Respiratory Lecture ILO’s Flashcards

1
Q

Describe the physiological relationships involved in V/Q matching.

A

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)

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2
Q

How is CO2 transported around the body?

A

Plasma (9%)
Carboamino had ogle in (10-13%)
Bicarbonate (78%)

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3
Q

Name the lungs lobes and fissures:

A

Right:
Lobes-
Superior
Inferior
Middle

Fissures-
Oblique
Horizontal

Left:
Lobes-
Superior
Inferior

Fissures-
Oblique

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4
Q

What is the hilum and what are the hilar structures?

A

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

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5
Q

What are the 10 bronchopulmonary segments?

A

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.

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6
Q

Structure of the bronchi tree:

A

Trachea divides into 2 main bronchi:
Primary Bronchi
Secondary Bronchi
Tertiary Bronchi

Bronchioles
Terminal bronchioles
Respiratory bronchioles
Alveolar ducts
Alveolar sacs
Alveoli

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7
Q

Describe asthma and it’s triggers

A

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

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8
Q

Describe COPD

A

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)

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9
Q

How to differentiate between COPD and asthma

A

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

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10
Q

Describe the mechanics of inspiration

A

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.

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11
Q

How does the respiratory control centre control rate of breathing?

A

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.

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12
Q

Role of the medulla in RCC

A

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.

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13
Q

Role of the pons in RCC

A

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.

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14
Q

What is the role and where are chemoreceptors found?

A

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.

  1. 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
  2. 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
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15
Q

Why shouldn’t pure oxygen be given to someone with chronic hypercapnia?

A

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).

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16
Q

What is a type 1 hypersensitivity reaction?

A

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

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17
Q

What is atopy?

A

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.

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18
Q

Pathology of an asthmatic airway:

A

• 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.

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19
Q

What is asthma?

A

§ 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

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20
Q

Pathophysiology of asthma

A

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

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21
Q

Epidemiology of asthma:

A

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

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22
Q

Signs and symptoms of asthma

A

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

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23
Q

History taking triggers during suspected asthma consultation

A

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

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24
Q

Differential diagnoses if asthma has been ruled out

A

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

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25
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
26
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
27
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
28
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.
29
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
30
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
31
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
32
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
33
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
34
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
35
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
36
Inhaler devices
§ MDI: Metered Dose Inhaler § Evohaler & Easibreathe § DPI: Dry Powder Inhaler § Turbohaler, Accuhaler, Easyhaler, Handihaler § SMI: Soft Mist Inhaler § Respimat
37
Colours of metered dose inhalers
§ Salbutamol (SABA) – Blue § Beclomethasone (ICS) – Brown § Salmeterol (LABA) – Green § Fostair (LABA/ICS) – Pink § Seretide (LABA/ICS) – Purple
38
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
39
Inhaler technique method:
1. Hold inhaler upright, remove cap and shake well 2. Stand/sit up and tilt chin upwards 3. Breath out fully 4. Place lips around mouthpiece to get a good seal 5. Breath in slowly and steadily, whilst simultaneously pressing the canister on the inhaler 6. Continue to breathe in slowly until lungs feel full 7. Remove the inhaler from your mouth and seal your lips 8. Hold your breath for 10 seconds, then gently breath out
40
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
41
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
42
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
43
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
44
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
45
Acute cardiac reasons for sob
Cardiac Severe pulmonary oedema Acute myocardial infarction Cardiac arrhythmia Pericarditis and pericardial effusion
46
Chronic pulmonary reasons for sob
● COPD ● Emphysema ● Bronchiectasis ● Fibrosis ● Pleural effusion ● Lung cancer ● Asthma ● Hereditary lung disorders (e.g. cystic fibrosis) ● Pulmonary Tuberculosis
47
Chronic cardiac reasons for SOB
Left ventricular disease Heart valve disease (mitral & aortic stenosis) Arrhythmias Pericardial causes
48
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?
49
Quantifying breathlessness MRC scale
1. Not troubled by breathless except on strenuous exercise 2. Short of breath when hurrying on a level or when walking up a slight hill 3. Walks slower than most people on the level, stops after a mile or so, or stops after 15 minutes walking at own pace 4. Stops for breath after walking 100 yards, or after a few minutes on level ground 5. Too breathless to leave the house, or breathless when dressing/undressing
50
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?
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
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
59
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
60
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
61
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
62
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
63
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
64
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)
65
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
66
What is the purpose of spirometry?
Measuring how the volume in the lungs empties
67
Which of the following is not an obstructive pathology? 1) Emphysema 2) Bronchiectasis 3) Idiopathic Pulmonary Fibrosis 4) Asthma
Idiopathic pulmonary fibrosis
68
What other measurements must be taken prior to performing spirometry?
Height Weight
69
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
70
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
71
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
72
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
73
Describe vital capacity
a. The volume of gas measured from a slow, complete exhalation after a maximal inspiration, without a forced effort
74
Bronchodilation is considered significant after what increase?
FEV1 increase by 12%
75
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
76
Residual volume definition
The volume of gas remaining in the lungs after a maximal exhalation
77
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
78
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
79
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
80
Inspiratory reserve volume
The extra volume of air that can be inspired with maximal effort after reaching the end of a normal, quiet inspiration
81
Tidal volume
The amount of air which moves in and out of the lungs during each respiratory cycle
82
Functional residual capacity
The volume remaining in the lungs after a normal passive exhalation
83
Total lung capacity
The volume of air in the lungs at different phases of the respiratory cycle
84
Define cor pulmonale
Right-heart disease resulting from Pulmonary Hypertension Not a diagnosis, but a complication of another disease Numerous causes
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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
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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
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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
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Acute vs chronic causes of cor pulmonale
Acute: pulmonary embolism Chronic: COPD
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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
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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
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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
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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.
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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
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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
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CXR findings in cor pulmonale
◦ Not very sensitive ◦ May show prominent pulmonary artery ◦ May show oligaemic (reduced blood flow) peripheral lung fields
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ECG findings in cor pulmonale
ECG ◦Abnormalities reflect the presence of right ventricular hypertrophy, strain or underlying pulmonary disease ◦ Right-axis deviation ◦ Increased P wave amplitude in leads II, II and aVF (p-pulmonale) ◦ Right bundle branch block ◦ Low-voltage QRS
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Treatment of cor pulmonale
Treat the underlying cause O2 therapy – consider LTOT (pO2 <8kPa on RA) Diuretics Vasodilators for PH – e.g Sildenafil Venesection – in severe polycythaemia
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Prognosis of cor pulmonale
◦ Poor prognosis ◦ LTOT improves prognosis ◦ Prognosis is worse in COPD patients with PH vs. COPD patients without PH ◦ In COPD Patients with a mild degree of Pulmonary Hypertension (20- 35mmHg) - 50% mortality at 5 years
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What investigations could be carried out for a suspected DVT?
D dimer - will increase as sign of a clot CXR Bloods - FBC, U+E ECG- T wave inversion lead 2-4, RBBB, sinus tachycardia, RAD
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Type 1 respiratory failure
Type 1: Low oxygen -> Cell death due to hypoxia (will kill you first) Aetiology: Shunt (Pneumonia), Diffusional (Covid), V/Q mismatch (PE), Ventilation (Coma), Altitude Mx: Oxygen, CPAP/PEEP, treat underlying disease, lung transplant
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Type 2 respiratory failure
Type 2: High carbon dioxide +/- low oxygen (2 things) Cell death from acidaemia Ventillational++ (Low RR, Low TV, bronchoconstriction) Coma, Opioids, COPD, Asthma Mx: Ventilate patient (awake with BIPAP, asleep with endotracheal tube), bronchodilators, treat underlying disease, lung transplant
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What causes a rightwards shift to the oxyhemoglobin curve?
Increase temp Decrease ph Increase CO2 Increase 2, 3 DPG Therefore oxygen is more readily released at the tissues Low affinity for oxygen at the tissues
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What causes a left shift of the oxyhaemoglobin curve?
Decrease in temperature Increase in pH Decrease in CO2 Decrease in 2,3 DOG Increased affinity for O2 so oxygen is not released readily at the tissues
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50 year-old woman with pneumonia, has been on 60% Venturi for 3 days Admission ABG FiO2 60% SaO2 95% PaO2 10 kPa ABG after 3 days FiO2 60% SaO2 98% PaO2 20 kPa What is going on? What should you do?
Patient is improving Can half FiO2 as don’t need PaO2 of 20, just need 10kPa And unnecessarily high FiO2 is bad for lungs and wastes oxygen supplies
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What physiological changes can be made for pH homeostasis to be altered?
Increase breathing rate Kidneys excrete more H+ or HCO3- CO2 +H2O<< carbonic anhydrase >>H2CO3 << >> H+ + HCO3-
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Normal range of CO2 and the affects if it goes outside of this
Carbon dioxide (4.7-6.0 kPa) Resp Acidosis (CO2 >6.0 kPa) Hypoventilation (low TV, low RR): fatigue/coma/opiates Bronchoconstriction (Asthma/COPD) Resp Alkalosis (CO2<4.7) Hyperventilation (high TV, high RR), panic attacks, pregnancy, high altitude, drug toxicity
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Bicarbonate normal range and affects if it goes outside of this
Bicarbonate (22-26 mmol/l) Base excess (BE) (+2/-2 mmol/l)...high values correlate with high bicarb (amount of strong acid or base that must be added to normalise pH) Metabolic Acidosis (BC<22): BE<-2 Causes: AGMA- lactic acidosis, ketoacidosis, renal insufficiency NAGMA- renal tubular acidosis, GI loss of H3CO3, GI fistulas Metabolic Alkalosis (BC>26): BE>+2 Causes: vomiting (loss of H+), hypovolemia, diuretics Cushing syndrome, hyperaldosteronism
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What is hypoxaemia?
Low O2 in the blood
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Describe intrapleural pressure and trans pulmonary pressure
• Intrapleural pressure is pressure in the pleural cavity. Usually a little less than atmospheric pressure (negative) • Transpulmonary pressure is the difference between intrapleural pressure and alveolar pressure.
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How does hypoxaemia occur?
Depressed breathing = hypoventillation / blocking the gas exchange Causing a ventilation perfusion mismatch as: Blood and gases aren’t going into the alveoli in the correct proportion Too much blood/ too little ventilation Too much ventilation/ too little blood
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Difference in ventilation/ perfusion in alveoli in the base and apex
APEX: (lungs pull more as less supported) Ventilation: • More negative intrapleural pressure • Larger trans mural pressure gradient • Alveoli with larger volume • Smaller Compliance • Less Ventilation Perfusion: Lower intravascular pressures Higher resistance Less blood flow BASE: Ventilation: • Less negative intrapleural pressure • Smaller Ptp • Alveoli with smaller volume • Larger Compliance • More Ventilation Perfusion: Greater vascular pressure Lower resistance Greater blood flow
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What is ventilation/ perfusion (VQ) mismatch
Ventilation perfusion mismatch or V/Q defects are defects in the total lung ventilation/ perfusion ratio. It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen. This happens if you have an obstructed airway, such as when you’re choking or if you have an obstructed blood vessel such as a blood clot in your lung.
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What are common viral causes of upper respiratory tract infections?
Upper Respiratory Tract Infections • Usually always viral • Viruses include: – Respiratory syncitial virus (RSV) – Adenovirus – Rhinovirus – Coranovirus – Influenza (A,B,C) – Para-influenza
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40 year old man presents with fever, cough and sore throat with photophobia. Preceded by 2 days of muscles aches, pains, fever and a headache. What’s the diagnosis?
Influenza (flu)
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Influenza info
Influenza (ie. Flu) • Caused by influenza which belong to orthomyxovirus group of viruses • RNA viruses • 3 types: A, B and C • Winter epidemics; or all year epidemics if close to equator • Influenza A responsible for pandemics – Aquatic birds act as natural reservoirs, several other animals can become infected – Spanish flu 1918, Bird flu 2004 • Influenza B responsible for more local, less severe outbreaks – Mostly humans act as reservoirs – Little antigenic diversity
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Influenza symptoms
Influenza: Symptoms • Initially fever, muscle aches, rigors • Later may develop: headache, sore throat, dry cough, conjunctivitis, photophobia • When symptoms resolve usually a phase of malaise/lethargy- usually occurs for weeks but can take months!!
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Influenza investigations and when would you investigate?
Influenza: Investigations • Tests usually not necessary • Naso-pharyngeal swabs • PCR Could test on: Vulnerable Going into hospital Immuno compromised
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Influenza complications
• Bronchitis • Viral pneumonia or secondary bacterial pneumonia • Sinusitis • Otitis media • Encephalitis • Pericarditis
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Influenza treatment
(Supportive) • Bed rest • Paracetamol, NSAID • In severe cases requiring hospital admission antibiotics may be given to prevent side effects (bacterial pneumonia) • Oseltamivir (Tamiflu) and Zanamivir (Relenza): – Active against influenza A + B – Recommended in UK for those over 65 years and under 65’s if “at risk” (immunosupressed, chronic respiratory disease etc.) – Reduce length of illness – Not clear whether reduce rate of complications/hospital admission
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Influenza prevention
• WHO tries to predict strain of influenza which will cause most suffering/cause biggest endemics • Vaccine formed depending on these strains • Immunity lasts just over a year • Vaccine available to: – >65 years – Pregnancy – Certain medical conditions (chronic lung diseases, CKD, diabetes, heart disease, immunosuppressive states) – Very overweight – Living in long-stay residential care home – Receive carer’s allowance/main carer for someone/Front line health care and social care worker
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30 year old man develops runny nose and watery eyes and mild sore throat. Symptoms fully resolve over 2-3 days. What is the diagnosis?
Acute coryzal illness (common cold)
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What virus can cause Acute coryza (common cold)?
Acute Coryza (Common Cold) • Usually caused by rhinovirus – Others: coranovirus, RSV, para-influenza
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Complications of acute coryza (common cold)
• Complications: otitis media, pneumonia,
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25 year old man complaining of sore throat, pyrexia and tender lymph nodes in neck. On inspection the mouth is red and inflamed. What is the diagnosis?
Pharyngitis
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Viral, bacterial and fungal causes of pharyngitis
Viral (majority) • Commonly caused by adenovirus • Can occur in the flu (influenza virus) • Can occur in acute coryza (rhinovirus, RSV, para-influenza etc.) • EBV- causes infectious mononucleosis • Herpes simplex- ulcers (labial/buccal ulcers and vesicles, gingivostomatitis Bacterial Causes • Group A beta-haemolytic streptococcus (GAS) • Diphtheria (grey membrane on throat) Fungal Causes (rare) • Candida albicans – usually underlying cause e.g. Immunosupression, steroid use
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Pharyngitis investigation:
• Non usually required • Rapid antigen testing for GAS or influenza – Negative test does not exclude ! • Throat culture (for bacteria) • Bloods if required Rapid test for step A if required
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FeverPAIN
FeverPAIN GAS vs Viral - Fever>38degreesC 1 - Purulence (pharnygeal/tonsillar exudate) - Attend rapidly (3 days or less) 1 - Severe Inflamed tonsils 1 - No cough or coryza 1 A score of 0 or 1 is associated with a 13% to 18% likelihood of isolating streptococcus. A score of 2 or 3 is associated with a 34% to 40% likelihood of isolating streptococcus. A score of 4 or 5 is associated with a 62% to 65% likelihood of isolating streptococcus.
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Centor criteria
Centor Criteria - Tonsilar exudate 1 - Tender anterior cervical lymphadenopathy or lymphadenitis - History of fever (>38degreesC) 1 - Absence of cough 1 A score of 0, 1 or 2 is thought to be associated with a 3 to 17% likelihood of isolating streptococcus. A score of 3 or 4 is thought to be associated with a 32 to 56% likelihood of isolating streptococcus.
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Pharyngitis treatment
• Treatment: – Supportive (salt water gargling, medicated lozenges, anaesthetic sprays) – Antibiotic treatment not required if bacterial infection • Phenoxymethylpenicillin (Clarithromycin= alternative) – Delayed antibiotic prescription – Give antibiotics if: marked systemic upset, at risk of serious complications, valvular heart disease, region of higher prevalence of rheumatic fever – Consider treatment with antibiotics if: high Centor or FeverPAIN score, immunosuppressed and other at risk co-morbidities (including history of rheumatic fever)
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28 year old develops sore throat, pyrexia, hoarseness and pain when speaking. What is the diagnosis?
Laryngitis
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What is laryngitis? What virus / bacteria can cause it? What are the symptoms? How is it treated?
• Inflammation of larynx • Sore throat, fever, cough • In addition pain on swallowing and pain when speaking and hoarse voice • Commonest cause is rhinovirus – Others: Influenza, parainfluenza, RSV • Bacterial causes: Group A strep, streptococcus pneumoniae • Self-limiting • Treatment:Supportive – Antibiotics rarely needed
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What is tonsillitis? What virus / bacteria can cause it? What are the symptoms? How is it treated? How is bacteria/ viral injection distinguished?
• Causes: Majority viral • Bacterial Causes (30%): – Group A beta-haemolytic streptococcus – Very rarely: Mycoplasma pnemoniae, diphtheria • Symptoms: Dysphagia, lymphadeonopathy, haliotosis • Treatment: Supportive - Antibiotics: If given Penicillin V - Corticosteroids can reduce inflammation - Tonsillectomy indicated if recurrent (>5 attacks a year for at least 2 years; quinsy with recurrent tonsillitis) Do the fever test to see if likely of bacterial or viral
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Peri-tonsillar Abscess/Quinsy
• Presentation: Along with tonsillitis symptoms may have trismus (pain on closing mouth) • Should be referred urgently to ENT for management (consideration of surgery)
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• 17 year old boy • General malaise with fever for several days • Now develops sore throat and has tender lymph nodes in neck- mainly cervical lymph nodes • Develops macular rash after Amoxicillin
Infective Mononucleosis (Glandular fever)
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What virus causes infective mononucleosis?
Infective Mononucleosis • Aka Glandular Fever • Commonly affects adolescents and young adults • Caused by ebstein barr virus (EBV) – DNA virus part of the herpes group of viruses • Incubation period: 4-5 weeks
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Infective mononucleosis symptoms and complications
Infective Mononucleosis (glandular fever) : Symptoms • Fever, headache, malaise, sore throat • Inflamed tonsils with white patches • Palatal petichiae • Transient macular skin rash – 90% who receive Ampicillin develop rash • Cervical lymphadenopathy • Splenomegaly • Hepatitis • Complications – Meningitis, Encephalitis, Myocarditis, Neuropathy, chronic fatigue syndrome (5 times more likely compared to other causes of URTI), haemolytic anaemia, thrombocytopenia No contact sport for 3 months
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Infective mononucleosis diagnosis
Infective Mononucleosis: Diagnosis • Paul Bunnel Test/Monospot Test/Heterophil Antibody Test: – Rapid test which gives results quickly – Detects heterophile antibodies (IgM) that agglutinate sheep erythrocytes – False positive in viral hepatitis, Hodgkin’s lymphoma, acute leukaemias, malaria • FBC/Blood Film: Lymphocytosis – Atypical mononuclear cells • Specific Ig Mantibodies • EBV PCR
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Infective mononucleosis treatment:
• Supportive treatment • Majority is self-limiting • Steroids may be needed if neurological complications or marked haemolysis and thrombocytopenia
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What is acute sinusitis and what can cause it?
• Infection in paranasal sinuses • Commonly viral infections (98%) • Usually always associated with some URTI • Bacterial Causes: Strep pneumoniae, Haemophilus influenzae, Staph
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Symptoms of acute sinusitis
• Symptoms: Frontal headache, rhinnorhoea, facial pain and tenderness, fever
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Treatment of acute sinusitis
• Treatment: Nasal decongestants, Abx (Co-Amoxiclav), Nasal corticosteroids, steam inhalation
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Complications of acute sinusitis
• Complications (rare): Meningitis, Orbital cellulitis/abscess, brain abscess
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67 year old man with a cough productive of green sputum, shortness of breath and chest tightness over the past week There is widespread wheeze and crackles on his chest He smokes 10 cigarettes per day What is the diagnosis?
Acute bronchitis
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What are the common causes and risk factors of acute bronchitis?
• Commonly caused by RSV – Others= rhinovirus, para-influenzae • Bacterial causes include Strep pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae • Risk Factors: Tobacco smoke, pollution, COPD • If underlying lung disease or smoker more likely to have bacterial cause
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Symptoms and treatment of acute bronchitis
• Symptoms:Productivecough,wheeze • Treatment: Supportive (usually self limiting and resolves in 4-8 days) – Abx usually not needed
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Pathogen incidence in pneumonia
• Streptococcus 30.4% • Mycoplasma 12.6% • Chlamydia 12.6% • Legionella 4.7% • Haemophilus Inf. 4.4% • Enterobacteriaceae 3.1% • Staphylococcus Aur. 0.5% • Other pathogens 20% • Not known 39.5%
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Classifications of pneumonia
Pneumonia • Infection/consolidationinthealveoli Classification • Location- Lobar vs bronchopneumonia – Lobar: Within the whole of one or more lobes – Bronchopneumonia: Affects lobules of lungs with bronchi and bronchioles - more diffuse consolidation • Hospital vs Community Acquired • Atypical pneumonia • Aspiration pneumonia • Ventilator acquired
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Bronchopneumonia
Bronchopneumonia • Infection diffuse throughout lobules and usually in bronchioles and bronchus • More diffuse • Differentiated from bronchitis as signs of pneumonia such as bronchial breathing, patchy changes on CXR, harsh breath sounds • Typically elderly patients with other medical conditions develop • Commoner in underlying lung disease • Common terminal event
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Aspiration pneumonia
Aspiration Pneumonia • Acute aspiration of gastric contents into lungs • Gastric acid can destroy lining of lungs • Causes: Impaired consciousness, reflux oesophagitis, poor swallow, oesophageal stricture • Persistent pneumonia can lead to anaerobic infection • Can progress to lung abscess or bronchiectasis
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Hospital acquired pneumonia
Hospital Acquired • Hospital Acquired: At least 48 hours into hospital admission – Usually gram negative baccillus (ie. Rod shaped) such as Pseudomonas and enterobaccili (such as Klebsiella) – Staphyloccocus aureus – MRSA – Pseudomonas – Klebsiella
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How is pneumonia presented on a chest x ray?
Pneumonia: CXR • CXR consolidation may lag behind symptoms • Consolidation may remain on the CXR for several weeks when the patient is recovered • Follow-up CXR usually done at 6-8 weeks and persistence of consolidation at this point usually implies a bronchial abnormality (usually carcinoma with persisting infection)
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Pneumonia investigations and management
• Investigations: – CXR – Blood Tests: FBC, U+E, CRP (inflammatory markers), LFTs, Blood Cultures, ABG • Mycoplasma antibodies – Urine for legionella and pneumococcal antigen – Sputum MC+S (microscopy, culture + sensitivity) • Management (Varies between trusts, this is only a guide): – Community Acquired: • CURB-65 1= Oral Amoxicillin • CURB-65 2= Oral Amoxicillin + Clarirthromycin • CURB-65 3-5= IV Co-Amoxiclav + Clarithromycin – Hospital Acquired: Co-Amoxiclav, IV Cephalosporin if severe – Aspiration: Co-Amoxiclav – Follow-up CXR in 6-8 weeks
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Streptococcal pneumoniae
• ie. Pneumococcal pneumonia • Commonest bacterial pneumonia • Gram +ve diplococci • Commoner in elderly, alcoholics, post-splenectomy, immuno-suppressed • Almost always a preceding viral infection • Followed by fever, pleuritic chest pain, cough productive of rusty coloured sputum • CXR= Lobar consolidation • Urine send for pneumococcal antigen • Treatment: Penicillin based Abx or cephalosporins • Prevention: Pneumococcal vaccine, 5 yearly
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Staphylococcus aureus pneumonia
• Staphylococcus aureus – Uncommon cause – Usually preceded by influenza infection – Risk if elderly, IV drug users, patients with long-term IV catheters, immunosuppression – Typically gives bronchopneumonia with cavities which later can form abscesses and empyema can develop
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Klebsiella pneumoniae pneumonia:
– Rare – Typically occurs in elderly, diabetics, alcoholics – Usually causes severe pneumonia (typically bronchopneumonia, and affects upper lobes) – Can cause a cavitating pneumonia, lead to abscesses
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Chlamydia pneumoniae pneumonia
• Chlamydia pneumoniae – Outbreaks in institutions and families – Person-to-person spread (not via animal reservoir) – Causes pharyngitis, laryngitis, sinusitis, followed by pneumonia – CXR= Segmental infiltrates
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• Chlamydia psittaci pneumonia
• Chlamydia psittaci – Causes psittacosis – History of exposure to birds- especially parrots – Causes headache, fever, dry cough, lethergy, arthalgia, hepato-splenomegaly
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• Haemophilus influenzae pneumonia
• Haemophilus influenzae: – Frequent cause of exacerbation of chronic bronchitis in COPD and can lead to pneumonia if COPD.
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Anaerobes pneumonia
• Anaerobes: – Usually occur if there is an underlying condition such as diabetes – Often associated with aspiration
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Viral pneumonia
Viral Pneumonia • Very uncommon • Usually due to influenza A virus – Others: adenovirus, measles, CMV, varicella zoster • SARS (Severe Acute Respiratory Syndrome): – Due to coranovirus – High mortality rate – Outbreak in 2003
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Legionella pneumophilia pneumonia
Atypical cause of pneumonia • Colonizes water tanks up to 60 degreesC • Causes outbreaks in hotels (hotel air conditioning/hot water systems) • Flu-like symptoms precede chest symptoms (usually dry cough) • CXR: Bi-basal consolidation, lymphopenia • Complications: D+V, hepatitis, hyponatraemia, haematuria • Diagnosis: Plasma serology – Urine testing for legionella antigen • Treatment: Macrolide e.g. Clarithromycin, Erythromycin +/- Rifampicin • Mortality= 10%
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Mycoplasma pneumonia pneumonia
Mycoplasma pneumonia • Epidemics usually occur every 4 years • Usually occurs in teens and those in 20s • Commoner in boarding institutions • Generalize malaise, headache, arthalgia before chest symptoms • CXR= Reticulo-nodular shadowing or patchy consoldiation • Investigations: Mycoplasma serology (ie. blood test for Mycoplasma IgM) – Cold agglutins- can cause haemolytic anaemia • Complications: Skin rash/erythema multiforme, myocarditis/pericarditis, haemolytic anaemia/low platelets, neurological abnormalities, GI symptoms • Treatment: Macrolides e.g. Clarithromycin, Erythromycin
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Erythema Multiforme
Complication of erythema multiforme Erythema Multiforme -Typically target lesions, raised, round, can appear oedemartous - Severe cases involve oral mucosa causing Steven Johnson Syndrome (severe Causes Drugs: NSAIDs, sufonamides, anti-conulsants, Allopurinol Infections: Herpes simplex, Mycoplasma, Orf, BCG, Idiopathic Non-Hodgkins lymphoma, leukaemia, multiple myeloma
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Lung Abscess
Lung Abscess • Localised infection in the lung within a cavity • Cavitation on CXR and usually with fluid level • Causes: – Aspiration (anaerobes) – Foreign body ingestion – Bronchial carcinoma – Staphylococcus or klebsiella pneumonia – Septic emboli (usually from staphylococcus) cause multiple metastasis • Additional sign may include finger clubbing • 20-30% develop empyema
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Empyema
Empyema • Presence of pus within pleural cavity • Usually from bacterial spread from a severe pneumonia or rupture of lung abscess into pleural space • 70% of empyema have anaerobes but usually mixed flora found • Investigations: Obtain sample of infection via: • Pleural tap, bronchoscopy, percutenous transthoracic aspiration – Ultrasound and CT chest • Treatment: Chest drain – Antibiotics (usually for several weeks)
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What test could you do to check for streptococcal pneumoniae? And how would you treat this?
• CXR= Lobar consolidation • Urine send for pneumococcal antigen • Treatment: Penicillin based Abx or cephalosporins • Prevention: Pneumococcal vaccine, 5 yearly
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What bacteria would cause a pneumonia in elderly, diabetics and alcohol ICS?
Klebsiella pneumoniae: – Rare – Typically occurs in elderly, diabetics, alcoholics – Usually causes severe pneumonia (typically bronchopneumonia, and affects upper lobes) – Can cause a cavitating pneumonia, lead to abscesses
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What pneumonia usually breaks out in boarding schools and families?
• Chlamydia pneumoniae – Outbreaks in institutions and families – Person-to-person spread (not via animal reservoir) – Causes pharyngitis, laryngitis, sinusitis, followed by pneumonia – CXR= Segmental infiltrates
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What pneumonia can be caused by bird exposure?
Chlamydia psittaci – Causes psittacosis – History of exposure to birds- especially parrots – Causes headache, fever, dry cough, lethergy, arthalgia, hepato-splenomegaly
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What pneumonia is usually caused after an exacerbation of chronic bronchitis in COPD patients?
Haemophilus influenzae: – Frequent cause of exacerbation of chronic bronchitis in COPD and can lead to pneumonia if COPD.
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What atypical pneumonia is likely after a holiday or cruise?
Legionella pneumophilia • Colonizes water tanks up to 60 degreesC • Causes outbreaks in hotels (hotel air conditioning/hot water systems) • Flu-like symptoms precede chest symptoms (usually dry cough) • CXR: Bi-basal consolidation, lymphopenia • Complications: D+V, hepatitis, hyponatraemia, haematuria • Diagnosis: Plasma serology – Urine testing for legionella antigen • Treatment: Macrolide e.g. Clarithromycin, Erythromycin +/- Rifampicin • Mortality= 10%
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What pneumonia is common in teens/ 20’s and in boarding institutions?
Mycoplasma pneumonia • Epidemics usually occur every 4 years • Usually occurs in teens and those in 20s • Commoner in boarding institutions • Generalize malaise, headache, arthalgia before chest symptoms • CXR= Reticulo-nodular shadowing or patchy consoldiation • Investigations: Mycoplasma serology (ie. blood test for Mycoplasma IgM) – Cold agglutins- can cause haemolytic anaemia • Complications: Skin rash/erythema multiforme, myocarditis/pericarditis, haemolytic anaemia/low platelets, neurological abnormalities, GI symptoms • Treatment: Macrolides e.g. Clarithromycin, Erythromycin
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Patient with swallow difficulty may be at risk of what type of pneumonia?
Aspiration
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37 year old man develops generazlied aches and pains, anorexia, blocked nose and headaches over 24 hours. Is pyrexic, has a productive cough of a little sputum. Recovers spontaneous after 5 days. But feels lethargic and tired for 3 more weeks
Influenza
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36 year old woman develops sore throat and blocked nose with watery discharge over a few hours. After 24 hours discharge becomes green/yellow and voice is hoarse. Able to continue normal activities and all symptoms resolve in 3 days.
Acute coryza
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19 year old woman with dry sore throat and hoarse voice which developed over 24 hours. Painful but unproductive cough and pain in her throat when tries to speak
Acute laryngitis
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5 year old body brought to GP, feeling sniffly on going to bed at night, but looks a lot worse now. Pyrexic, complains of sore throat and making a wheezing noise on inspiration. Child holds his head tilted upwards
Acute epiglottis
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79 year old lady with end stage lung cancer admitted with pyrexia, productive cough and SOB, widespread crackles heard throughout chest
Bronchopneumonia
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16 year old body suffered from sore throat with headache, muscle pains and macular rash several weeks ago, this settled after about 1 week but since feeling tired, lethergic and wanting to sleep for at least 12 hours/day.
Infectious mononucleosis
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What virus in a common cause of acute respiratory syndrome (SARS)
Coronavirus
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What virus is a common cause of erythema multiforme?
Herpes simplex virus
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What virus is the commonest cause of pharyngitis?
Adenovirus
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What virus causes large pandemics of flu?
Influenza A
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What virus causes a positive Paul- Brunnel Test Name of the disease?
Ebstein-barr virus Infectious mononucleoise
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26 year old man with 2 days of malaise, fever, SOB with pain on right side. Developed a cough and expectorating rusty sputum. CXR shows consolidation at right lower lobe
Streptococcus pneumoniae Right lower lobe pneumonia
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67 year old woman with 5 days of malaise, cough productive of yellow sputum, nil on examination but CXR shows two cavities with air-fluid levels
Assess caused by Staphylococcus aureus Probably because of excess IV use
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28 year old man presents with productive cough SOB, preceded by headache, joint pain and malaise. CXR reveals patchy consolidation, He is anaemic with a raised MCV
Mycoplasma pneumoniae pneumonia
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53 year old man brought to A+E after a fit. Wife says complaining of malaise, muscle aches and dry cough for 7 days since return from holiday. Bloods reveal Na of 124mmol/L, K= 4.2mmol/L
Legionella pneumoniae
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62 year old man who has parrots at home presents with 2 weeks of SOB associated with dry cough and widespread joint ache with fever. Enlarged liver and spleen. CXR shows patchy consolidation in both lobes
Chlamydophila psittaci
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56 year old man presents with pleuritic chest pain, SOB and pyrexia. He has a history of alcohol abuse, is drowsy, and smells very strongly of alcohol. You notice coughing of a currant jelly like sputum. Which organism is associated?
Klebsiella
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23 year old man is admitted to the neuro rehab unit following an RTA after where he sustained a spinal cord fracture at C2. He is 3 days into his admission and was making good progress but has now developed a purulent productive cough over the past 3 hours. His temperature is 36.7degreesC, P= 120, BP= 119/80, SATs= 91% in RA. There is reduced air entry at his right base, and you note he has a tracheostomy and NG tube in situ. What is the most likely organism?
Aspiration of stomach contents
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An 82 year old man presents to A+E with shortness of breath and a productive cough. He is unable to give you a history but on examination his temperature is 38.1degreesC, HR is 76bpm, BP= 108/76, RR= 31/min, SATs= 92% (RA), bibasal creps are heard at his lung bases, worse on the right side. Which treatment would be most appropriate?
Do CURB-65 score IV Co-Amoxiclav and oral Clarithromycin
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What factors affect respiratory function?
Neural stimulus to breathe Respiratory mechanics • Respiratory muscle/ thoracic cavity effectiveness Airway resistance Elastic recoil of lungs Gas exchange interfaces • Lungs to blood • Blood to tissues
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How is CO2 transported?
Physically dissolved (10%) Bound to Hb (30%) • Carbaminohaemoglobin (HbCO2) • Binds to globin rather than haem part As bicarbonate (60%) • CO2 +H2O=H+ +HCO3- • Driven by enzyme carbonic anhydrase in erythrocytes • Generates acid which triggers respiration
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High concentration O2 therapy
Safe in uncomplicated Type 1 Respiratory Failure • Pneumonia,pneumothorax,PE,shock Oxygen low Carbon dioxide low or normal Respiratory centres functioning normally Little risk of hypoventilation or carbon dioxide retention Give 100% oxygen or 15L/min via mask
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Low concentration O2 therapy
Used where patients are at risk of CO2 retention, or low O2 requirements Blunting of hypercapnic drive due to overproduction of bicarbonate and mopping up of excess H+ Drive to breathe now from hypoxic stimulus Too much oxygen can cause hypoventilation and worsening of CO2 retention Patient may carry oxygen alert card with documented target saturations
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O2 delivery methods
O2 delivery methods Wall oxygen - Readily available in hospital Up to 15L/min Oxygen cylinders - Medium (2L/min) or high (4L/min) flow Oxygen concentrators - More economical than cylinder and Useful for LTOT
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Nasal cannula
• Comfortable • Easy to wear • Non-obstructive to eating and drinking • Should only go up to 4L/min • Unable to control exact inspired O2 concentration • Can lead to dry nasal mucosa • Used in LTOT Not good for mouth breathers
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Venturi masks
Controlled O2 therapy ¡ Put a number of L/min through a valved mask to achieve a specific concentration ¡ Colour-coded O2 concentration range: ¡ Blue: 24%V = 2L ¡ White: 28%V = 4L ¡ Yellow: 35%V = 8L ¡ Red: 40%V = 10L ¡ Green: 60%V = 15L Good for COPD patients as very controlled
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O2 DELIVERY METHODS – NON- REBREATHE MASK
O2 DELIVERY METHODS – NON- REBREATHE MASK Rebreather Around 1/3 patient’s exhaled air goes into reservoir bag. Rebreathed CO2 acts as respiratory stimulus Non-rebreather One way valves means most exhaled air escapes so inhaled oxygen concentrations are higher Emergency O2 therapy A+E or ambulance 15 litre non rebreather = about 85% oxygen Emergency scenario where patient is hypoxic
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O2 DELIVERY METHODS – HIGH-FLOW O2
O2 DELIVERY METHODS – HIGH-FLOW O2 • High-Flow Nasal Cannula • Wide-bore nasal cannula • O2 driven through a humidified circuit otherwise conc would be too high causing nose bleed • Delivers up to 100% O2 therapy • Improves work of breathing Very thick nasal cannula T1 resp failure Usually HDU
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CONTINUOUS POSITIVE-AIRWAY PRESSURE/BI-LEVEL POSITIVE AIRWAY PRESSURE – CPAP/BIPAP
NIV - non invasive ventilation Obstructive sleep apnoea patients- splints airways open to stop hypoxia BIPAP/CPAP ¡ Tight fitting mask that supplies higher than atmospheric pressure to splint open airways and prevent them from collapsing ¡ Can be used with/without oxygen ¡ CPAP ¡ Pressure constant throughout respiratory cycle ¡ Used in neonates, mild obstructive sleep apnoea ¡ BIPAP ¡ Pressure drops during expiration phase to encourage more movement of air in and out of lungs ¡ Used in hypercapnic respiratory failure, severe OSA
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LONG-TERM O2 THERAPY ¡ Only prescribed after careful assessment ¡ Patient must have stopped smoking due to explosion risk ¡ 16 hours daily of 1-2L/min may prolong survival in COPD ¡ Arterial PO2 <7.3 kPa or <8kPa with complications (measured with ABG) ¡ Polycythaemia, pulmonary hypertension, peripheral oedema ¡ Prescribe using HOOF form – usually with Community Respiratory Team input
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Indications for acute O2 therapy
Exacerbation of longstanding lung disease • Eg. COPD, cystic fibrosis, other fibrosis Severe kyphosis • Restrictive lung defect caused by physical inabilty to fully inflate lungs Respiratory muscle weakness • Eg. Motor neurone disease Overdose of drugs causing respiratory depression • Opiates/ benzodiazepines
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INDICATIONS FOR ACUTE O2 THERAPY – T2RF
Patients at risk of developing Type 2 Respiratory Failure: • COPD • Kyphoscoliosis • Motor Neurone Disease ¡ Initially give controlled concentration of 28%V and adjust appropriately ¡ Aim for oxygen saturations of 88-92% ¡ Monitor patient condition and ABG’s regularly for signs of CO2 retention and acidosis ¡ May require BIPAP (biphasic positive airways pressure)
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A 24-year-old woman presents to A&E with sudden onset breathlessness and severe right sided chest pain on inspiration. No history of cardiac/ respiratory disease. O/E dyspnoea, distress. Chest clear. HS normal. P 110 reg, RR 30, SpO2 90%, BP 120/80,T 36.5 How much oxygen would you give? How? What would you expect an ABG to show? What are the possible causes?
15L non rebreather aim for >94% ABG = Type 1 respiratory failure Possible causes: PE, asthma, pneumonia, pneumothorax
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15 year old boy attends A&E. Short of breath and distressed.Audible wheeze. Using accessory muscles. Unable to complete sentences. ¡ Uses brown and blue inhalers for asthma ¡ O/E P 120 reg, RR 30, BP 100/60,T 36.7, SpO2 88%. HS normal. Chest – wheeze throughout ¡ How would you manage? ¡ What would an ABG show? Part 2 Given 100% oxygen via non- rebreathe mask, nebulisers and steroids You notice he is tiring and his breathing becomes slower and quieter You repeat his ABG. What might it show now? Would this change your oxygen therapy?
Bronchodilator 15L non rebreather T1 resp failure T2 resp failure Controlled O2 therapy
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¡ 85 year old man attends A&E with increasing SOB for several days. Coughing up green sputum. ¡ Ex smoker, 60 pack years. Known COPD, on maximal therapy. Normally becomes breathless with ADL’s. ¡ O/E Barrel chest, thin, dyspnoeic. Raised JVP, ankle/ sacral oedema. P 90 reg, RR 24, BP 120/80,T 37.7, SpO2 83%. HS normal. Chest wheezy with poor air entry bilaterally. Possible diagnosis? What might an ABG show? What would your oxygen therapy be? He improves over several days. He feels back to normal and is keen to go home.You check a final blood gas. It shows PaO2 is 7.7 kPa on room air.Would you suggest any further treatment?
Cor pulmonale ABG would show increased CO2 O2 therapy- 15L non rebreather, do ABG to see if CO2 retainer Further treatment- cut off is 7.3 for normal but 8 for pulmonary hypertension, do echo to see if right sided HF
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Clinical features of suspected pulmonary embolism , pneumothorax or sepsis
Respiratory rate of more than 30 breaths per minute. • Tachycardia greater than 130 beats per minute. • Systolic blood pressure less than 90 mmHg, or diastolic blood pressure less than 60 mmHg (unless this is normal for them). • Oxygen saturation less than 92%, or central cyanosis (if the person has no history of chronic hypoxia). • Peak expiratory flow rate less than 33% of predicted. • Altered level of consciousness. • Use of accessory muscles of respiration (particularly if the person is becoming exhausted). • Features of foreign body aspiration
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Time definitions for cough
Time definitions for cough • Acute • < 3 weeks • Sub-acute • 3 – 8 weeks • Chronic • > 8 weeks
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What are the causes of an acute cough?
What are the causes of an acute cough? Respiratory causes: • URTI • Foreign body aspiration • Pulmonary embolism • Pneumothorax • Acute bronchitis • Pneumonia • Acute asthma • Exacerbation of COPD • Pertussis (whooping Cough) • Lung cancer Non Respiratory Causes • Aortic aneurysm Cardiac failure – pulmonary oedema • GORD
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Causes of a cough
• Upper Airway Syndrome • Pertussis • Acute Bronchitis • Asthma • COPD • COVID 19 • Allergies • Heart Failure • Side Effect ACE Inhibitors • Foreign Body Aspiration • PE • Pneumothorax • Lung Ca • URTI • Bronchitis • Pneumonia • Pertussis • Bronchiectasis • Post Infectious Cough • TB • Smokers Cough • GORD • Heart Failure • Interstitial Lung Disease
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Acute cough history taking questions (likely OSCE station)
• Started suddenly or developed over time? • Did anything trigger the cough? • How long has cough lasted? • When do you cough? • Is the cough worse when you exercise • Are you breathless even when your not coughing? • Have you got any chest pain when you are coughing? • Are you coughing up any phlegm (mucus)? • What colour is the phlegm? • Is there any blood in the phlegm? • Do you generally feel ill? • Do you have a high temperature? • Has there been any unintentional weight loss? • Any recent contacts with anyone with Tuberculosis? • Are you a smoker or recent smoker? • What is your current and past occupation if retired? • Have you started any new medication recently particularly for high blood pressure? • Travel/Hotels
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Acute causes of upper respiratory tract infections
ACUTE CAUSE Includes: • Sinusitis • Rhinitis • Pharyngitis • Laryngitis • Usually self diagnosed • Cough usually develops after nasal symptoms have cleared and can take up to 3 weeks to resolve Children • Restlessness or irritability • Nasal congestion/discharge and sneezing — severe nasal congestion may interfere with feeding, breathing, and sleep • Cough — occasionally, vomiting may follow a bout of coughing. • Fever Management • Fluid, healthy food, rest • Paracetamol/NSAID • Safety net
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Foreign body aspiration
Foreign Body Aspiration • Vary from life-threatening obstruction and death to non-specific symptoms of cough, wheezing, fever, haemoptysis, or dyspnoea. • large objects can completely occlude the trachea and result in asphyxiation and death • small objects can lodge in the lower lobar airways and cause wheezing and coughÒatelectasis, post- obstructive pneumonia, bronchiectasis, or lung abscess. • Can lead to misdiagnosis of asthma, reactive airways disease, bronchitis, or pneumonia. • The right lower lobe of the lung is the more common site – right bronchus is wider and steeper than the left - objects to enter more easily than the left side At risk groups • Children, >70 years • Stoke, dementia • Impaired cough reflex • medications, alcohol, drugs Present with • Acute intractable cough • Followed by side effects
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Foreign body aspiration investigations
Foreign Body Aspiration • Investigations • CXR • Most aspirated objects are radiolucent • Non-specific findings that suggest foreign body aspiration include atelectasis, pneumonia, air trapping, and pneumomediastinum. Bronchiectasis, lung abscess, and empyema are usually late findings. • A normal chest x-ray does not rule out foreign body aspiration, and CT scan or bronchoscopy is warranted for confirmation. • CT • More sensitive, non invasive Investigation/Management • Bronchoscopy • Flexible for stable • Rigid for unstable
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Post infectious cough
Post Infectious Cough • Sub acute cough (3-8 weeks) • Following URTI • Can be dry or productive • Thought to be • Inflammatoryresponse • Increased sensitivity • Normal respiratory examination • Diagnosis is clinical and one of exclusion • Investigations to consider • CXR - normal • Sputum sample • Explain that the cough may persist for several months and advise the person to re-attend for assessment if the cough does not improve after 2 months.
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Pertussis
Pertussis (whooping cough) • Resurgence of pertussis in highly vaccinated populations, the disease continues to be a public health and medical concern. • Three stages: catarrhal, paroxysmal, and convalescent. cough may persist for several months • Initial symptoms may be similar to a cold, with rhinorrhoea and lacrimation, or a dry cough followed by episodes of severe coughing. Fever may be absent or low-grade. • There may be vomiting after coughing, or an inspiratory whoop • Inspiratory whooping is a characteristic symptom • Bordetella pertussis • Notifiable disease!
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Chronic cough causes
COPD • Asthma • Cough variant asthma • Allergies • Upper airway cough syndrome • Gastroesophageal reflux • Medication side effects • Cancer • TB Post nasal drip
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Upper airway cough syndrome (UACS)
• CHRONIC Cause • Cough present for > 8 weeks • Non productive • Presence of abnormal sensations arising from the throat - patients describe something stuck in the throat • There are no definitive tests • A trial of empirical therapy • antihistamine • plus a decongestant • Recommended to confirm the diagnosis in the presence of a supportive history and exam • Chlorphenamine 4 mg orally every 4-6 hours, maximum 24 mg/day plus pseudo ephedrine 60mg orally every4-6hours, maximum 240 mg/day; 120 mg orally (extended- release) twice daily Approximately 60% of patients improve with this approach •improvement is usually seen within 2 weeks
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Gastroesophageal Reflux Disease
• Gastroesophageal reflux disease(GORD) is a common cause of chronic cough • Risk factors • Smokers, alcohol, NSAIDs, diet • May not have typical reflux symptoms • Cough, throat clearing, voice changes, worse on lying flat • Trial of PPIs
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ACEI Induced Chronic Cough
• ACE inhibitor cause a non productive cough in 5-20% of patients, affecting women more than men • The effect is not dose related, and the cough can occur after one week or to six months after therapy has been initiated. • The cough should spontaneously resolve a few days to several weeks after the ACE inhibitor is discontinued. • A four week trial of withdrawal is usually sufficient to determine whether the medication caused the cough • Cough related to ACEI usually subsides within 2 weeks but some reports suggest up to four weeks
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Suspected lung cancer
Suspected lung Ca Patient must have a CXR within 2 weeks if: • Cough • Fatigue • Shortness of breath • Chest pain • Weight loss • Appetite loss • 2 of the above unexplained or.. • 1 of the above unexplained and have ever smoked • CXR 2 weeks: Age >40 and any of... • Persistent or recurrent chest infection. • Finger clubbing. • Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy. • Chest signs consistent with lung cancer. • Thrombocytosis
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Suspected Mesothelioma referral pathway
Mesothelioma CXR within 2 weeks if: • Cough • Fatigue • Shortness of breath • Chest pain • Weight loss • Appetite loss • 2 of the above unexplained or.. • 1 of the above unexplained and have ever smoked • 1 OF THE ABOVE AND ASBESTOS EXPOSURE
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Red flags in cough
• A cough that lasts more than three weeks should be thoroughly investigated • Systemic symptoms – fever sweats, weight loss (possible Tuberculosis, lymphoma, bronchial carcinoma) • Coughing up blood (haemoptysis) could be sign of tuberculosis, bronchial carcinoma. • Cough associated with copious sputum production (might indicate bronchiectasis) • Night sweats associated with coughing (consider Tuberculosis and also consider lymphoma) • Associated with significant dyspnoea (heart failure, COPD, Fibrotic lung disease) • Hoarseness. Laryngeal problem • Peripheral oedema with weight gain. • Prominent dyspnoea, especially at rest or at night. • Smokers aged over 45 years with a new cough, change in cough, or coexisting voice disturbance • Trouble swallowing.
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Haemoptysis classification
• From a small amount of blood-streaked sputum • To massive bleeding with life-threatening consequences due to airway obstruction and haemodynamic instability. • Mild haemoptysis: <30 mL over 24 hours • Frank or moderate haemoptysis: ≥30 mL and <600 mL over 24 hours • Massive haemoptysis: 600 mL or more over 24 hours • Consider >150 mL haemoptysis as life-threatening, as this volume of blood could flood the conducting airways completely
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Haemoptysis – Taking a History
• Most important to confirm that the bleeding is from the lungs. • Is there any bleeding from the nose/pharynx? • Any dental problems? • Any gastro-oesophageal reflux? • Any vomiting? • Is the blood mixed with the sputum?
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Information from sputum
• Is it frothy and pink sputum (suggests heart failure?) • Purulent or rusty coloured suggests a bacterial infection • Any suggestion of infection in sputum? Is the sputum yellow/green coloured sputum? • Any possible exposure to tuberculosis? (check recent travel) • White sputum with blood streaks might suggest possible tumour • Frequency of haemoptysis (recurrent?) – any suggestion of recurrent bleeding might suggest malignancy • Has blood in the sputum over a prolonged time led to anaemia? Any obvious signs and symptoms of anaemia • Past medical history & drug history – any known bleeding tendencies or medications that could cause these? • Any clues to possible undiagnosed malignancy (smoking history?)
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Common Causes of haemoptysis
Common causes • Acute Bronchitis • Chronic Bronchitis (COPD) • Pneumonia • Lung Cancer • Metastasis • Pulmonary Embolism • Infections can cause haemoptysis by causing necrosis of adjacent bronchial vessels or local mucosal ulceration. • In bronchiectasis - recurrent inflammatory destruction and healing lead to bronchopulmonary vascular anastomoses. • Cardiac • In left ventricular failure and mitral stenosis, blood-streaked sputum is caused by rupture of pulmonary veins or capillaries, or by anastomoses between the bronchial and pulmonary arteries distended by elevated intravascular pressure or pulmonary venous hypertension. Neoplastic. (Cancer) • increase in the bronchial artery supply to the region of the tumour. • Haemoptysis results from necrosis, mucosal invasion, or direct local invasion of a blood vessel. • Massive haemoptysis • invasion into a blood vessel and its adjacent airway results in vascular airway fistula.
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Covid-19
Severe Acute Respiratory Distress Syndrome Coronavirus-2 Infection with the SARS-CoV-2 virus Spread by aerosols, small droplets and surfaces Diagnosis: reverse transcription PCR of nasopharyngeal and oropharyngeal swab samples
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Covid-19 symtoms
¡ Fever ¡ Dry Cough ¡ Fatigue ¡ Change in sense of smell/taste ¡ Shortness of Breath ¡ Myalgia ¡ Up to 1/3 of cases are totally asymptomatic ¡ Some patients continue to experience symptoms for over 12 weeks – Long COVID
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Why might liver function test rise in covid?
Covid causes livid congestion so liver function markers rise
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Case study- arterial blood gas on 40% V • Interpret this blood gas • What type of failure is the patient in? pH 7.51 pCO2 3.3 pO2 8.9 Bicarb 23.7 SATs 95.8
Respiratory alkalosis Type 1 resp failure as hyperventilating
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Covid complications
Pneumonia Acute Respiratory Distress Syndrome Multi-Organ Failure VTE – prevalence of approximately 8% in initial wave Superadded bacterial infection – prevalence of approximately 7% in initial wave Long covid
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Treatment options for covid
RECOVERY Trial – Dexamethasone and Tocilizumab Dexamethasone approved for use in July 2020 – reduces 28-day mortality in patients requiring O2 Tocilizumab approved for use in March 2021 (Steroids to treat the cytokines storm)
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Levels of care
Level 1 Care •Ward-Based Care •For example: O2 via a venturi mask, IV Antibiotics/IV Fluids Level 2 Care (single organ support) •May be ward-based or High- Dependency Unit •For example: Continuous Positive Airway Pressure (CPAP) or Nasal High-Flow O2 (NHF) Level 3 Care •Intensive Care Unit •For example: Inotropic Support, Intubation and Ventilation (multi organ failure)
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Acronym to break bad news to patients
DIFFICULT COMMUNICATION ¡ SPIKES Setting (no interruptions) Perception (what do you know so far) Invitation (are you happy for me to proceed) Knowledge (deliver news pause do you understand) Empathy Summary (next steps)