanding pathophysiology in acute care to know what physiotherapy can influence and what requires medical/pharmacological management. A guiding quote from readings: if problems can be influenced by physical means, physiotherapy is indicated; also indicated when preventive measures can be taken.
The session centres on acute insults on otherwise normal lungs and examples include trauma, post-surgical changes with infection, inflammatory conditions, pulmonary oedema, and pulmonary embolus. All of these can affect ventilation–perfusion (V/Q) matching and thus oxygen delivery, which is a primary problem to address.
Key pathophysiological concepts
Ventilation–perfusion matching (V/Q) is central to gas exchange; disruptions lead to impaired oxygen delivery to tissues.
Primary clinical focus: problems that reduce ventilation (airflow into the alveoli) versus problems that reduce perfusion (blood flow to the alveoli).
Inflammation and infection can impair gas exchange and may accompany each other or occur independently.
Pulmonary oedema represents a mixed picture with cardiac origin causing venous congestion and interstitial/alveolar fluid, impairing ventilation.
The clinician must distinguish whether physiotherapy will help (ventilation problems) or not (perfusion problems like pulmonary embolus), as treatment priorities differ.
Ventilation-focused acute events
Atelectasis
Definition: collapse of alveoli (alveolar collapse).
Causes (multiple pathways):- Airway obstruction by sputum or other material (e.g., foreign body in larger bronchi).
Lung compression (e.g., pleural effusion; external compression).
Diaphragm elevation (post-thoracic or abdominal surgery; posture-related).
Reduced inspiratory volume leading to hypoventilation and reduced functional residual capacity (FRC).
Range of involvement: from microatelectasis to full lobar collapse.
Practical examples and orientation cues:- Chest X-ray signs: when viewing the film as if the patient is facing you, the left side of the image corresponds to the patient’s right side.
Radiopaque structures (bone, muscle, blood) appear white; aerated lung appears darker.
Example given: right upper lobe collapse due to a large tumour obstructing the right upper lobe bronchus; the horizontal fissure (which separates upper and middle lobes) should be at the level of the fourth rib; shift of fissure upward indicates air has been sucked out (collapse).
Functional consequence: alveoli lose air, reducing gas exchange; difficult to re-expand due to surface tension; FRC reduction worsens oxygenation.
Physiotherapy implications: if atelectasis is present and ventilation is impaired, techniques to increase lung volume are indicated (see below).
Infection and consolidation (pneumonia) and aspiration
Pneumonia:- Alveoli filled with inflammatory debris, bacterial/viral organisms, and cellular byproducts, impairing gas exchange.
Consolidation differs from atelectasis in imaging: alveolar space is filled with inflammatory exudate, not collapsed air spaces; fissures and borders may stay in place.
Aspiration:- Entry of oropharyngeal materials into the lung; debris fills alveoli causing consolidation and impaired gas exchange.
Radiographic example described: right middle lobe consolidation with white (opacity) area near the heart border on the chest X-ray, indicating alveolar filling instead of air.
Consolidation versus collapse:- In consolidation, fissures may remain in their normal positions while the lung tissue is filled with dense material.
In atelectasis, there is often displacement of fissures/diaphragms due to volume loss.
Practical relevance: both processes disrupt gas exchange; however, their management and interpretation in imaging differ.
Inflammation (inflammatory processes with or without infection)
Inflammation as a broader immune response to irritants (smoke, pollutants) or infection; can occur in airways (e.g., asthma) or alveoli (e.g., ARDS).
Key distinction: inflammation without infection is possible; infection is typically accompanied by fever, whereas pure inflammation may not have fever.
Mechanism: recruitment of inflammatory cells (leukocytes) and release of chemicals that can damage lung tissue.
Clinical implication: inflammation can narrow airways and impair ventilation, contributing to V/Q mismatch.
ARDS example (acute respiratory distress syndrome): severe lung disease where pulmonary vascular permeability is increased and fluid leaks into the alveolar space, significantly impairing ventilation and gas exchange.
Perfusion-focused acute events
Pulmonary embolus (embolism)
Pathophysiology: occlusion of a pulmonary artery leading to reduced perfusion to the affected lung region; gas exchange impaired due to lack of blood flow to ventilated tissue.
Classic clinical picture: acute onset chest pain, shortness of breath, tachypnoea, tachycardia, and sometimes fever.
Hypoxic response: low oxygen levels trigger hypoxic pulmonary vasoconstriction, redirecting blood to better-oxygenated lung regions (redistribution of perfusion).
Diagnostic approach: CT pulmonary angiography (CTPA) is a common diagnostic test; has many features overlapping with other respiratory conditions, so accurate assessment is critical.
Physiotherapy considerations: since perfusion is the primary issue, increasing ventilation alone does not resolve the underlying problem; management typically requires pharmacological treatments (e.g., anticoagulation, thrombolysis in select cases). Mobilisation may be unsafe during an acute embolus until it is medically managed.
Pulmonary oedema (cardiogenic oedema)
Pathophysiology: usually due to left-sided heart failure; backlog of blood in the left atrium then pulmonary vasculature; capillary pressure increases, causing leakage of fluid into the interstitium and alveoli.
Consequence: oedema reduces ventilatory capacity and impairs gas exchange (ventilation is reduced in affected areas).
Clinical note: part of the spectrum of V/Q mismatch; ABG changes and hypoxia are common.
Practical implication: pharmacological management (e.g., diuretics, rate control, and optimisation of cardiac function) is typically needed; physiotherapy can assist with ventilation strategies but cannot resolve the underlying perfusion problem without medical treatment. Mobilisation may be contraindicated or delayed until stabilisation.
Gas exchange implications and clinical reasoning
Reduced ventilation leads to deoxygenated blood and altered arterial blood gases (ABGs) with hypoxia; the clinician looks for signs of gas exchange impairment and tries to identify the underlying cause.
In atelectasis, reinflation is challenging due to increased surface tension once alveoli collapse, reinforcing the role of physiotherapy techniques to restore lung volume.
In perfusion-limited conditions (embolus), increasing ventilation alone is unlikely to correct gas exchange; targeted medical therapy is essential, and mobilisation may be unsafe until stabilised.
Across conditions, many observations (e.g., breath sounds, cough, sputum production, oxygenation status) may appear similar, highlighting the need for pathophysiological reasoning to guide management.
Physiotherapy interventions in acute lung conditions
Goals and general approach
Increase lung volume and prevent/reverse atelectasis to improve ventilation.
Clear secretions when airway clearance is impaired by infection, inflammation, or mucus obstruction.
Limit further airflow obstruction when inflammation narrows airways (e.g., asthma, bronchitis).
Recognise situations where physiotherapy will not directly treat the primary problem (e.g., pulmonary embolus, oedema due to heart failure) and coordinate with medical management.
Techniques to increase lung volume and improve ventilation
Positioning strategies to optimise ventilation (e.g., upright positions, lateral positioning to recruit dependent regions).
Mobilisation and gradual ambulation (standing, stepping) to enhance regional ventilation and promote lung expansion.
Thoracic expansion exercises to improve chest wall/knee mobility and inspiratory capacity.
Practical clinical rationale: these strategies aim to counteract atelectasis, improve FRC, and optimise oxygenation.
Airway clearance and secretion management
When secretions hinder clearance (e.g., pneumonia, post-operative atelectasis), employ airway clearance techniques (ACTs):- Active Cycle of Breathing Techniques (ACBT)
Positive Expiratory Pressure (PEP)
Effective Forced Expiratory Technique (FET)
Positioning to facilitate drainage
Goals: mobilise secretions, improve airway patency, and facilitate gas exchange.
Role in inflammation and airway obstruction
If airway inflammation narrows airways, physiotherapy can help minimise further reductions in airflow through techniques that support airway clearance and promote optimal ventilation.
Note: the effectiveness of physiotherapy depends on the underlying cause (ventilation impairment vs perfusion impairment).
Distinguishing scenarios and clinical decision-making
If V/Q mismatch is due to reduced ventilation (e.g., atelectasis, pneumonia with secretion burden, inflammation causing airway narrowing), physiotherapy interventions to improve ventilation and clear secretions are likely beneficial.
If V/Q mismatch is due to reduced perfusion (e.g., pulmonary embolus), physiotherapy should not substitute medical therapy; mobilisation may be contraindicated until embolus is treated.
The clinician uses pathophysiology to generate hypotheses about physiotherapy involvement and to prioritise interventions accordingly.
Risk factors, comorbidity, and patient groups
Acute lung conditions can occur in anyone, including those with otherwise healthy lungs (e.g., trauma, pneumonia).
Higher-risk groups include:- Current smokers: reduced mucociliary clearance, increased secretions, plus potential structural damage.
Older adults: reduced lung elasticity and FRC due to aging, possible cardiac comorbidities.
Comorbidity definition: any additional medical condition beyond the primary or index condition that can influence management and outcomes.
These factors influence assessment, prognosis, and the suitability/direction of physiotherapy in acute care.
Clinical relevance and next steps
In clinical practice, initial assessment should reveal problems that physiotherapy can influence and identify those that require medical/pharmacological management.
The session prepares students for integrating theory with clinical reasoning in acute care settings and highlights the need for multidisciplinary collaboration.
The course will include a video of an acute care patient with acute lung injury to illustrate these concepts in a real-world context.
Connections to prior learning and real-world relevance
Builds on foundational physiology of the respiratory system and prior lectures on secretion clearance.
Bridges to future content on pneumonia, asthma, and chronic lung conditions.
Emphasises practical clinical decision-making: differentiating problems amenable to physiotherapy from those requiring pharmacological or surgical management, and recognising when mobilisation is contraindicated.
Key formulas and numerical concepts (LaTeX)
Functional residual capacity concept: FRC = RV + ERV where RV is residual volume and ERV is expiratory reserve volume.
Ventilation–perfusion ratio concept: \text{V/Q} =\frac{V}{Q} where V is ventilation and Q is perfusion; disruptions lead to hypoxaemia and altered gas exchange.
Note on imaging and clinical signs (summary)
Chest X-ray interpretation cues: orientation with the patient facing you; the L marker corresponds to the patient’s left; radiopaque structures (bone, muscle) appear white; air-filled lung appears darker.
Distinguishing atelectasis from consolidation on imaging: atelectasis may shift fissures/diaphragms due to volume loss; consolidation typically does not shift fissures but shows focal area of opacity near the heart border.
PE and oedema share symptoms with other acute lung conditions; diagnosis relies on imaging (e.g., CT pulmonary angiography for embolus) and clinical context, and management is disease-specific.
LECTURE 2: Secretion Clearance
Overview
Secretion clearance is a vital topic in cardiopulmonary physiotherapy. This session covers the physiology of secretion clearance, main clearance mechanisms, factors that alter physiology, and practical measures to assess and improve clearance.
Key clearance mechanisms in the healthy lung:
Alveolar clearance (small role)
Mucociliary clearance (primary mechanism)
Cough (secondary mechanism)
Special focus on forced expiratory techniques (FET) and dynamic compression/equal pressure point concepts to facilitate secretion clearance in clinical practice.
Impairments in physiology can necessitate assistance from airway clearance techniques (ACT) and other strategies.
Outcome measures for secretion clearance include symptom scales, auscultation, sputum volume, and imaging (research context).
The Three Main Clearance Mechanisms
Alveolar clearance occurs at the level of the alveoli.
If particles reach the alveoli:
Soluble particles: pass through the alveolar-capillary membrane into the bloodstream.
Insoluble particles: phagocytosed by macrophages and transported to ciliated airways for removal.
This is a minor pathway; only a small amount is typically removed here.
Mucociliary clearance (the mucociliary escalator)
Primary defence mechanism in healthy lungs; active continuously.
Airway lining and key cell types:
Goblet cells: produce mucus.
Ciliated cells: contain 200 cilia per cell that beat to transport mucus.
Epithelium lines airways from nasal cavity to terminal bronchioles.
Mucus layers:
Sol (watery) layer: lies closest to the cilia; cilia beat within this layer.
Gel layer: atop the sol layer; produced by goblet cells; provides a chemical shield with antimicrobial substances.
Function: cilia beat in the watery sol layer to move mucus (and trapped secretions) upward toward the throat where it can be swallowed or cleared.
Normal functioning depends on: intact cilia, mucus of appropriate watery consistency for cilia to move effectively.
Disruptors of mucociliary clearance include:
Cilia damage or destruction (e.g., cigarette smoke can paralyse or destroy cilia).
Abnormal mucus properties (too thick or excessive).
Airway or lung tissue damage (airway remodelling, tissue injury).
Environmental and disease factors that impair mucus clearance:
Smoking and smoke exposure; dust and pollution can damage cilia.
Inflammation and infection causing ciliary damage and increased mucus production.
Chronic lung diseases with airway narrowing or tissue damage, leading to mucus retention and impaired clearance.
Consequences of impaired mucociliary clearance:
Retained mucus creates a site for recurrent infections.
Toxic mucus can cause airway damage and structural changes (e.g., bronchiectasis).
Airway narrowing and wall inflammation reduce airflow and gas exchange; can hinder inhaled medication delivery.
Symptoms include shortness of breath, reduced exercise tolerance, wheeze; cough can have emotional and social impacts.
Cough (secondary defence mechanism; activated when mucociliary clearance is insufficient)
Four stages of an effective cough:
§ Irritation: reflex or voluntary initiation.
Inspiration: deep enough inspiration to generate large lung volume.
Compression/closure: vocal cords/glottis close to build up intrathoracic pressure.
Expulsion: rapid contraction of expiratory muscles (especially the abdominal muscles) to generate a strong expulsion of air through a partially opened glottis.
Distinctions:
Cough: forced expiration with closed glottis (closed glottis).
Huff: forced expiration with an open glottis (no strong expulsive force like a cough).
Documentation in assessment:
Assess whether cough is strong or weak; dry vs moist (presence of mucus); effective vs ineffective; productive vs nonproductive.
An ineffective cough may involve impairment in any of the four stages (e.g., post-surgical impairment of inspiration or expiration).
Precautions/contraindications to coughing:
Respiratory system: risk of bronchospasm, airway trauma, laryngeal trauma; paroxysms of coughing.
Hemodynamic: increased intrathoracic pressure can reduce venous return or cause hypertension and arrhythmias; could raise intracranial pressure (contraindicated in traumatic brain injury, ocular surgery, aneurysm, etc.).
Genitourinary: chronic cough can cause stress incontinence or prolapse.
Clinical implications: coughing is a key target for airway clearance but must be managed safely in patients with instability or contraindications.
What Happens in Normal Secretion Clearance: Physiological Interplay
Secretion clearance depends on three interconnected factors:
1) Airflow to mobilise secretions behind them.
2) Dynamic compression of the airways during forced expiration.
3) Position and behaviour of the equal pressure point (EPP) along the airway tree.
Two-phase gas-liquid flow principle (relevance to secretion movement):
Gas flow over a liquid-lined airway transmits momentum to the liquid ( mucus ) layer.
Greater air velocity leads to greater movement of mucus.
Practical implication: increasing lung volume and airflow helps mobilise secretions.
Notation: if vg is air velocity, and L̇ is mucus movement rate, then a simple proportional relation can be written as: dot{L} = alpha vg where alpha is a geometrical or system-specific constant.
Dynamic compression during expiration:
During forced expiration, mucus movement relies on pressure gradients between alveolar pressure (PA) and external airway pressure (P, from pleural pressure + elastic recoil).
In a tract from alveolus to mouth, P_A decreases from a peak (e.g., 20) toward atmospheric pressure (0) at the mouth.
There exists a point along the airway where PA equals P; this is the equal pressure point (EPP).
Proximal to the EPP, external pressure exceeds internal pressure, causing airway narrowing; distal to EPP, airway may stay open due to the gradient.
Example from the visualisation described: initial alveolar pressure P*A = 20, external airway pressure P*= 10; EPP occurs when PA = P= 10
The EPP is denoted on diagrams; a red cross marks the EPP where internal and external pressures are equal.
Effect of lung volume on EPP location:
Low lung volume (low tidal volume) shifts EPP to more peripheral airways, enabling clearance from very small airways when using a forceful expiration.
High lung volume shifts EPP more centrally toward larger airways (closer to the throat), enabling clearance from more central airways.
In summary: EPP peripheral low lung volume; quad EPP central high lung volume
Manipulating EPP to enhance clearance (clinical strategy):
Use low-volume huffs to target peripheral secretions; progress to higher-volume huffs to clear central secretions.
This combination of huff plus breathing control is called Forced Expiratory Technique (FET).
FET principles apply to structurally normal lungs, but effectiveness is reduced in chronic lung disease due to:
Airway obstruction reducing driving pressure during expiration.
Loss of elastic recoil shifting EPP peripherally even during normal expiration.
To counteract reduced driving pressure and peripheral EPP in disease, apply Positive Expiratory Pressure (PEP) at the mouth to:
Keep airways open during expiration, maintaining expiratory flow.
Move EPP toward larger airways (trachea) with more cartilaginous support, reducing airway collapse.
Practical Implications for Chronic Lung Disease
Chronic airway obstruction and loss of elastic recoil shift the EPP peripherally and reduce expulsive efficiency.
Implication: FET effectiveness is reduced; adjuncts like PEP can improve airway patency and clearance.
Other disease features that impair secretion clearance:
Airway narrowing, lung tissue damage, mucus hypersecretion, and inflammation can all hinder clearance.
Therapeutic strategies to improve clearance in disease:
PEP devices and breathing strategies to increase expiratory pressure and maintain airway patency.
Postural drainage and positioning to maximise gravity-assisted clearance.
Exercise to improve overall airflow and mucus clearance.
Hydration and humidification to optimise mucus rheology.
Summary Diagrammatic Concepts (Key Takeaways)
The three mucociliary clearance systems, and how impairment leads to reliance on cough.
How factors like smoke, infection, and inflammation impair mucociliary clearance and how physiotherapy can compensate.
The role of cough stages, and how to document cough quality (strength, dryness/moisture, effectiveness, productivity).
The equal pressure point concept and how EPP location is affected by lung volume and external pressures.
Techniques to manipulate EPP (low-volume vs high-volume huffs) and the use of PEP to enhance expiratory flow.
Impairments and Related Pathologies
Mucociliary clearance impairment consequences:
Increased risk of infection due to retained mucus.
Toxic mucus can cause airway damage and bronchiectasis with involved airway dilation, wall inflammation, and airway obstruction.
Reduced gas exchange due to airway obstruction and mucus plugging.
Interference with delivery of inhaled medications.
Cough-related issues:
Bronchospasm, airway trauma, laryngeal trauma, paroxysms.
Hemodynamic effects: reduced venous return with low blood pressure, or increased blood pressure and arrhythmias with coughing-induced intrathoracic pressure changes.
Raised intracranial pressure, posing risk in patients with brain injury, ocular surgery, or cerebral aneurysms.
Genitourinary effects: stress incontinence or pelvic organ prolapse with repeated coughing.
Measuring Secretion Clearance: Outcome Measures and Validity
Symptom-based (patient-reported) measures:
COPD Assessment Test (CAT): simple 0–5 scale questions on cough and phlegm, among others; supports assessment of symptom burden and quality of life.
Breathlessness, Cough, and Sputum Scale: 0–4 scale rating for dyspnoea, cough, and sputum.
Objective measures and their limitations:
Auscultation: listening for crackles or wheezes; common in practice but limited validity/reliability.
Sputum volume measurement: not reliably indicative of clearance; clearance can improve without immediate sputum production.
Imaging-based measures (research context): SPECT (Single Photon Emission Computed Tomography) using radiolabelled aerosols to visualise mucus clearance before and after interventions.
Practical considerations:
Symptom measures provide useful, non-invasive insights, but may not perfectly reflect clearance efficacy.
Auscultation and sputum measurements may have limited reliability; re-evaluation after clearance strategies is important.
In practice, improvements may take time (e.g., 20 minutes or more) for peripherally moved secretions to appear in the central airways.
Practical Techniques for Secretion Clearance
Forced Expiratory Techniques (FET): cough and huff as core components; emphasis on equal pressure point manipulation via lung volume and expiratory effort.
Active Cycle of Breathing Technique (ACBT): a combination of breathing control, thoracic expansion exercises, and FET components; details available in technique handbooks and bronchiectasis toolbox.
Postural drainage and positioning: optimising gravity effects to assist mucus clearance.
Hydration and humidification: improving mucus rheology to facilitate clearance.
Exercise: increasing overall airflow and cardiovascular efficiency to aid secretion movement.
Devices to aid clearance:
Positive Expiratory Pressure (PEP) devices to maintain airway patency during expiration.
Other devices as introduced in subsequent teaching sessions.
Practice resources:
Learn online videos on Active Cycle Breathing Technique and Forced Expiratory Technique from the bronchiectasis toolbox for theory and technique demonstrations.
Connections to Practice and Real-World Relevance
This session provides background for practical sessions on secretion clearance techniques and the rationale for using FET, huffs, and ACBB in acute care and chronic lung disease.
Understanding the equal pressure point and dynamic compression informs how to tailor techniques to target peripheral vs central secretions.
Recognising impairments (smoking, pollution, infection, inflammation, bronchiectasis, COPD) helps clinicians anticipate challenges and choose appropriate ACT strategies.
Ethical and practical implications: ensure safety when employing cough-based techniques in patients with cardiovascular instability or intracranial pressure concerns; use non-invasive symptom measures when appropriate; monitor for adverse effects (bronchospasm, trauma).
Quick Summary for Exam Prep
The three main clearance mechanisms: alveolar clearance, mucociliary clearance (mucociliary escalator), and cough.
Mucociliary clearance depends on functional cilia, appropriate mucus consistency, and intact airway epithelium; impairment due to smoke, dust, infection, inflammation, and chronic lung disease leads to mucus retention and infection risk.
Cough stages: irritation, inspiration, compression (glottis closed), expulsion; documentation factors include strength, moisture, effectiveness, and productivity; precautions include bronchospasm, trauma, hemodynamic effects, intracranial pressure, and genitourinary stress incontinence.
Secretion clearance relies on airflow, dynamic airway compression, and EPP location; EPP moves with lung volume; manipulating EPP via low/high-volume huffs and external PEP improves clearance.
In chronic lung disease, obstructions and loss of elastic recoil shift EPP peripherally; PEP and other ACTs help counteract these changes.
Outcome measures include symptom scales (CAT; breathlessness, cough, sputum scale), auscultation, sputum volume, and advanced imaging (SPECT) in research.
Practical techniques: ACBB/ACBT, FET, cough/huff, positioning, hydration/humidification, exercise, and PEP devices.
Additional resources: bronchiectasis toolbox videos and online materials for technique demonstrations.
