Respiratory Flashcards
IgE Hypersensitivity
Risk Factors Asthma
Definition
Asthma may be defined as a chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity. The symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction.
- FH of Atopy
- Antenatal factors : maternal smoking, viral infection during pregnancy (especially RSV)
- Low birth weight
- Not being breastfed
- Maternal smoking around child
- Exposure to high concentrations of allergens (e.g. house dust mite)
- Air pollution
- ‘Hygiene hypothesis’: Studies show an increased risk of asthma and other allergic conditions in developed countries. Reduced exposure to infectious agents in childhood prevents normal development of the immune system resulting in a Th2 predominant response
Pt could suffer from hayfever (allergic rhinitis) or Eczema (dermatitis)
A number of patients with asthma are sensitive to aspirin. Patients who are most sensitive to asthma often suffer from nasal polyps
Presentation of Asthma
Signs & Symptoms
Symptoms
- Cough (dry)
- Dyspnea (SOB)
- Wheeze (tight chest)
Signs
- Expiratory wheeze on auscultation
- Reduced Peak Expiratory Flow Rate (PEFR)
Reduced PEFR indicates a decrease in the ability to blow air out forcefully, which can be a sign of breathing difficulties
(aetiology)
Pathophysiology of Asthma
is it reversible or irreversible obstruction?
Epidiemologically: It affects over 10% of children and around 5-10% of adults, can also be caused by occupation.
- Inhalation of Allergen or Irritant (T1 Hypersensitivity reaction)
- Inflammation of Airway -> Bronchoconstriction/Bronchospasm -> Airflow Obstruction
- Asthma is Reversible Obstruction (generally) caused by:
- Inflammatory Cells infiltration
- Mucus Hypersecretion - with Mucus Plug Formation
- Smooth Muscle Contraction
What is Type 1 Hypersensitivity Reaction
People susceptible to T1 hypersensitivity have excesss T Helper 2 cells
- Inhalation of allergen causes release of IL 14, 12 + 5 from excess T helper 2 cells
- IL 14 + 12 cause IgE release from Plasma cells
- IgE causes degranulation of Mast cells
- Mast cells release Histamines, Leukotriens, Prostglandins
- These cause Obstruction (mentioned in Pathophysiology of Asthma Card)
Excess T helper 2 cells commonly found in Atopic Conditions
IL5 causes released of Eosinophils which cause degranulation of Mast cells
Pathologically what could cause Asthma to become irreversible obstruction?
Due to uncontrolled Asthma
Irreversible obstruction is caused by:
- Basement Membrane Thickening
- Collagen deposits causing Fibrosis
- Airway Remodelling by Smooth Muscle Hyperplasia and Hypertrophy
Asthma is reversible obstruction (usually) which is caused by: 1. Inflammatory Cells 2. Mucus Hypersecretion 3. Smooth Muscle Contraction
What is FEV1:FVC
Separate FEV1, FVC, FEV1:FVC
What is the normal FEV1:FVC Value
FEV1: Force Exipratory volume in 1 second (amount of air forcefully inhaled in one second - SPEED)
FVC: Forced Vital capacity is the volume of air that can forcibly be blown out after full inspiration (AMOUNT-CAPACITY)
FEV1:FVC: is the ratio of the forced expiratory volume in the first one second to the forced vital capacity of the lungs. (How fast you can blow out to how much you store)
these are measured in L
Normal value of FEV1:FVC is above 0.75-85, though this is age dependent.
- Values less than 0.70 are suggestive of obstruction
- Restrictive lung diseases often produce a FEV1/FVC ratio which is either normal or higher
- Obstruction usually has reduced FEV1 compared to normal lungs
- Restrictive usually has normal or high FEV1 but reduced capactiy (FVC)
Investigations for Asthma (In Order)
Give positive results for asthma below
- Identify whether its caused occupationally (refer to specialist)
- Spirometry with Bronchodilator reversibility
- Fractional Exhaled Nitric Oxide (FeNO) -Test of Inflammation
- Peak Flow Variablity Diary - Usually 2 - Weeks
- Direct Bronchial Challenge Testing (w/ Histamine)
Results of tests
- FEV1/FVC ratio less than 70% (or below the lower limit of normal if this value is available) is considered obstructive
- Greater than 12% increase in FEV1 on reversibility testing supports a diagnosis of asthma.
- 40ppb in FeNO considered diagnostic/positive (some guidelines see FeNO as useless)
- In children perfrom spiro with broncho dilator - if spiro +ve but bronchodilator -ve then reinvestigate using FeNO
- Serial peak flow measurements at work and at home are used to detect occupational asthma
Long term Management of Asthma?
Mix of NICE and British Throcacic Society
Clarify MART Therapy too
- Newly Diagnosed start Short acting Beta Agonist (SABA - Salbutamol)
- If uncontrolled add inhaled corticosteroid (ICS - Fluticasone)
- if symptoms persist then add Leukotriene Receptor Antagonist (LTRA - Montelukast)
- If they persist then SABA + low-dose ICS + Long-acting beta agonist (LABA - Salmeterol) - continue LTRA depending on patient
- If persisting then swap ICS/LABA for MART (see below) ( SABA +/ LTRA + MART (symbicot))
- If they still persist then consider medium dose of MART
- Persistence: then ditch the MART and add high dose ICS
- Consider Theophyline or long-acting muscarinic receptor antagonist Such as Tiotropium (Theophyline can be toxic due to narrow therapeutic window)
MART: (Maintenance and reliever therapy) -
* a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required
* MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)
What are the features of Acute asthma?
what does an ABG show for Acute Asthma?
- Worsening Dypnea, Wheeze, Cough, Tachypnea
- Accessory Muscle Use
- Salbutamol use of no or limited help
- Usually triggered by infection, excercise, cold weather
On ABG = Respiratory Alkalosis
- Tachypnea leads to drop in CO2
- Normal or Raised CO2 or Low O2 = Respiratory Acidosis - LIFE THREATENING
Grading of Acute Asthma Exacerbations
3 Grades and their descriptions
Moderate
- PEFR 50-70%
- Speech Normal
Severe
- PEFR 33-50%
- RR >25
- HR 110bpm
- Struggling to complete sentences
Life Threatening
- PEFR <33%
- Oxygen Below 92%
- Tired, Confused, Cyanosis, Bradycardia
- No Wheeze/Silent Chest
- Haemodynamically Instablity
- pa O2 <8%
Management of Acute Asthma
give criteria for discharge too
Admit Pts to hospital who:
Low O2 Sats
Pregnant
History of Acute Asthma Attacks
Moderate
- Inhaled Salbutamol
- 4 dose ICS - 2weeks
Severe
- Nebulised Salbutamol
- Corticosteroids (50mg Oral Prednislone) or (IV hydrocortisone)
Life threatening
- Oxygen therapy
- Nebulised Ipratropium Bromide
- IV Magnesium sulfate
- IV Aminophyline (consult senior)
- Consider intubation (for intubation start early as bronchoconstriction can cause difficulty to intubate)
Abx given if there is evidence of bacterial Ix
Criteria for discharge:
* been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
* inhaler technique checked and recorded
* PEF >75% of best or predicted
How does stepping down treatment work with Asthma?
- Should try and step down treatment every 3 months
- When reducing the dose of inhaled steroids the BTS advise us to do this by 25-50% at a time.
Clearly patients with stable asthma may only have a formal review on an annual basis but it is likely that if a patient has recently had an escalation of asthma treatment they would be reviewed on a more frequent basis.
What causes Occupational Asthma?
and how should PEFR be measured for diagnosis?
- Most Common cause : Isocyanates (Spray Paint, Foam Moulding)
- platinum salts
- soldering flux resin
- glutaraldehyde
- flour
- epoxy resins
- proteolytic enzymes
Serial measurements of PEFR are recommended at work and away from work.
How does Obstructive Lung disease differ from Restrictive Lung disease?
Give Examples of each one
Obstructive lung diseases involve difficulty exhaling due to narrowed airways, while restrictive lung diseases result in difficulty inhaling with reduced lung expansion, and mixed patterns may coexist.
Restrictive
- Pulmonary fibrosis
- Asbestosis
- Sarcoidosis
- Acute respiratory distress syndrome
- Infant respiratory distress syndrome
- Kyphoscoliosis e.g. ankylosing spondylitis
- Neuromuscular disorders
- Severe obesity
Obstructive
- Asthma
- COPD
- Bronchieactasis
- Bronchiolitis Obliterans
Define Pulmonary Emobolism
what makes up VTE?
Clot (thrombus) which is found in Pulmonary artery.
Usually travels from lower extremities of the body.
The thrombus will block the blood flow to the lung tissue and strain the right side of the heart
DVTs and PEs are collectively known as venous thromboembolism (VTE).
Risk Factors for Pulmonary Embolism?
- Immobility - long haul journey/surgery
- Pregnancy
- HRT - Oestrogen Specificallly
- Malignancy
- Polycythemia
- SLE
VTE Prophylaxis given to all hospital patients: low molecular weight heparin (Contraindication: currently bleeding or already on anticoagulation therapy)
Anti-embolic compression stockings are also used unless contraindicated (e.g., peripheral arterial disease).
Pathophysiology of Pulmonary Embolism
- Thrombus breaks off from lower extremities travels via Inferior Vena Cava into RA -> Rv then into Pulmonary circulation
- Thrombus blocks perfusion (Q) of CO2 + O2 in Alveoli leading to V/Q mismatch (as ventilation (V) is normal)
- Theres an Increase in V/Q -> Increased Alveolar Arterial Gradient
- Low O2 in blood (due to low perfusion) = Hypoxemia.
- Hypoxemia triggers chemoreceptors in aortic/carotid bodies stimulating CNX and CNIX
- CNX and CNIX trigger breathing centre in brain (medulla) -> Tachypnoea. (causing CO2 exhalation)
- This in turn reduced CO2 -> Hypocapnia -> Respiratory Alkalosis
- Pulmonary Vasoconstriction -> reduces O2 supply to lungs -> Lung Infarction -> Haemoptysis
- Increased Afterload -> Pulmonary HTN -> RV dilation/dysfunction -> Raised JVP (as blood flows back in to superior vena cava)
Chemoreceptors for Resp, Baro receptors for Cardiac
Signs & Symptoms of Pulmonary Embolism
- Pleuritic Chest pain
- Dyspnoea (SOB)
- Cough - leading to Haemoptysis
- Tachycardia
- Tachypnoea
- Fever
- Hypotension
There may also be signs and symptoms of a deep vein thrombosis, such as unilateral leg swelling and tenderness.
What is Virchow’s Triad and how is it linked to PE?
Presence of 3 factor that predisposes development of vascular thrombosis
- Stasis of Blood Limited movement of blood can cause clots (blood flow should be laminar)
- Hypercoaguability Coagulation gives rise to clots (incl. hypercoaguble conditions)
- Endothelial Injury Platelet aggregation causes clot formation
Causes of each below.
- Limited movement (planes, post-op, paralysis post CVA), Obesity; causes obstruction of veins, Pregnancy; uterus can compress iliac vein, Varicose veins; prevent flow of blood
- Factor V lieden, Prothrombin gene mutation, Oestrogen, Lung + Pancreatic Cancer, Nephrotic Syndrome
recommended by the NICE guidelines (2020)
What is the PERC rule
Pulmonary embolism rule-out criteria (PERC)
- Only performed when low clinical suspiscion
- All the criteria must be absent to have negative PERC result, i.e. rule-out PE
If suscpicion is >15% then move straight to Wells Score
Includes: Age>50, Tachypnoea, Hypoxaemia, Prev DVT, Unilateral leg swellin, haemoptysis, recent surgery, Oestrogen use.
What is the Well’s Score?
- The Wells score predicts the probability of a patient having a PE
- Score of > 4 PE likely
- Score of <4 PE less likely
- If score above 4 then perform CTPA
- If there is a delay in getting the CTPA then interim therapeutic anticoagulation should be given until the scan is performed.
- if CTPA -ve then perform doppler (proximal leg vein) ultrasound to rule out DVT
If score less than 4 then perform D-dimer to be on safe side
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1
More info on Wells Card
Investigations for Diagnosing Pulmonary embolism
including gold standard
D Dimer if low wells score
- All patients to have chest x-ray to exclude other pathology. (normally clear, sometimes wedge-shaped opacification seen)
- Perform CTPA if not contraindicated
- V/Q scan if CTPA contraindicated - RENAL DISEASE as CTPA requires contrast medium
- Classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. Sinus Tachycardia - most common
CTPA is Gold Standard
things which can raise D Dimer
* Pneumonia
* Malignancy
* Heart failure
* Surgery
* Pregnancy
Management of Pulmonary Embolism
Outpatient for haemodynamic stable, lack of comorbidities + home support
Pulmonary Embolism Severity Index (PESI) score used to determine to treat for outpatients or inpatients
- Hospital admission for some - give O2 + analgesia as required
- 1st line DOAC (apixaban - rivoraxaban) - LMWH is alternative followed by Warfarin (Vit K antagonist)
- Provoked PE: 3mths Treatment Unprovoked: 6mths
Haemodynamically Unstable
- Hypotension
- Begin thrombolysis with fibrinolytic such as alteplase
- alongside continuous infusion of unfractionated heparin
- risk of bleeding with thrombolysis
- thrombolysis given via peripheral canula or central catheter
ORBIT score can be used to help assess the risk of bleeding
Contraindications for DOAC include: severe renal impairment, antiphospholipid syndrome.
What alternative is there for Patients with constant PEs on adequate anticoagulation
Patients who have repeat pulmonary embolisms, despite adequate anticoagulation, may be considered for inferior vena cava (IVC) filters. These work by stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries. IVC filter use is currently supported by NICE