Respiratory Lecture ILO’s Flashcards
Describe the physiological relationships involved in V/Q matching.
Alveolar ventilation (V) should match perfusion (Q)
Matching Ventilation and perfusion (VQ) perfectly would maximise gas transfer between lungs and pulmonary circulation.
– Both V and Q are greater towards the bottom of the lung
– VQ >1 = well ventilated, poorly perfused
– VQ <1 = poorly ventilated, well perfused
– On average the VQ matching (or V/Q ratio) is between 0.8 and 1
VQ matching is achieved by altering bronchiole and pulmonary arteriole radius. Bronchioles dilate due to hypercapnia. Pulmonary arterioles constrict due to hypoxia (diverting blood to alveoli with more oxygen)
How is CO2 transported around the body?
Plasma (9%)
Carboamino had ogle in (10-13%)
Bicarbonate (78%)
Name the lungs lobes and fissures:
Right:
Lobes-
Superior
Inferior
Middle
Fissures-
Oblique
Horizontal
Left:
Lobes-
Superior
Inferior
Fissures-
Oblique
What is the hilum and what are the hilar structures?
The hilum is where structures enter and leave the lung, important nerves are related to it
Hilar structures
• Main bronchi (right lobar), post/superior
• Pulmonary arteries, ant/superior
• Pulmonary veins, inferior
• Bronchial arteries and veins
• Bronchopulmonary lymph nodes
• Pulmonary plexus of nerves (CN X and sympathetic)
• Point of pleural reflection and pulmonary ligament
Phrenic nerves run anterior to the hilum to supply diaphragm, motor and sensory (C3,4,5) = referred pain to the shoulder
Vagus nerves run posterior to the hilum
What are the 10 bronchopulmonary segments?
A bronchopulmonary segment is a portion of lung supplied by a specific segmental bronchus and its vessels. These arteries branch from the pulmonary and bronchial arteries, and run together through the center of the segment. Veins and lymphatic vessels drain along the edges of the segment.
In general, each lung has 10 segments: the upper lobes contain 3 segments, the middle lobe / lingula 2 and the lower lobes 5.
Structure of the bronchi tree:
Trachea divides into 2 main bronchi:
Primary Bronchi
Secondary Bronchi
Tertiary Bronchi
Bronchioles
Terminal bronchioles
Respiratory bronchioles
Alveolar ducts
Alveolar sacs
Alveoli
Describe asthma and it’s triggers
Common chronic inflammatory condition characterised by
localised type 1 hypersensitive reaction & variable reversible airway obstruction
Episodes of – Breathlessness , wheeze & cough
AIRFLOW limitation – usually reversible
AIRWAY hyper responsiveness
INFLAMMATION of the bronchi – eosinophils, T –lymphocytes & mast cells
Triggers
Exercise
Air pollutants
Hypersensitivity
Respiratory infections
Describe COPD
COPD is predominantly caused by smoking and is characterised by airflow obstruction that:
- is not fully reversible (different to asthma)
- does not change markedly over several months
- is usually progressive in the long term
• Exacerbations often occur, where there is a rapid and sustained worsening of symptoms beyond normal day-to-day variations requiring a change in treatment (chronic condition with acute exacerbations)
How to differentiate between COPD and asthma
Clinical Features COPD Asthma
Smoker Usually all Occasional
Under 35 Very rare Often
Chronic productive
cough Common Uncommon (usually dry and tickly at night)
Breathlessness Persistent/
progressive Variable
Describe the mechanics of inspiration
Diaphragm – flattens, extending the superior/inferior dimension of the thoracic cavity.
External intercostal muscles – elevates the ribs and sternum, extending the anterior/posterior dimension of the thoracic cavity.
The action of the inspiratory muscles results in an increase in the volume of the thoracic cavity. As the lungs are held against the inner thoracic wall by the pleural seal, they also undergo an increase in volume.
As per Boyle’s law, an increase in lung volume results in a decrease in the pressure within the lungs. The pressure of the environment external to the lungs is now greater than the environment within the lungs, meaning air moves into the lungs down the pressure gradient.
How does the respiratory control centre control rate of breathing?
The respiratory centers contain chemoreceptors that detect pH levels in the blood and send signals to the respiratory centers of the brain to adjust the ventilation rate to change acidity by increasing or decreasing the removal of carbon dioxide (since carbon dioxide is linked to higher levels of hydrogen ions in blood).
There are also peripheral chemoreceptors in other blood vessels that perform this function as well, which include the aortic and carotid bodies.
Role of the medulla in RCC
The Medulla
The medulla oblongata is the primary respiratory control center. Its main function is to send signals to the muscles that control respiration to cause breathing to occur. There are two regions in the medulla that control respiration:
The ventral respiratory group stimulates expiratory movements.
The dorsal respiratory group stimulates inspiratory movements.
The medulla also controls the reflexes for nonrespiratory air movements, such as coughing and sneezing reflexes, as well as other reflexes, like swallowing and vomiting.
Role of the pons in RCC
The Pons
The pons is the other respiratory center and is located underneath the medulla. Its main function is to control the rate or speed of involuntary respiration. It has two main functional regions that perform this role:
The apneustic center sends signals for inspiration for long and deep breaths. It controls the intensity of breathing and is inhibited by the stretch receptors of the pulmonary muscles at maximum depth of inspiration, or by signals from the pnuemotaxic center. It increases tidal volume.
The pnuemotaxic center sends signals to inhibit inspiration that allows it to finely control the respiratory rate. Its signals limit the activity of the phrenic nerve and inhibits the signals of the apneustic center. It decreases tidal volume.
The apneustic and pnuemotaxic centers work against each other together to control the respiratory rate.
What is the role and where are chemoreceptors found?
Arterial O2, CO2 and pH are the most important influences on breathing.
• Detected by two sets of chemo receptors to stabilise PaO2, PaCO2 and pH in health.
- Peripheral chemoreceptors
– Carotid & aortic bodies in carotid arteries & aortic arch respectively
– Send signals via the glossopharyngeal and the vagus nerves respectively
- respond by altering their firing rate due to all or nothing affect
Primarily respond to decreased PAO2
Sensitive to changes in arterial ph
Respond to hypercapnia - Central chemoreceptors – In the medulla oblongata of the brain close to RCC
Main source of passive breathing
Primary source for feedback on assessing ventilation effectiveness
Elicit 80% of the ventilatory change due to PACO2
Insensitive to hypoxia
Why shouldn’t pure oxygen be given to someone with chronic hypercapnia?
As hypoxia is relied on to drive breathing rate
– Increased PaCO2 gives resp. acidosis
– Bicarbonate compensations return the brain pH back to normal so central chemoreceptors are less sensitive to further changes in PaCO2
– With central chemoreceptor drive depressed, minute ventilation depends on hypoxia via the carotid bodies
– If pure O2 given – this depresses carotid response output and will reduce hypoxic ventilation drive
– This could depress ventilation, increase PaCO2 and induce coma (CO2 narcosis).
What is a type 1 hypersensitivity reaction?
Type I hypersensitivity is also known as an immediate reaction and involves immunoglobulin E (IgE) mediated release of antibodies against the soluble antigen. This results in mast cell degranulation and release of histamine and other inflammatory mediators.
Eg allergies, hayfever
What is atopy?
Atopy is a predisposition to an immune response against diverse antigens and allergens leading to CD4+ Th2 differentiation and overproduction of immunoglobulin E (IgE). The clinical consequence is an increased propensity to hypersensitivity reactions.
Pathology of an asthmatic airway:
• 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.
• Inflammation / Swelling: the inside walls of the airways are often swollen and inflamed, leaving less space inside.
• Mucus: mucus production is normally a protective response, but in severe asthma, it is excessive and can block the inside of the airways.
• 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 asthma?
§ Most common chronic respiratory disorder encountered in clinic practice
§ Chronic inflammatory disorder of the airways secondary to hypersensitivity
§ Reversible bronchospasm resulting in airway obstruction - paroxysmal
Pathophysiology of asthma
Chronic inflammation of the airways
§ Heightened contractability of the smooth muscle
§ Causes narrowing of the airways, which leads to wheeze
§ Typically reversible, but chronic inflammation can lead to airway remodelling
Epidemiology of asthma:
5.4 million people have asthma in the UK
§ 1 in 11 children, 1 in 12 adults
§ Every 10 seconds, someone in the UK is having a potentially life- threatening asthma attack
§ Every day, the lives of three families are devastated by the death of a loved one
Signs and symptoms of asthma
Probability of asthma is increased by the patient having more than one of:
§ Shortness of Breath
§ Wheeze
§ Cough
§ Chest tightness
Especially if:
§ Worse at night/early morning
§ Related to exercise/cold/allergen exposure
§ Occurs after taking NSAIDs/Beta-Blockers
History taking triggers during suspected asthma consultation
Upper respiratory tract infections
Cold air
Exercise- symptoms during/after
Pollution including cigarette smoke
Allergens ie pollen and animals
Time of day- diurnal variation
Work related- symptoms better at work/holiday
Differential diagnoses if asthma has been ruled out
COPD
• Significant smoking history • Less reversibility
Heart Failure
• Orthopnoea
• Cardiac wheeze
Angina
• Chest pain – triggered by cold/exercise
Gastro-Oeosophageal Reflux
• Symptomatic following food
Post-Nasal Drip
• Worse on lying down
Malignancy
• Consider in smokers – red flags
Diagnosis and investigation of asthma
Asthma is a clinical diagnosis
Based upon a convincing history
Supported by positive response to bronchodilator therapy
Investigated using peak expiratory flow and spirometry
Peak expiatory flow technique
§ Stand up & take a deep breath in
§ Lips form a tight seal around plastic
§ Like blowing a dart
§ Don’t obstruct the tab
§ Best out of 3 attempts
§ Monitor throughout the day
Contraindications to spirometry
Angina
Heart problems
Recent concussion
Recent surgery on the brain, middle ear, sinuses, eyes, chest or abdomen
Uncontrolled high or low blood pressure
Pulmonary hypertension
Pulmonary embolism
Pneumothorax
Late term pregnancy
Aneurysms
FEV1 and FVC
§ FEV1 – Forced Expiratory Volume in 1 second. Normal >80% Predicted.
§ FVC – Forced Vital Capacity – total volume expired from maximal inspiration to maximal forced expiration. Normal >80% Predicted.
§ FEV1/FVC Ratio as a percentage § Normal: 70-80%
§ <70%: Obstructive Defect
§ >80%: Restrictive Defect
§ Patients will also have a predicted FEV1 and FVC value based on the predicted normal for a patient of the same age, sex and height.
§ % Your Value/Predicted Value = % Predicted FEV1 or FVC.
Obstructive vs restrictive defect in spirometry
Obstructive= FEV1/FVC reduced <0.7
Airway collapse causes significant reduction in FEV1
Restrictive= FEV1/FVC >0.8
Significant reduction in FVC
Flow volume loops
Patient takes a deep breath in, which starts the graph at 0
Patient then forces air out
Volume is measured in Litres along the X-Axis
FEF – Forced Expiratory Flow
FIF – Forced Inspiratory Flow
Each are measured at 25%, 50% and 75% of FVC
Different patterns of flow volume loops are seen in different conditions
Flow loop patterns obstructive vs restrictive
Normal:
PEF normal
Pattern initially rapid, decreasing steadily
Volume normal
Restrictive:
PEF normal or slightly reduced
Pattern normal
Volume reduced
Obstructive:
PEF reduced
Pattern concaved
Volume normal or reduced
DLCO
A.K.A. Transfer Factor - DLCO
Ability for gaseous transfer across the alveolar to the blood supply
Transfer capacity of the lung, for uptake of carbon monoxide
It is reduced in emphysema, acute asthma, anaemia and interstitial lung disease
It is increased in chronic asthma, left heart failure, polycythaemia and exercise
What is bronchodilator reversibility?
Bronchodilator responsiveness assess whether your lung function improves with SABA therapy
Spirometry is done before and 15 minutes after inhaling SABA
Assesses any improvement in lung function – improvement suggests a diagnosis of Asthma or COPD
What are the management goals of asthma?
Aim to control symptoms – including nocturnal and exercise-induced
Prevent exacerbations and need for rescue medication
Achieve best possible lung function – aim for PEFR >80% predicted
Minimise side- effects
Maintain patients on lower possible dose of inhaled corticosteroid
Investigate reasons for poor control, such as poor inhaler technique
Patient education and empowerment is key
Name some inhaled therapies for asthma
Short-acting B2-Agonists (SABA)
• Salbutamol • Terbutaline
Long-acting B2-Agonists (LABA)
• Salmeterol • Formeterol
Muscuranic Antagonists
• Tiotropium • Ipratropium
Inhaled Corticosteroids
• Budesonide
• Beclometasone
• Fluticasone
Inhaler devices
§ MDI: Metered Dose Inhaler § Evohaler & Easibreathe
§ DPI: Dry Powder Inhaler
§ Turbohaler, Accuhaler,
Easyhaler, Handihaler
§ SMI: Soft Mist Inhaler § Respimat
Colours of metered dose inhalers
§ Salbutamol (SABA) – Blue
§ Beclomethasone (ICS) – Brown
§ Salmeterol (LABA) – Green
§ Fostair (LABA/ICS) – Pink
§ Seretide (LABA/ICS) – Purple
Inhaler technique consolation
Introduce yourself and confirm patient details
Explain what you will be doing and confirm patient understanding
Explain what the inhaler is and why it is needed
Explain how the inhaler works and when it should be used
Demonstration of technique
Observe patient and provide feedback
Inhaler technique method:
- Hold inhaler upright, remove cap and shake well
- Stand/sit up and tilt chin upwards
- Breath out fully
- Place lips around mouthpiece to get a good seal
- Breath in slowly and steadily, whilst simultaneously pressing the canister on the inhaler
- Continue to breathe in slowly until lungs feel full
- Remove the inhaler from your mouth and seal your lips
- Hold your breath for 10 seconds, then gently breath out
Further medications for asthma if initial treatment is failing
Leukotriene Receptor Antagonists
• Montelukast
Phosphodiesterase inhibitors and non-selective adenosine receptor antagonists
• Theophylline
• Aminophylline
Oral Corticosteroids
• Prednisolone
Annual asthma review
• Any difficulty sleeping due to symptoms?
• Any asthma symptoms during the day?
• Has your asthma interfered with your usual activities?
Measurement of PEF or spirometry
Review:
flow or spirometry
• Exacerbations in past 12 months
• Any time off work or school
• Use of oral corticosteroids
Check inhaler technique
Check patient adherence
Patient ownership and use of an asthma action plan
When should an acute asthma patient be referred to ICU?
Patients with acute severe or life- threatening asthma who have:
§ Persistent or worsening hypoxia
§ Hypercapnia
§ Acidosis
§ Exhaustion
§ Feeble respiration
§ Deteriorating PEF
§ Reduced GCS
§ Confusion
§ Respiratory arrest
Case study- Miss Crampton
§ 27 year old female attending ED
§ PC: SOB
§ PMH: Asthma, Hayfever
§ DH: Seretide 250 Inhaler 2 puffs BD, Loratadine 10mg, Salbutamol Inhaler prn, Microgynon
§ SH: Accountant, Social drinker, never smoked
§ A – Managing Own Airway
§ B – RR 30, SATs 93% RA, Bilateral wheeze on auscultation, Equal expansion, PEFR 250 (Normal 600), Speaking broken sentences
§ C – HR 120, HS normal, Peripherally cyanosed, BP 128/74, CRT <2s
§ D – Alert, GCS 15/15, BM 6.9
§ E – Calves soft non-tender, no erythema, no visible rashes, Temp
§ What classification of Asthma exacerbation did Miss. Crampton have?
§ Why did Miss. Crampton have an Asthma Exacerbation?
Severe acute asthma
Poor compliance to inhaler therapy
Miss Crampton will have a primary care follow up
Acute pulmonary reasons for SOB
● Pneumonia
● Pneumothorax
● Pulmonary embolism
● Asthma
● Acute exacerbation of COPD
● Acute Respiratory Distress Syndrome ie covid sars
● Large airway obstruction: e.g.
anaphylaxis, foreign body, epiglottitis
Acute cardiac reasons for sob
Cardiac
Severe pulmonary oedema
Acute myocardial infarction
Cardiac arrhythmia
Pericarditis and pericardial effusion
Chronic pulmonary reasons for sob
● COPD
● Emphysema
● Bronchiectasis
● Fibrosis
● Pleural effusion
● Lung cancer
● Asthma
● Hereditary lung disorders
(e.g. cystic fibrosis)
● Pulmonary Tuberculosis
Chronic cardiac reasons for SOB
Left ventricular disease
Heart valve disease (mitral & aortic
stenosis)
Arrhythmias
Pericardial causes
How to take a history of presenting complaint of SOB?
● Onset & duration: When did it start? Acute or gradual?
● Timing: e.g. diurnal variation with asthma
● Severity: MRC scale / able to talk in full sentences?
● Course: worsening, improving, fluctuating?
● Exacerbating and relieving factors: on exertion? Inhaler?
● Previous Episodes? What has made you come in today?
Quantifying breathlessness MRC scale
- Not troubled by breathless except on strenuous exercise
- Short of breath when hurrying on a level or when walking up a slight hill
- Walks slower than most people on the level, stops after a mile or so, or stops after 15 minutes walking at own pace
- Stops for breath after walking 100 yards, or after a few minutes on level ground
- Too breathless to leave the house, or breathless when dressing/undressing
Associated features of SOB
● Cough: Productive? Colour? Volume?
● Wheeze: Time of day? Triggers?
● Haemoptysis: How much?
● Chest pain: SOCRATES
● Red Flags / Systemic: Fever? Night sweats? Unintentional Weight loss?
What to ask in past medical history/drug history when presenting with shortness of breath
Respiratory conditions? Cardiac conditions? Allergies?
Other medical co-morbidities? Anxiety?
Hospital admissions / ITU admissions?
Drug history:
Inhalers, steroids, diuretics, antibiotics, home oxygen Beta-blockers, amiodarone, nitrofurantoin, methotrexate, heroin
What to ask in a social history when presenting with shortness of breath
Social History
● Smoking: calculate pack years
● Recreational drugs: cannabis
● Baseline: activities of daily living
● Occupation: shipyard, miner, farmer
● Travel History
● Recent immobilisation
What investigations can be done due to SOB?
Investigations
Pulse oximetry
CXR
ECG
Lung function tests - eg, peak flow measurement, spirometry.
Venous blood tests: FBC, brain natriuretic peptides (BNPs) Arterial blood gases
Imaging:
Echocardiogram.
High-resolution CT scan
V/Q scan.
Radioallergosorbent test (RAST) measurement or skin prick testing to common aero-allergens
What is interstitial lung disease
Interstitial Lung Disease
Group of disorders that affect the lung interstitium (alveolar & capillary epithelium, basement membrane etc.)
Cause fibrosis (scarring) and loss of elasticity of the lungs
Interfere with gas transfer Symptoms: SOB, dry cough
>200 causes. Examples:
Idiopathic Pulmonary Fibrosis
Hypersensitivity
Pneumonitis
Sarcoidosis
Asbestosis
Drug side effect e.g. methotrexate
Idiopathic pulmonary fibrosis clinical features and investigations
Clinical Features
IPF is reserved when no underlying cause exists
Typically 50-70yrs
Progressive exertional dyspnoea
Bi-basal crackles on auscultation
Dry cough
Clubbing
Low saturations / cyanosis
Investigations
● Spirometry
● Reduced TLCO
● CXR
● High-Resolution CT:
○ Ground Glass
○ Honeycombing
Idiopathic pulmonary fibrosis: management
● No cure
● Pulmonary rehab
● Few medications shown to benefit
● Pirfenidone (antifibrotic agent) may
be useful- when caught early
● Supplementary O2
● Lung transplant
● Poor Prognosis: life expectancy 3-4 years- progressive condition
What is sarcoidosis and what are its clinical features?
• Multisystem chronic inflammatory condition
• Non-caseating granuloma across body (predilection for lungs)
• Mid 20s-Mid 40’s
• Many present as an incidental CXR finding
• 1/3 asymptomatic, 1/3 non-specific symptoms (lethargy, cachexia), 1/3 acute admission
• Worse prognosis in black patients
Sarcoidosis: Clinical Features
Constitutional symptoms e.g. fevers, night sweats Lungs (90%) – cough, fever, SOB
Erythema nodosum, lupus pernio (rash)
Eyes (>20%) – anterior uveitis, dry eyes, glaucoma
Sarcoidosis investigations
• FBC: eosinophila, lymphopenia
• ESR, PO4, ALP, Ca – can be raised
• (unusual to have renal impairment)
• If Ca high – check 24 hour urinary Ca – hypercalciuria
• Serum ACE (up in 60%)
• CXR 5 stages (0-4)
• BAL – lymphocytes, raised CD4:CD8
Sarcoidosis management
Sarcoidosis: Management
Test eyes in all new diagnoses
Steroids
Most resolve spontaneously, 20% can result in pulmonary fibrosis Osteoporosis protection, flu vaccine, stop smoking
What is bronchiecstasis?
Bronchiectasis
Chronic airway inflammation with dilation of bronchi or their branches (larger bronchioles)
Extra mucus is made in the abnormal airways which is not cleared due to loss of cilia escalator
Collection of thick viscous mucus results in the patient becoming more prone to chest infections
Bronchiectasis causes
• In ~ 1⁄2 of cases, a cause cannot be found
• History of serious lung infection is the most common cause: e.g. tuberculosis, whooping cough, pneumonia or measles
• Immunosuppression: e.g. AIDS, transplant patients, hypogammaglobulinaemia
• Immune hyperactivity: e.g. Ulcerative colitis, Crohn’s disease and
rheumatoid arthritis
• Inherited diseases: e.g. cystic fibrosis an Kartageners syndrome
• Airway Obstruction: bronchial ca, foreign body
• Aspiration: e.g. GORD, chronic alcoholics
Bronchiectasis presenting symptoms and diagnosis
Bronchiectasis: Diagnosis
Main symptom = cough with lots of phlegm
Recurrent chest infections
Mucus in the airway forms a broth for bacteria to grow
Sputum turns green / yellow when infected
Bad breath can indicate active infection
Tiredness and poor concentration
Wheeze (common)
Breathlessness, particularly when exerting
Occasional may cough up small amounts of blood from an inflamed airway
Gold standard = C.T. imaging
Width of the branching airways (bronchi) can be determined
Widened bronchi seen on the CT scan can confirm bronchiectasis (signet rings)
Chest X-ray: useful screening tool but limited sensitivity and specificity - ring shadows and tramlines
Pulmonary MRI scanning is evolving (lack of ionising radiation) - developing in use for bronchiectasis of cystic fibrosis
Bronchiectasis management
Bronchiectasis: Management
Antibiotics
Respiratory physiotherapy Inhalers:
Bronchodilator inhalers (SABAs and SAMAs) are used if wheezing and breathlessness are prominent in an acute attack
Used only for those patients who find they help their symptoms.
If they are not helpful they should be stopped
Steroid inhalers are not recommended anymore for bronchiectasis unless there is underlying asthma
Other medications: e.g. aminophylline or theophylline are occasionally used to help symptoms
Antibiotic use in Bronchiectasis
Bronchiectasis: Management (Antibiotics)
Mainstay of treatment
Mild disease: occasional antibiotics would be prescribed
When to prescribe:
Worsening cough and breathlessness or systemically unwell
May not be required if the phlegm turns green
Most commonly amoxicillin (check local guidance & allergies)
Long-term antibiotics:
Severe cases, almost continuous infections
Some antibiotics can administered via nebuliser: high doses of antibiotic directly into the airways
Complications: antibiotic resistance, GI problems (e.g. diarrhoea) and genital fungal infections (e.g. candida)
How is physio used to manage Bronchiectasis?
Bronchiectasis: Management (Physio)
The aim of physiotherapy and other exercise therapies is to help cough up and clear the mucus from the chest (airway clearance)
This helps to prevent a build up of infected mucus
Typically patients with bronchiectasis would be encouraged to get someone in their family to co perform their chosen airways clearance therapy for 20-30 minutes once or twice daily
What is the purpose of spirometry?
Measuring how the volume in the lungs empties
Which of the following is not an obstructive pathology?
1) Emphysema
2) Bronchiectasis
3) Idiopathic Pulmonary Fibrosis
4) Asthma
Idiopathic pulmonary fibrosis
What other measurements must be taken prior to performing spirometry?
Height
Weight
Which of the following would produce a Restrictive Pattern?
1) Severe Anaemia
2) Kyphoscoliosis
3) Cystic Fibrosis
4) Bronchiectasis
2) Kyphoscoliosis (extrathoracic restriction)
3) Cystic Fibrosis
Which of the following is suggestive of an Obstructive Pathology?
1) FEV1 <4.0L
2) FVC < 80% Predicted
3) FVC <4.0L
4) FEV1/FVC Ratio <0.7
4) FEV1/FVC Ratio <0.7
Mr. Lovejoy is a 68 year old gentleman who is seen in his annual review at the Respiratory Clinic, he has COPD controlled with inhalers. His Pulmonary Function Tests show:
FEV1 1.54 – 47% Predicted
FVC 3.40 – 80% Predicted
FEV1/FVC Ratio – 0.45
What severity of COPD does he have?
Severe COPD
In patients with FEV1/FVC <0.7
What are the mild, moderate, severe and very severe classifications for COPD patients
Mild = FEV1 greater or equal to 80% of predicted
Moderate = FEV1 50 - 80% of predicted
Severe = FEV1 30-50% of predicted
Very severe = FEV1 < 30% of predicted
Describe vital capacity
a. The volume of gas measured from a slow, complete exhalation after a maximal inspiration, without a forced effort
Bronchodilation is considered significant after what increase?
FEV1 increase by 12%
Mr. Burns, a 55 year old gentleman, who works as a teacher presents to his GP. He tells you he is suffering from recurrent chest infections. He produces an eggcup-size amount of green sputum daily. He tells you the sputum often sticks in his throat. This has been going on for almost a year.
His only Past Medical History is a severe bout of Whooping Cough as a child.
Which further tests should be complete?
What is the most likely cause of this presentation?
Sputum sample
CXR
Spirometry
Bloods
Bronchiectasis
Residual volume definition
The volume of gas remaining in the lungs after a maximal exhalation
Inspiratory capacity
The maximum volume of air that can be inspired after reaching the end of a normal quiet expiration
Tidal volume + inspiratory reserve volume
Expiratory reserve volume
The extra volume of air that can be expired with maximum effort beyond the level reached at the end of normal, quiet expiration
Vital capacity
The amount of air a person can expel from the lungs after a maximum inhalation. It is equal to the sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume
Inspiratory reserve volume
The extra volume of air that can be inspired with maximal effort after reaching the end of a normal, quiet inspiration
Tidal volume
The amount of air which moves in and out of the lungs during each respiratory cycle
Functional residual capacity
The volume remaining in the lungs after a normal passive exhalation
Total lung capacity
The volume of air in the lungs at different phases of the respiratory cycle
Define cor pulmonale
Right-heart disease resulting from Pulmonary Hypertension
Not a diagnosis, but a complication of another disease
Numerous causes
Cardiac dysfunction-> cardiac failure
Heart Failure is divided into systolic and diastolic
Systolic heart failure–ventricles unable to pump blood hard enough during systole.
Diastolic heart failure–ventricles unable to fill fully during diastole
Can affect either ventricle, or both
Biventricular heart failure
CorPulmonale is when an issue with the lungs causes right-sided cardiac dysfunction which can lead to right-sided heart failure
How does cor pulmonale happen?
Respiratory conditions such as COPD Lead to persistent hypoxia
Hypoxia leads to pulmonary vasoconstriction
Leads to increased resistance
This causes pulmonary hypertension
Pulmonary blood pressure goes to > 25mmHg
Causes of Pulmonary Hypertension, which leads to Cor Pulmonale
Damage to lung tissue
• E.g. COPD
Damage to pulmonary vessels
• E.g. CTEPH
Altered anatomy
• E.g. Kyphoscoliosis
Acute vs chronic causes of cor pulmonale
Acute: pulmonary embolism
Chronic: COPD
What diagnostic methods and what would the results show in an acute causing cor pulmonale eg a PE
CXR
• Usually normal
• May show pulmonary artery dilation in hila or a wedge
infarct
ECG
• Sinus tachycardia
• RA dilatation – tall peaked T waves in lead II
• RV strain and dilatation – RBBB, R axis deviation, T wave inversion
• S1Q3T3 rare
ABG
• Hypoxia
• May show hypocapnia
ECHO
• Enlarged RV, Flattened intra-ventricular septum
Why could chronic COPD lead to cor pulmonale
Pulmonary vasoconstriction due to hypoxia/acidosis Initially intermittent, with exacerbations
Becomes persistent
Heart responds with muscular hypertrophy Increased pressure load – strain on RV
RV dilates and reduces in function
Blood forced back through tricuspid valve into RA Backup of blood into venous circulation
Right ventricular strain
Raised pulmonary blood pressure makes it harder for the RV to pump blood into pulmonary circulation – back pressure
RV is thin-walled and made for pumping blood against a low pressure
In RVH,the muscle mass is increasing, eventually encroaching into the RV, meaning less space for blood to fill the RV -> diastolic heart failure
The increase in muscle mass leads to an increase in oxygen demand as well as squeezing the coronary arteries
Increased demand and reduced supply can lead to RV ischaemia
This leads to weaker contractions and systolic heart failure
Blood often forced backward through the tricuspid valve
Left sided heart failure vs right sided heart failure in cor pulmonale
Left-Sided Heart Failure can cause Pulmonary Hypertension but it would not cause Cor Pulmonale, as the cause is inherent in the heart, not the lungs
Primary Right-Sided Heart Failure, which could occur following a RV MI, or Pulmonary Valve Stenosis – underlying defect is cardiac nor pulmonary. Pure right-sided heart failure is rare.
Signs and symptoms of cor pulmonale
Shortness of Breath
Fatigue
Syncope
Jugular Venous Distension
Right Ventricular Heave
Hepatomegaly
Peripheral Oedema
Chest pain (seen in RV ischaemia)
Sudden death
Diagnosis of cor pulmonale
Echocardiogram
• Increased pressure in pulmonary arteries and RV dilatation/hypertrophy
• Will show intra-cardiac shunts if present
Spirometry
• Assist diagnosis of underlying lung conditions
Right-Heart Catheterisation – GOLD STANDARD
• Measure pulmonary pressures
• Assesses response to vasodilators
