Respiratory PBL ILO’s Flashcards
Structure and function of the chest wall:
The chest wall is compromised of skin, fat, muscle and the thoracic Skelton. It provides protection to vital organs (eg heart and major vessels, lungs and liver).
Structure and function of the pleural cavity:
The pleural cavity is a space between the visceral and parietal pleura. The space contains a tiny amount of serous fluid, which has two key functions:
The serous lucid continuously lubricates the pleural surface and makes it easy for them to slide over each other during lung inflation and deflation.
The serous fluid also generates surface tension which ills the visceral and parietal pleura adjacent to each other allowing the thoracic cavity to expand during inspiration.
Name the respiratory muscles of inspiration:
Sternocleidomastoid
Scalenes
Pectoralis major and minor
Sarratus anterior
External intercostals
Diaphragm
Nam the expiratory muscles of respiration:
Internal intercostals
Obliques
Transverse Abdominis
Recuts Abdominis
Structure and function of the sternum:
Maubrium
Body
Xiphisternum
Protection. Your sternum, along with your ribs, works to protect the organs of your torso, such as your heart, lungs, and chest blood vessels.
Support. Your sternum also provides a connection point for other parts of your skeletal system, including your collarbone and most of your ribs.
Function of the ribs:
The ribs are the bony framework of the thoracic cavity. The ribs form the main structure of the thoracic cage protecting the thoracic organs, however their main function is to aid respiration. There are twelve pairs of ribs. Each rib articulates posteriorly with two thoracic vertebrae by the costovertebral joint.
Function of thoracic vertebrae:
Your thoracic spine consists of 12 vertebrae, labeled T1 through T12. Vertebrae are the 33 individual, interlocking bones that form your spinal column. These bones help protect your spinal cord from injury while allowing you to twist and turn. Your thoracic spine and ribcage also protect your heart and lungs. The joints in your thoracic spine are tight enough to protect these vital organs but loose enough to allow for the movements of breathing — inhaling and exhaling.
Structure and function of the thoracic inlet/ outlet
The thoracic inlet/ outlet (clinically) is defined as the space in the lower neck between the thorax and axilla through which the subclavian vein, subclavian artery, and brachial plexus travel from their central origins to their peripheral termini.
Intercostal spaces
The intercostal spaces are the spaces between the ribs, there are 11 on each side and are numbered according to the rib which is the upper border of the space. They contain three layers of muscle, the external, internal and innermost layers, with the neurovascular bundle found between the internal and innermost layers.
Describe and explain the 3 types of Intercostal muscles:
The external intercostal muscles
• Outermost muscle, has fibres which run in a downwards, forwards and medial direction from the inferior border of the superior rib to insert on the outer lip of the inferior rib.
The internal intercostal muscle • The middle layer of the intercostal space. This muscle has fibres which run in a downwards, backwards and lateral direction from the inferior border of the superior rib to insert on the superior border of the inferior rib, The innermost intercostals • 3 muscles which are collectively known as the transverse thoracic group.
What is the neurovascular bundle and where would it be found?
The neurovascular bundle consist of a nerve, artery and a vein between the internal and innermost muscles.
Where does posterior intercostal artery arise from?
Thoracic aorta
Where o the anterior intercostal arteries arise from?
Internal thoracic musculophrenic
Where do posterior intercostal veins drain to?
Azygos system
Where do anterior intercostal veins drain in to?
Internal thoracic or musclophrenic
What do the intercostal nerves supply?
• The intercostal nerves supply the intercostal muscles, the parietal pleura and overlying skin and supply somatic innervation.
Diaphragm:
Diaphragm
• Dome shaped skeletal muscle with a central tendon, it has a left and right dome.
• The origin of the diaphragm consists of three parts, the sternal which rises at the posterior surface of the xiphisternum, the costal which rises at the lower 6 ribs and their costal margins and the vertebral which rises from the right crus (from bodies L1-3), and left crus (from L1-2), medial & lateral arcuate ligaments.
• T5 of the thoracic vertebrae during expiration
• Openings for the inferior vena cava (T8) oesophagus (T10) and aorta (T12)
• Fibrous pericardium fused to the central tendon.
The costophrenic recess is the area between the chest wall and the dome
Functional anatomy of ventilation - inspiration/ inhalation:
• Inhalation is initiated by the contraction of the diaphragm.
• Contents of the abdomen are moved downward and the ribcage to expands
• Chest cavity expands so the lungs can also expand into it.
• Larger thoracic volume and a negative pressure (with respect to atmospheric pressure) inside the chest.
• The external intercostal muscles also contract to pull the ribcage both upward and outward when you inhale to further help enlarge the chest cavity, decreasing the pressure and causing air to flow in via the pressure gradient.
Functional anatomy of ventilation - expiration/ exhalation:
• Exhalation is generally a passive process since the lungs have a natural elasticity
• They recoil from the stretch of inhalation and air flows back out until the pressures in the chest and the atmosphere reach equilibrium therefore air travels out.
Inspiratory accessory muscles:
• There are accessory muscles of inspiration which are recruited during exercise or patients with breathing difficulties.
• The pectoralis major and pectoralis minor, the serratus anterior, the sternocleidomastoid is and scalene all assist in elevating the rib cage during inhalation.
Costochondral joint:
- Costochondral joint
• The costochondral joint is the connection between a rib and its costal cartilage.
• The joint is formed by two articular surfaces: the roughened cup-shaped anterior end of the rib and the rounded lateral end of the costal cartilage.
• They costochondral articulations themselves are immobile, they do not permit movement.
• But the costal cartilages provide a flexible attachment for the anterior ends of the ribs to the sternum and may undergo slight bending and twisting movements that facilitate widening of the thoracic diameters during breathing.
Costovertebral joint:
- Costovertebral joint
• The costovertebral joints are the joints that connect the ribs to the vertebral column.
• The movements of these joints are called ‘pump handle’ or ‘bucket-handle’, the long axes of the necks of the rib move in this motion, resulting in raising and lowering the sternal ends.
• During inspiration, the transverse diameter of the thorax is increased by the ribs swinging outward.
Sternocostal joint:
- Sternocostal joints
• The sternocostal joints lie between the costal cartilages of the first to the seventh ribs and the sternum.
• The joint between the first rib and the sternum is cartilaginous, but all others are synovial.
• Each is surrounded by a capsule and supported by radiate movements. The main function of the sternocostal joint is to facilitate the mechanical ventilation by allowing the costal cartilage to glide with the ribs during inspiration and expiration.
Three stage stress response:
The stress response is considered to include three stages—alarm, resistance, and exhaustion:
Alarm stage: activation of the hypothalamus, sympathetic nervous system and adrenal glands
Resistance stage: hormone levels raised, essential body systems are at peak performance
Exhaustion stage: body is unable to respond further/is damaged by the increased demands of the stress
Physiological features of stress response:
Physiological features of stress response:
Significant effects of the stress response include the following:
• Increased cardiac output (Elevated blood pressure and increased heart rate)
• Bronchodilation and increased ventilation
• Increased blood glucose levels (resulting from glycogenolysis and gluconeogenesis in the liver and protein catabolism in muscle, as well as lipolysis )
• Arousal of the central nervous system
• Decreased inflammatory and immune responses (cortisol reduces the early and later stages)
What is lidocaine and how does it work?
Local anaesthetic involves numbing an area of the body without causing someone to lose consciousness
This is usually for smaller operations or procedures
Can recover from them quicker than the use of general anaesthetic
How do they work:
• Stop the nerves in a part of your body sending signals to your brain
• Won’t feel any pain but can feel pressure / movement
• Takes a few minutes to lose feeling
• Medication usually wears off after a couple of hours
Forms of local anaesthetic:
• Injections
• Creams
• Gels
• Sprays
• Ointments
Uses of local anaesthetics:
Uses of local anaesthetics:
• Treating pain ○ e.g. sprays and gels can help with mouth ulcers and sore throats ○ e.g. long term joint pain can be treating by combination of local anaesthetic and steroid injection • Preventing pain during + after surgery ○ Usually in minor procedures such as wisdom tooth removal, minor skin operations on lesions, some eye surgeries, biopsies, performing a lumbar puncture, inserting a central line, hand surgery, sutures ○ Can be used in major surgery if the patient needs to be away e.g. certain brain surgeries • Epidurals and spinal anaesthetics ○ Local anaesthetic injected into the epidural space or spine ○ Numb large areas of the body by stopping pain signals travelling along nerves in the spine ○ Child birth, hip replacements • Peripheral nerve block ○ Inject local anaesthetic to numb nerves supplying a particular part of the body e.g arm ○ Ultrasound scan is used to pinpoint the nerve when injecting ○ Takes 30mins to become effective
Risks and side effects of lidocaine:
Risks and side effects
• Some discomfort when injection is given
• Tingling sensation as medication wears off
• Minor bruising, bleeding or soreness at site of injection
• Can sometimes get temporary side effects:
○ Dizziness
○ Headaches
○ Blurred vision
○ Twitching muscles/shivering
○ Continuing numbness, weakness or pins and needles
○ Find it hard to urinate/leaking after epidural
• Very rarely can have an allergic reaction. Can lead to fits (seizures) or cardiac arrest
Demonstrate knowledge of the changes in pleural pressure during respiration:
· The alveolar and atmospheric pressures are greater than the intrapleural pressure. Therefore, connections between the alveoli and pleural space, or surrounding atmosphere and pleural space, will lead to air moving down a pressure gradient into the pleural space.
· This increases the intrapleural pressure, potentially compressing the lungs. Air will continue to move into the pleural space until the pressure gradient equilibrates or the connection into the pleural space seals off.
What happens in a tension pneumothorax?
· In a tension pneumothorax, air enters the pleural space through a one-way valve and is therefore unable to leave the pleural space. The intrapleural pressure exceeds the atmospheric pressure, leading to collapse of the ipsilateral lung and a shift of the mediastinum away from the pneumothorax.
· In severe cases, the increased intrapleural pressure can compress the heart and surrounding vasculature, reducing cardiac output and venous return. If untreated, this may lead to cardiac arrest.
Pleural pressure during inspiration:
Inspiration:
· Diaphragm and inspiratory intercostal muscles actively contract expansion of thorax. Interpleural pressure drops (usually ~-4mmHg at rest) becomes more subatmospheric/more negative
· Intrapleural pressure drops
· Lower alveolar pressure compared to atmospheric pressure allows air to flow
1. Diaphragm contracts which causes thorax to expand
2. This pulls the outer pleural membrane (the one facing the thoracic cavity) causing a drop in intrapleural pressure
3. The inner pleural membrane then pulls on the lungs, causing the lungs to expand, this causes the pressure gradient, allowing air to flow into the lungs
*opposite in expiration
Pleural pressure during expiration:
Expiration
· Relaxation of the diaphragm and elastic recoil of tissue decreases thoracic volume increasing intraalveolar pressure and intrapleural pressure
· Higher alveolar pressure compared to atmospheric pressure allows air to flow out of lungs, alveoli shrink due to elastic recoil
*If intrapleural pressure becomes positive e.g. lungs become punctured/damaged) – causes lungs to collapse
First and second step of taking a chest x ray:
First step: confirm details
• Patient details: name, date of birth and unique identification number. • Date and time the film was taken • Previous imaging: useful for comparison.
Second step: check the quality of the chest radiograph (RIPE)
Rotation
The medial aspect of each clavicle should be equal distance from the spine.
The spinous processes should also be in vertically orientated against the vertebral bodies.
Inspiration
The 5-6 anterior ribs, lung apices, both costophrenic angles and the lateral rib edges should be visible.
Good inspiration by the patient during the X-ray will stretch the thoracic cavity outwards and separate the pulmonary vessels, allowing for greater visualisation.
Projection
Note if the film is front to back (anterior to posterior - AP) or back to front (posterior to anterior - PA)
If there is no label, then assume it’s a PA film (if the scapulae are not projected within the chest, it’s PA).
Exposure
The left hemidiaphragm should be visible to the spine and the vertebrae should be visible behind the heart.
ABCDE interpretation to a chest x ray:
Third step: structured interpretation of a chest X-ray
• Airway: trachea, carina, bronchi and hilar structures. • Breathing: lungs and pleura. • Cardiac: heart size and borders. • Diaphragm: including assessment of costophrenic angles. • Everything else: mediastinal contours, bones, soft tissues, tubes, valves, pacemakers and review areas.
Trachea observations in a chest x ray:
Trachea
Inspect the trachea for evidence of deviation:
• The trachea is normally located centrally or deviating very slightly to the right. • If the trachea appears significantly deviated, inspect for anything that could be pushing or pulling the trachea. Make sure to inspect for any paratracheal masses and/or lymphadenopathy.
True tracheal deviation:
Pushing of the trachea: large pleural effusion or tension pneumothorax.
Pulling of the trachea: consolidation with associated lobar collapse.
Apparent tracheal deviation:
Rotation of the patient can give the appearance of apparent tracheal deviation, so as mentioned above, inspect the clavicles to rule out the presence of rotation.
Carina and bronchi observation on a chest X ray:
Carina and bronchi
The carina is cartilage situated at the point at which the trachea divides into the left and right main bronchus.
On appropriately exposed chest X-ray, this division should be clearly visible.
The right main bronchus is generally wider, shorter and more vertical than the left main bronchus. As a result of this difference in size and orientation, it is more common for inhaled foreign objects to become lodged in the right main bronchus - aspiration pneumonia.
Depending on the quality of the chest X-ray you may be able to see the main bronchi branching into further subdivisions of bronchi.
Hilar structure observations on a chest X ray:
Hilar structures
The hilar consist of the main pulmonary vasculature and the major bronchi. Each hilar also has a collection of lymph nodes which aren’t usually visible in healthy individuals.
The hilar are usually the same size, so asymmetry should raise suspicion of pathology.
Causes of hilar enlargement or abnormal position
• Bilateral symmetrical enlargement is typically associated with sarcoidosis or TB. • Unilateral/asymmetrical enlargement may be due to underlying malignancy (cancer). • Abnormal hilar position can also be due to a range of different pathologies. You should inspect for evidence of the hilar being pushed (e.g. by an enlarging soft tissue mass) or pulled (e.g. lobar collapse).
Lung observation on a chest x ray:
Lungs
When interpreting a chest X-ray you should divide each of the lungs into zones.
Compare each zone between lungs, noting any asymmetry (some asymmetry is normal and caused by the presence of various anatomical structures e.g. the heart).
Some lung pathology causes symmetrical changes in the lung fields, which can make it more difficult to recognise, so it’s important to keep this in mind (e.g. pulmonary oedema).
Increased airspace shadowing in a given area of a lung field may indicate pathology (e.g. consolidation/malignant lesion).
The complete absence of lung markings should raise suspicion of a pneumothorax.
Egs- lung cancer, pneumonia, pneumothorax,
Pleura observations on a chest X ray:
Pleura
The pleura are not usually visible in healthy individuals. If the pleura are visible it indicates the presence of pleural thickening which is typically associated with mesothelioma.
Inspect the borders of each lung to ensure lung markings extend all the way to the edges of the lung fields (the absence of lung markings is suggestive of pneumothorax).
Fluid (hydrothorax) or blood (haemothorax) can accumulate in the pleural space, resulting in an area of increased opacity on a chest X-ray. In some cases, a combination of air and fluid can accumulate in the pleural space (hydropneumothorax), resulting in a mixed pattern of both increased and decreased opacity within the pleural cavity.
Tension pneumothorax
A tension pneumothorax is a life-threatening condition which involves an increasing amount of air being trapped within the pleural cavity displacing (pushing away) mediastinal structures (e.g. the trachea) and impairing cardiac function.
If a tension pneumothorax is suspected clinically (shortness of breath and tracheal deviation) then immediate intervention should be performed without waiting for imaging as this condition will result in death if left untreated.
Cardiac observation on a chest X ray:
Cardiac
In a healthy individual, the heart should occupy no more than 50% of the thoracic width.
• This rule only applies to PA chest X-rays (as AP films exaggerate heart size), so you should not draw any conclusions about heart size from an AP film.
Cardiomegaly is said to be present if the heart occupies more than 50% of the thoracic width on a PA chest X-ray.
Assess the heart’s borders
Inspect the borders of the heart which should be well defined in healthy individuals:
• The right atrium makes up most of the right heart border. • The left ventricle makes up most of the left heart border.
The heart borders may become difficult to distinguish from the lung fields as a result of pathology which increases the opacity of overlying lung tissue:
Reduced definition of the right heart border is typically associated with right middle lobe consolidation.
Reduced definition of the left heart border is typically associated with lingular consolidation.
Diaphragm observation on a chest x ray:
Diaphragm
The right hemidiaphragm is, in most cases, higher than the left in healthy individuals (due to the presence of the liver).
The diaphragm should be indistinguishable from the underlying liver in healthy individuals on an erect chest X-ray, however, if free gas is present (often as a result of bowel perforation), air accumulates under the diaphragm causing it to lift and become visibly separate from the liver.
There are some conditions which can result in the false impression of free gas under the diaphragm, known as pseudo-pneumoperitoneum, including Chilaiditi syndrome.
Chilaiditi syndrome involves the abnormal position of the colon between the liver and the diaphragm resulting in the appearance of free gas under the diaphragm (because the bowel wall and diaphragm become indistinguishable due to their proximity).
Costrophrenic angles observed by a chest x ray:
Costophrenic angles
In a healthy individual, the costophrenic angles should be clearly visible on a normal chest X-ray as a well defined acute angle.
Loss of this acute angle, sometimes referred to as costophrenic blunting, can indicate the presence of fluid or consolidation in the area. Costophrenic blunting can also develop secondary to lung hyperinflation as a result of diaphragmatic flattening and subsequent loss of the acute angle (e.g. chronic obstructive pulmonary disease).
Name some types and what a pneumothorax is:
What is pneumothorax?
Pneumothorax occurs when air gets into the pleural space separating the lung from the chest wall. It can occur spontaneously or secondary to trauma, medical interventions (“iatrogenic”) or lung pathology.
Types:
Primary pneumothorax: occurs in a patient without a known respiratory disease.
Secondary pneumothorax: occurs in a patient with pre-existing respiratory disease.
Tension pneumothorax is caused by trauma to chest wall that creates a one-way valve that lets air in but not out of the pleural space.
Causes of primary pneumothorax:
Causes of primary pneumothorax include:
• Often unknown
• May be due to rupture of a subpleural air bleb (found in the pleural space).
• The bleb itself is caused by alveolar rupture, which lets air travel through the interlobular septum into the subpleural space.
Causes of secondary pneumothorax:
Causes of secondary pneumothorax include:
• COPD: (70% of secondary pneumothorax): rupture of air bulla (air-filled space in lungs, caused by emphysematous destruction of lung tissue).
• Asthma: rupture of air bulla or subpleural air bleb, though the mechanism is still poorly understood.
• Cystic fibrosis: endobronchial obstruction causing increased pressure in the alveoli, leading to alveolar rupture.
• Marfan syndrome: abnormal lung connective tissue leads to increased formation of air bulla (which rupture), and tall body habitus increases mechanical stress on lung apices (exacerbating bulla rupture).
Causes of a tension pneumothorax:
Causes of tension pneumothorax include:
• Penetrating/blunt trauma
• Mechanical ventilation or non-invasive ventilation (NIV)
• Conversion of simple pneumothorax to tension pneumothorax
How is normal physiological function affected by a pneumothorax?
How is normal physiological function affected by pneumothorax?
• The one-way valve means that during inspiration air is drawn into the pleural space and during expiration, the air is trapped in the pleural space.
• Therefore, more air keeps getting drawn into the pleural space with each breath and cannot escape = intrapleural pressure exceeds the atmospheric pressure, leading to collapse of the ipsilateral lung
• This is dangerous as it creates pressure inside the thorax that will push the mediastinum across away from the pneumothorax.
• The mediastinum kinks the big vessels in the mediastinum and cause cardiorespiratory arrest.
In severe cases, the increased intrapleural pressure can compress the heart and surrounding vasculature, reducing cardiac output and venous return. If untreated, this may lead to cardiac arrest.
Signs of tension pneumothorax:
Signs of Tension Pneumothorax
• Tracheal deviation away from side of pneumothorax
• Reduced air entry to affected side
• Increased resonant to percussion on affected side
• Tachycardia
• Hypotension
Clinical examination and usual findings for suspected pneumothorax:
Investigations:
Clinical examination
A full respiratory examination should be performed in suspected cases of pneumothorax.
Typical clinical findings in pneumothorax include – on the same side as the pneumothorax.
• Hyper-resonant lung percussion
• Reduced breath sounds.
• Reduced lung expansion.
Typical clinical findings in tension pneumothorax include:
• Tracheal deviation away from the pneumothorax
• Severe tachycardia
• Hypotension
Peripheral chemoreceptors:
Peripheral chemoreceptors
• Located in carotid body and aortic body
• Detect large changes in partial pressure of oxygen (pO2) as arterial blood supply leaves the heart
• When oxygen levels are low, afferent impulses trave via glossopharyngeal and vagus nerves to medulla oblongata and pons in the brainstem
• A number of responses are then coordinated which aim to restore pO2:
○ Respiratory rate and tidal volume are increased to allow more oxygen to enter lungs and diffuse into blood
○ Blood flow directed towards kidneys and brain
○ Cardiac output is increased to maintain flow
Central chemoreceptors:
Central chemoreceptors
• Located in the medulla oblongata of the brainstem
• Detect changes in arterial partial pressure of pCO2
• When changes are detected, the receptors send impulses to the respiratory centres in the brainstem that initiate changes in ventilation to restore normal pCO2
○ Detection of an increase pCO2 = increased ventilation
○ Detection of decrease pCO2 = decreased ventilation
Mechanism behind how central chemoreceptors detect changes in arterial pCO2 is more complex, and is related to changes in pH of the cerebral spinal fluid
• pH of CSF is established by ratio of pCO2 : HCO3-
• The pH of the CSF is inversely proportional to the arterial pCO2
○ A small decrease in pCO2 leads to an increase in pH of CSF which stimulates the respiratory centres to decrease ventilation
○ A small increase in pCO2 leads to a decrease in the pH of the CSF which stimulates the respiratory centres to increase ventilation
What is hypoxia?
• Hypoxia is when the tissues of your body don’t have enough oxygen
• Lung disease and heart disease both increase your risk of hypoxia
Right lung
The right lung has three lobes and two fissures. Normally, the lobes are freely movable against each other because they are separated, almost to the hilum, by invaginations of visceral pleura. These invaginations form the fissures:
▪ The oblique fissure separates the inferior lobe ( lower lobe ) from the superior lobe and the middle lobe of the right lung .
▪ The horizontal fissure separates the superior lobe ( upper lobe ) from the middle lobe.
What important structures are on the medial surface of the right lung?
The medial surface of the right lung lies adjacent to a number of important structures in the mediastinum and the root of the neck ( Fig. 3.45B ). These include the:
▪ heart,
▪ inferior vena cava,
▪ superior vena cava,
▪ azygos vein, and
▪ esophagus.
The right subclavian artery and vein arch over and are related to the superior lobe of the right lung as they pass over the dome of the cervical pleura and into the axilla.
Left lung
The left lung is smaller than the right lung and has two lobes separated by an oblique fissure. The oblique fissure of the left lung is slightly more oblique than the corresponding fissure of the right lung.
The inferior portion of the medial surface of the left lung, unlike the right lung, is notched because of the heart’s projection into the left pleural cavity from the middle mediastinum.
From the anterior border of the lower part of the superior lobe a tongue-like extension (the lingula of the left lung ) projects over the heart bulge.
The medial surface of the left lung lies adjacent to which important features?
The medial surface of the left lung lies adjacent to a number of important structures in the mediastinum and root of the neck. These include the:
▪ heart,
▪ aortic arch,
▪ thoracic aorta, and
▪ esophagus.
The left subclavian artery and vein arch over and are related to the superior lobe of the left lung as they pass over the dome of the cervical pleura and into the axilla.
Where is the trachea and where does it bifurcate?
The trachea is a flexible tube that extends from vertebral level CVI in the lower neck to vertebral level TIV/V in the mediastinum where it bifurcates into a right and a left main bronchus.
Bronchial tree order
Each main bronchus enters the root of a lung and passes through the hilum into the lung itself. The right main bronchus is wider and takes a more vertical course through the root and hilum than the left main bronchus ( Fig. 3.47A ). Therefore, inhaled foreign bodies tend to lodge more frequently on the right side than on the left.
Secondary bronchi (supplies a lobe)
Tertiary bronchi (supply bronchopulmonary segments)
Terminal bronchioles
… conducting zone
Respiratory zone….
Respiratory bronchioles
Alveolar ducts
Alveolar sacs
What is a bronchopulmonary segment?
Bronchopulmonary segments
A bronchopulmonary segment is the area of lung supplied by a segmental bronchus and its accompanying pulmonary artery branch.
Tributaries of the pulmonary vein tend to pass intersegmentally between and around the margins of segments.
Each bronchopulmonary segment is shaped like an irregular cone, with the apex at the origin of the segmental bronchus and the base projected peripherally onto the surface of the lung.
A bronchopulmonary segment is the smallest functionally independent region of a lung and the smallest area of lung that can be isolated and removed without affecting adjacent regions.
There are ten bronchopulmonary segments in each lung ( Fig. 3.48 ); some of them fuse in the left lung.
Anatomical names of the lungs
Apex (top)
Hilum:
A pulmonary artery
Two pulmonary veins
A main bronchus
Bronchial vessels
Nerves
Lymphatics
Anterior border
Posterior border
Inferior border
Costal surface (attaches to ribs)
Mediastinal surface
Diaphragmatic surface (base)
• Each lung has: ○ Base on the diaphragm ○ Apex projecting above rib I and into the root of the neck ○ Two surfaces § Costal surface lies immediately adjacent to ribs and intercostal spaces of thoracic wall § Mediastinal surface lies against mediastinum anteriorly and vertebral column posteriorly □ Contains hilum which structures enter and leave through ○ Three borders § Inferior border → sharp and separates the base from costal surface § Anterior/posterior borders → separate costal surface from medial surface □ Anterior border is also sharp □ posterior border is smooth and rounded
Why is the right lung slightly bigger than the left lung?
• Right lung is slightly larger than left. Middle mediastinum contains the heart and bulges more to the left than to right
The conducting portion
The conducting portion
• Conducting piece = nasal cavity, trachea, bronchi & bronchioles
• Luminal surfaces of this entire portion → ciliated pseudostratified columnar epithelium & contain goblet cells
○ Role → excrete mucus that serves as first line of defense against incoming environmental pathogens
○ Cilia move mucus-bound particulate up and away for expulsion from the body
• In most proximal airway, hyaline cartilage rings support the larger respiratory passages (trachea & bronchi) to facilitate passage of air
○ Three major cell types in this region
1. Ciliated
□ Each lined with 200-300 cilia, account for more than half of all epithelial cells in conducting airway
2. Non-ciliated Secretory cells
3. Basal cells
• As the degree of branching within the airway tree continues, the epithelium gradually changes from pseudostratified to simple cuboidal…the predominant cells become non-ciliated cells
Functions:
• Conducting portion (nose, pharynx, larynx, trachea, bronchi and bronchioles) → serve to humidify, warm and filter air
○ Humidification → requires serous and mucous secretions
○ Warming → relies on the extensive capillary network that lays within alveoli
○ Filtration → occurs by trapping mechanism of mucus secretions and ciliary beating
§ Goblet cells → columnar epithelial cells that secrete high molecular weight mucin glycoproteins into the lumen of the airway and provide moisture to epithelium while trapping incoming particulate and pathogens
The gas exchange portion
The gas-exchange portion
• Composed of millions of alveoli → lined by an extremely thin, simple squamous epithelium
○ This allows for the easy diffusion of oxygen and carbon dioxide
• Additionally, cuboidal, surfactant-secreting cells, Type II pneumocytes are also found lining the walls of alveoli
○ Surfactant has a vital role in lowering the surface tension of water to allow for effective gas exchange
• Type I pneumocytes → flattened cells that create a very thin diffusion barrier for gases
○ Tight junctions connect one cell to another
○ Principal functions are gas exchange and fluid transport
• Type II pneumocyte → secrete surfactant, this decreases surface area between thin alveolar walls, and stops alveoli from collapsing uring exhalation
○ These cells connect to the epithelium and other constituent cells by tight junctions
○ Also play a vital role in acting as progenitor cells to replace injured or damaged Type I pneumocytes
Functions:
• Gas exchange → inhaled air diffuses through alveoli into the pulmonary capillaries. CO2 diffuses at same time from capillaries into the alveoli
How is ventilation controlled in the brain?
Ventilation Control: The Brain
• Involuntary ventilation occurs subconsciously
• The organs involved in ventilation (diaphragm and intercostal muscles) are stimulated by the pons and the medulla (located in the brain)
• Pons + medulla (respiratory centre of the brain) send impulses to the primary respiratory muscles, via the phrenic and intercostal nerves, which stimulates contraction.
What are the groups of neurones called involved in breathing?
Groups of neurons involved in ventilation
• Ventral: expiration
• Dorsal: inspiration
Pontine: rate and pattern of breathing
Short acting beta 2 adrenergic receptor agonists
Short acting beta 2 adrenergic receptor agonists, for example salbutamol. These work quickly but the effect only lasts for an hour or two. Adrenalin acts on the smooth muscles of the airways to cause relaxation. This results in dilatation of the bronchioles and improves the bronchoconstriction present in asthma. They are used as “reliever” or “rescue” medication during acute exacerbations of asthma when the airways are constricting.
Inhaled corticosteroids (ICS)
Inhaled corticosteroids (ICS), for example beclometasone. These reduce the inflammation and reactivity of the airways. These are used as “maintenance” or “preventer” medications and are taken regularly even when well.
Long acting beta 2 agonists (LABA)
Long-acting beta 2 agonists (LABA), for example salmeterol. These work in the same way as short acting beta 2 agonists but have a much longer action.
Long acting muscarinic antagonists (LAMA)
Long-acting muscarinic antagonists (LAMA), for example tiotropium. These block the acetylcholine receptors. Acetylecholine receptors are stimulated by the parasympathetic nervous system and cause contraction of the bronchial smooth muscles. Blocking these receptors leads to bronchodilation.
Leukotriene receptor antagonists
Leukotriene receptor antagonists, for example montelukast. Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways. Leukotriene receptor antagonists work by blocking the effects of leukotrienes.
Theophylline
Theophylline. This works by relaxing bronchial smooth muscle and reducing inflammation. Unfortunately it has a narrow therapeutic window and can be toxic in excess so monitoring plasma theophylline levels in the blood is required. This is done 5 days after starting treatment and 3 days after each dose changes.
Maintenance and reliever therapy (MART)
Maintenance and Reliever Therapy (MART). This is a combination inhaler containing a low dose inhaled corticosteroid and a fast acting LABA. This replaces all other inhalers and the patient uses this single inhaler both regularly as a “preventer” and also as a “reliever” when they have symptoms.
Adverse effects of anti inflammatory drugs used in asthma treatment:
Adverse effects of anti-inflammatory drugs
· Dysphonia (effect of voice box, altered voice)
· Oropharyngeal candidiasis
· Adrenal suppression
· Osteoporosis
· hyperglycaemia
What is the aim of step wise asthma treatment:
Aim of treatment:
§ No daytime symptoms
§ No night-time awakening due to asthma
§ No need for rescue medication
§ No asthma attacks
§ No limitations on activity including exercise
§ Normal lung function (FEV and/or PEF >80%) predicted or best
§ Minimal side effects from medication
Step wise treatment for asthma therapy:
Intermittent reliever therapy (usually blue inhaler-short term, short acting β2 agonist) and regular preventer therapy (usually brown inhaler – corticosteroid) *see table below on doses
Initial add-on therapy – long-acting β2 agonist, which should be considered before increasing dose of inhaled corticosteroid
Combination inhalers recommended to:
o Guarantee that long acting β2 agonist is not taken without inhaled corticosteroid
o Improve inhaler adherence
Additional controller therapies
o If control remains poor on low-dose inhaled corticosteroids plus a long-acting β2 agonist, recheck diagnosis, assess adherence to existing medication and check inhaler technique before increasing therapy
o Increase the dose of inhaled corticosteroids from low dose to medium dose, if not already on these doses
o Consider adding a leukotriene receptor antagonist
Referred to specialist care
Grading acute asthma:
Moderate
• PEFR 50 – 75% predicted • Speaking full sentences
Severe
• PEFR 33-50% predicted • Resp rate >25 • Heart rate >110 • Unable to complete sentences in one breath
Life-threatening
• PEFR <33% • Sats <92% • Becoming tired • Altered consciousness level • No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
Near fatal asthma- raised PCO2 and/or requiring mechanical ventilation with raised inflation pressures
Treatment of moderate acute asthma:
Treated at home or in primary care
Admit people with a moderate asthma exacerbation with worsening symptoms despite initial bronchodilator treatment and/or who have had a previous near-fatal asthma attack.
Medication:
β2 agonist bronchodilators
In most cases nebulised β2 agonists given in high doses act quickly to relieve bronchospasm with few side effects.
Ipratropium bromide
Combining nebulised ipratropium bromide with a nebulised β2 agonist produces significantly greater bronchodilation than β2 agonist alone, leading to faster recovery and shorter duration of admission.
• Ipratropium bromide is a type of anticholinergic medication which opens up the medium and large airways in the lungs.
Dose:
Salbutamol 2.5 mg (to be repeated x2 over 60 min if required)
Add nebulised ipratropium bromide (250–500 micrograms 3–4 times a day) to β2 agonist treatment
Acute severe asthma treatment:
Acute severe asthma
Admit patients with any feature of a severe asthma attack persisting after initial bronchodilator treatment.
Medication:
Oxygen
Give controlled supplementary oxygen to all hypoxaemic patients with acute severe asthma via a face mask, Venturi mask or nasal cannula.
Hypercapnia indicates the development of near-fatal asthma and the need for emergency specialist/anaesthetic intervention.
Steroid therapy
Steroids reduce mortality, relapses, subsequent hospital admission and requirement for β2 agonist therapy. The earlier they are given in the acute attack the better the outcome.
Give steroids in adequate doses to all patients with an acute asthma attack.
Intravenous aminophylline
In an acute asthma attack, IV aminophylline is not likely to result in any additional bronchodilation compared with standard care with inhaled bronchodilators and steroids.
Some patients with near-fatal asthma or life-threatening asthma with a poor response to initial therapy may gain additional benefit from IV aminophylline.
Antibiotics
If there is convincing evidence of bacterial infection!
Dose
Maintain saturation levels >88-92%
Oral prednisolone (40–50 mg daily) until recovery (minimum 5 days)
IV hydrocortisone (100 mg six hourly) continued for 5 days
Life threatening asthma treatment
Life threatening asthma
Admit patients to ICU if:
Persistent or worsening hypoxia
Hypercapnia
Feeble respiration
Reduced GCS
Respiratory arrest
Confusion
Deteriorating PEF
Exhaustion
Acidosis
V magnesium sulphate infusion
• Should only be used following consultation with senior medical staff. • PEF < 50% best or predicted
Intravenous salbutamol
Intravenous hydrocortisone
Admission to ICU/HDU
Intubation in worst cases
This decision should be made early because it is very difficult to intubate with severe bronchoconstriction
Dose:
1.2–2 g IV infusion over 20 minutes in saline
When should you arrange emergency admission for a person with breathlessness?
Arrange emergency admission for people with:
• Rapid onset or worsening of symptoms of suspected heart failure. • Suspected sepsis. • Anaphylaxis. • ECG suggesting a cardiac arrhythmia or myocardial infarction. • Clinical features of: ○ Pulmonary embolism. For more information, see the CKS topic on Pulmonary embolism. ○ Pneumothorax. ○ Cardiac tamponade. ○ Pulmonary oedema. ○ Superior vena cava syndrome. • Any features of a severe or life-threatening asthma attack. ○ Altered level of consciousness or acute confusion. ○ Arrhythmia. ○ Cyanosis. ○ Elevated respiratory rate. ○ Exhaustion. ○ Hypotension. ○ Oxygen saturation less than 92%. ○ Peak expiratory flow rate less than 50% of predicted. ○ Poor respiratory effort. ○ Silent chest. • Any features of a severe or life-threatening chronic obstructive pulmonary disease (COPD) exacerbation. ○ Acute confusion or impaired consciousness. ○ Already receiving long-term oxygen therapy. ○ Cyanosis. ○ Oxygen saturation less than 90% on pulse oximetry. ○ Poor or deteriorating general condition including significant comorbidity (such as cardiac disease or insulin-dependent diabetes). ○ Rapid onset of symptoms. ○ Severe breathlessness. ○ Worsening peripheral oedema.
Managing acute breathlessness whilst waiting for emergency admission
Managing acute breathlessness whilst waiting for emergency admission
1) Sit the person up. 2) If the person has an oxygen saturation of 94% or less, give oxygen and continuously monitor their oxygen saturation levels while waiting for transfer to hospital. • Use a 24% Venturi mask at 2-3 L/min for people with suspected chronic obstructive pulmonary disease (COPD), morbid obesity, a chest wall deformity, or a neuromuscular disorder. ○ This is because they are at risk of hypercapnic respiratory failure. 3) Aim for an oxygen saturation of 88-92%. • If the oxygen saturation remains below 88% following oxygen administration with a 28% Venturi mask, change to either a nasal cannula at 2-6 L/min or a simple face mask at 5 L/min and aim for an oxygen saturation of 88-92% — the A&E department should be alerted in advance that the person is a high priority. 4) Identify and treat people with clinical features of: • Acute exacerbation of chronic obstructive pulmonary disease (COPD) • Acute severe asthma (peak expiratory flow rate less than 50% of predicted) • Anaphylaxis • Pulmonary oedema • Silent myocardial infarction • Supraventricular tachycardia (SVT) • Tension pneumothorax
Managing breathlessness when emergency admission is not required
Managing breathlessness when emergency admission is not required
1) For people who do not require emergency admission or urgent referral, manage the underlying cause of breathlessness. • Anxiety-related breathlessness • Asthma • Bronchiectasis • Chronic obstructive pulmonary disease (COPD) • Community-acquired pneumonia • Interstitial lung disease • Lung/lobar collapse • Pleural effusion
Managing breathlessness that remains of uncertain cause
Reassess for risk factors and clinical features that may indicate a serious underlying condition that requires emergency admission. If emergency admission is not required, arrange routine referral.
Common cardiac causes of breathlessness
Common cardiac causes of breathlessness include:
• Silent myocardial infarction. • Cardiac arrhythmia. • Acute pulmonary oedema. • Chronic heart failure.
Common causes of pulmonary breathlessness
Common pulmonary causes of breathlessness include:
• Asthma. • Chronic obstructive pulmonary disease (COPD). • Pneumonia. • Pulmonary embolism. • Lung cancer. • Pleural effusion.
Epidemiology of asthma
• Asthma affects more than 300 million people worldwide including 11.6% of children aged 6 to 7 years.
• In the UK, over 8 million people, or approximately 12% of the population, have been diagnosed with asthma. However, some may have grown out of the condition, and 5.4 million people are receiving asthma treatment.
• Approximately 160,000 people in the UK are diagnosed with asthma each year, however, incidence rates went down by around 10% between 2008 and 2012.
• The incidence of asthma is higher in children than in adults.
• In early childhood, asthma is more common in boys than in girls, but by adulthood, the sex ratio is reversed.
• Asthma accounts for 2-3% of primary care consultations, 60,000 hospital admissions, and 200,000 bed days per year in the UK.
• Occupational asthma may account for 9–15% of adult-onset asthma. It is reported to be the most common industrial lung disease in the developed world.
• Every 10 seconds someone is having a potentially life threatening asthma attack. And on average 3 people die from an asthma attack a day in the UK.
• The cost of asthma to the NHS is around 1 billion per year.
Aetiology of asthma
People with asthma have swollen (inflamed) and “sensitive” airways that become narrow and clogged with sticky mucus in response to certain triggers. Genetics, pollution and modern hygiene standards have been suggested as causes, but there’s not currently enough evidence to know if any of these do cause asthma.
Symptoms:
Infection
Night time or early morning
Exercise
Animals
Cold/damp
Dust
Strong emotions
Occupational exposure
Pollutants
Pathophysiology of asthma and what type of inhaler is used.
• Airway Muscle: the thin layer of muscle within the wall of an airway can contract to make it tighter and narrower. In people with asthma, this muscle is often “twitchy” and contracts more easily and more strongly than in people who do not have asthma. (Reliever inhaler)
• Inflammation / Swelling: the inside walls of the airways are often swollen and inflamed, leaving less space inside. (Preventer) • Mucus: mucus production is normally a protective response, but in severe asthma, it is excessive and can block the inside of the airways. (Preventer) • Fibrosis or Scarring: ongoing inflammation in the airways can lead to development of scar tissue and “tissue remodelling”. This results in thickened airway walls and increased smooth muscle.
What is atopy?
When you have atopy, your immune system is more sensitive to common allergic triggers that you breathe in or eat. So you have a stronger-than-normal reaction to these allergens, such as dust, pollen, peanuts, or shellfish. If you have allergies or asthma, there’s a chance atopy is behind it. Atopy is a problem with your immune system that makes you more likely to develop allergic diseases. Your genes cause this problem.
What conditions are related to atopy?
Atopy makes you more likely to have allergic conditions like these:
• Asthma
• Eczema
• Allergic rhinitis (hay fever)
• Allergies to shell fish, eggs and nuts
Bronchial hyperresponsiveness
• Bronchial hyperresponsiveness is defined as an increase in sensitivity to a wide variety of airway narrowing stimuli, which can be both chemical and physical.
• The hyper-activity of the bronchial smooth muscle leading to bronchoconstriction, increasing air flow resistance and decreased air flow.
• Those with bronchial hyperresponsiveness experience excessive responses to even small doses of stimuli. Although different stimuli may provoke different responses among different individuals.
• Providing evidence that bronchial hyperresponsiveness is heterogenous.
Hypersensitivity
• Th2 cells can promote the Type 1 hypersensitivity response.
• This is an immediate reaction which involves the Th2 cells activating downstream B cells to produce immunoglobulin E (Ig-E), which mediates the release of antibodies against the soluble antigen.
• This results in mast cell degranulation and release of histamine and other inflammatory mediators, including proteinoids, platelet activating factor and leukotrienes, creating a cycle of chronic inflammation. • The process causes bronchoconstriction and epithelial damage, leading to remodelling of the airway and bronchospasm.
