Respiratory Flashcards
accessory inspiratory muscles
sternocleidomastoid,
thescalenusanterior, medius, and posterior, thepectoralis majorandminor,
the inferior fibres ofserratus anteriorandlatissimus dorsi,
theserratus posterior superiormay help in inspiration also theiliocostalis cervicis
accessory expiratory muscles
theabdominal muscles:rectus abdominis,external oblique,internal oblique, andtransversus abdominis
layers before alveoli out to in
capillary endothelium, RBC’S, capillary endothelium, surfactant, alveolar membrane
diffusion barrier
alveolar membrane, surfactant, capillary endothelium, cell membrane
Lung Volumes
inspiratory reserve volume
tidal volume
expiratory reserve volume
residual volume
inspiratory capacity
inspiratory reserve volume + tidal volume
functional residual capacity
expiratory reserve volume + residual volume
vital capacity
inspiratory reserve volume + tidal volume + expiratory reserve volume
why are lung volumes calculated?
assessment of the mechanical condition of the lungs, musculature, airway resistance and effectiveness of gas exchange at the alveolar membrane.
why should ventilation and perfusion of the lungs be adequately matched?
ensuring continuous delivery of oxygen
and removal of carbon dioxide from the body
ventilation rate
volume of gas inhaled and exhaled
from the lungs in a given time period`
perfusion
total volume of blood reaching the pulmonary capillaries in the same time period
ideal V/Q ratio
1
how can a mismatch in ventilation and perfusion occur?
reduced ventilation of part of the lung or reduced perfusion,
and clinically manifests in several respiratory conditions
differential diagnosis of breathlessness
asthma, COPD, cystic fibrosis, PE, iron deficient anaemia, anything causing issues with perfusion or ventilation
asthma
chronic inflammatory disorder of the airways characterized by bronchial wall hyper-reactivity and airway obstruction which is reversible
risk factor for asthma
family history,
prematurity (& low birth weight), tobacco smoke exposure,
obesity and exposure to allergens in the case of atopic asthma
types of asthma
- extrinsic/atopic asthma
- intrinsic/ non atopic asthma
extrinsic asthma
known cause
Airway inflammation in this type
of asthma is due to allergen exposure
atopy
Atopy is a group of disorders that typically occur together and includes rhinitis, eczema, hay-fever and asthma. It is associated with the ADAM33 and PHF11 genes, and as such, typically runs in families
atopic individuals have type 1 hypersensitivity reactions
intrinsic asthma
no identified cause
airway inflammation not due to allergen exposure
patient specific triggers
features of an asthmatic airway
increased mucus,
immune cells,
goblet cells,
thicker basement membrane,
muscle layer
Characteristic features of asthma
airflow limitation
airway hyper responsiveness
airway inflammation
asthma pathway
- asthmatic individual inhales allergen
- stimulates immune response CD4 differentiates into t helper 2
- th2 release cytokines interleukin 4 and 5
- b cells diff into plasma
- interleukin 4 recruits eosinophils
- plasma releases IgE
- igE binds to mast cells - mast cell IgE complexes
- allergen binds to complex
- causes mast cell degranulation
- causes inflammatory mediators histamine, leukotrienes, prostaglandins release
- causes airway inflammation and bronchostriction → clinical symptoms
histamine
amine which causes inflammation
stridor
sound obstruction of in upper airway
intrinsic asthma triggers
- emotion
- viral infection
- smoking
- occupational allergens
- drugs
- cold air
- exercise
- atmospheric pollution
- NSAIDs
spirometry
gold-standard test to diagnose asthma, and is a method of assessing lung function by measuring the volume of air that the patient is able to expel from the lungs after a maximal inspiration. It is a reliable method of differentiating between obstructive airways disorders and restrictive diseases and to monitor disease severity
key measures in spirometry
– FEV1; Volume of air forcibly exhaled after deep inspiration in 1 second.
– FVC; Total volume of air forcibly exhaled in one breath.
– FEV1/FVC ratio
– FEV1 and FVC are expressed as percentages of a ‘predicted normal’ based on
aged, gender and height.
normal ranges for fev1, fvc, fev1/fvc ratio
- FEV1: >80% predicted
- FVC: >80% predicted
- FEV1/FVC ratio: >0.7
typical spirometry findings in obstructive lung disease
– Reduced FEV1 (<80% of the predicted normal).
– Reduced FVC (but to a lesser extent than FEV1).
– FEV1/FVC ratio reduced (<0.7).
airway inflammation pharmacological management
corticosteroids
leukotriene receptor antagonists
monoclonal antibody therapies
corticosteroid examples
beclometasone, budenoside, fluticasone, prednisolone
side effects of corticosteroids
Dysphonia, Oral Candida, Hyperglycaemia, Osteoporosis, Cushing’s
Syndrome
mechanism of action of corticosteroids
bind to intracellular glucocorticoid within bronchial smooth cells to form receptor complexes
complexes interfere in gene transcription
formation of PLA2 inhibited
result - decreased prostaglandin and leukotriene formation → decreased inflammation
mechanism of action of leukotriene receptor agonists
bind to leukotriene receptors on mast cells, eosinophils and alveolar macrophages
prevent leukotrienes from binding
reduced bronchostriction, reduced cytokine release, overall reduced airway oedema
side effects of leukotriene receptor agonists
headache, GI disturbance
examples of leukotriene receptor agonists
montelukast
mechanism of action of monoclonal antibody therapies
binds to IL5 and prevents this from binding to eosinophils
reduces inflammation and subsequent cytokine release
examples of monoclonal antibody therapies
mepoluzimab benraluzimab
airway obstruction pharmacological management
beta 2 agonists
muscarinic antagonists
theophyllines
beta 2 agonists mechanism of action
bind to beta 2 receptors on bronchial smooth muscle
adenylyl cyclase activated and generation of cAMP
PKA activated
bronchial smooth muscle relaxation via potentiation of the SNS
side effects of monoclonal antibody therapies
Abdominal pain, fever, headache, hypersensitivity
side effects of beta 2 agonists
fine tremor
palpitations
hyperkalaemia
arrhythmia
examples of beta 2 agonists
salbutamol, formoterol, tertubuline
mechanism of action of muscarinic antagonists
bind to M2 receptors on bronchial smooth muscle
prevent Ach from binding
minimises activation of PNS, reduced bronchoconstriction
side effects of muscarinic antagonists
dry mouth/eyes
examples of muscarinic antagonists
Ipratropium Bromide, Tiotropium Bromide
mechanism of action of theophyllines
inhibit phosphodiesterase enzyme (normally breaks down cAMP to AMP)
this means more cAMP remains within bronchial smooth muscle and can
go on to activate PKA and induce bronchial smooth muscle relaxation (potentiating SNS)
side effect of theophyllines
arrhythmia, GI disturbance, seizures, hypokalaemia
what is COPD?
an obstructive airways disease that is most commonly the result of a combination of chronic bronchitis and emphysema and characterised by airflow limitation
chronic bronchitis
productive cough for more than 3 months each year for 2 or more consecutive years
emphysema
destruction of the alveolar wall with dilation of airspaces
risk factors for COPD
cigarettes
chemical dust
exposure to atmospheric pollution including biofuels
low birth weight
genetic - alpha-1-antitrypsin deficiency
difference in a cross section of the airway for COPD
increased mucus
damaged cilia
extra goblet cells
impact of COPD on ventilation/perfusion
abnormal V/Q resulting in respiratory acidosis - low O2 high CO2
what is used to stage COPD?
spirometry
stage 1 mild copd
fev1/fvc<0.7
fev1> 80% predicted
stage 2 moderate copd
fev1/fvc<0.7
fev1 50-80% predicted
stage 3 severe copd
fev1/fvc<0.7
fev1 30-50% predicted
stage 4 very severe copd
fev1/fvc<0.7
fev1<30% predicted
pharmacological management in copd
airway obstruction - beta agonists, muscarinic antagonists, theophyllines
airway inflammation - corticosteroids
non pharmacological management in copd
smoking cessation/nicotine replacement
pulmonary rehab
long term oxygen therapy
non invasive ventilation
occasional lung surgery
why does cor pulmonale occur?
increased right ventricular filling pressures from longterm pulmonary hypertension
pulmonary arterial pressure >20mmHg
pathophysiology of cor pulmonale
- COPD and other diseases damage the lungs
- low oxygen leads to hypoxic pulmonary vasoconstriction - limits blood flow to hypoxic alveoli
- vascular remodelling
- increased pulmonary arterial pressure
- increased right ventricular afterload leading to RV dysfunction and failure
diagnosis of cor pulmonale
ECHO - RV enlargement with tricuspid valve regurgitation
CXR - cardiomegaly (enlarged heart), chunky vessels, signs consistent with COPD
V/Q scan - rule out other causes of pulmonary hypertension
right heart catheterisation findings - pulmonary artery pressure >20mmHg
management of cor pulmonale
optimise COPD treatment
long term oxygen treatment
some cases - heart-lung transplant
differences between asthma and COPD
- AGE - asthma any, COPD typically older
- COUGH - asthma dry + night, COPD productive + anytime
- VARIATION OF SYMPTOMS - asthma diurnal variation, COPD consistent and progressive
- REVERSIBILITY OF AIRWAY OBSTRUCTION - asthma yes, COPD no
- CELL INVOLVEMENT - asthma eosinophils and CD4, copd - neutrophils, macrophages and CD8
- SMOKING HISTORY - asthma smoker or non smoker, COPD - typically smoking historu
Pneumonia
type of lower respiratory tract infection, characterized by inflammation of lung tissue due to bacterial, viral, or fungal lung infection
risk factors for pneumonia
smoking
underlying lung disease
immunocompromised
malnourished
underlying cardiovascular disease
types of pneumonia
- community acquired pneumonia
- hospital acquired pneumonia
- aspiration pneumonia
Pathophysiology of bacterial pneumonia
- bacteria is inhaled and uncontrollably replicates and colonises alveolus
- macrophages release cytokines
- vasodilation of pulmonary capillaries - vascular permeability
- more neutrophils recruited which go through leakt junction
- cell debris + neutrophils form pus
- improper ventilation - ventilation perfusion mismatch
- back flow of pus into other alveoli
pathophysiology of viral pneumonia
- virus inhaled and enters cells in alveolar membrane and replicates in alveolar epithelium cell
- cell swells and bursts - cell lysis
- virus infects other cells lining alveoli
- inflammatory mediators and cytokines released during lysis - attracts macrophages
- macrophages release more cytokines - vascular permeability
- lymphocytes attracted and leak into alveoli
- pus build up
- ventilation perfusion mismatch and backflow
key difference between viral and bacterial pneumonia?
viral - lymphocytes
bacterial - neutrophils
expect coryzal symptoms in viral
alveolar congestion presents as:
chest pain, productive cough, breathlessness
clinical symptom: reduced air entry, bronchial breathing, dull to percussion, coarse crackles
cytokines entering systemic circulation presents as:
fevers/rigors, fatigue, confusion
clinical symptom; hypotension, tachypnoea, altered mental state
airway inflammation presents as:
wheeze, breathlessness, chest pain
clinical symptoms: respiratory distress, hypoxia
investigations for pneumonia
- blood tests - WBC and which
- blood cultures - which pathogens
- urinary antigen testing - which pathogens
- viral swabs - flu/rhinovirus
- CXR/CT scan - see blocks
what is the CURB-65 scoring system used for
to see whether to admit to hospital
considers confusion, respiratory rate, BP, age
treatment for pneumonia
- antibiotic therapy
amoxicillin 500mg
OR
amoxicillin 1g + consider doxycycline
OR
co-amoxiclav 1.2g IV + clarithromycin 500mg oral
supplemental oxygen
fluids
analgesics
chest physiotherapy
What is a pulmonary embolism
the obstruction of the pulmonary artery or one of its branches by material – usually a thrombus (blood clot)
risk factors for PE
previous PE/DVT
malignancy
recent surgery
immobility
pregnancy
age
smoking
obesity
clotting problems
acute infection/inflammation
cardiac/neuro comorbidities
oral contraceptives
HRT
how does a thrombus form?
virchows triad
vessel wall injury + hypercoagulability + stasis
thrombus migration embolisation
deep vein → right atrium → right ventricle → pulmonary trunk → branch of pulmonary artery
pathophysiology of persistent hypotension
thrombus lodged in pulmonary artery
→ inc pulmonary vascular pressure
→ inc in right ventricular pressure
→ right heart failure
→ reduced CO and hypotension
→ stimulation of sympathetic nervous system - tachycardia and vasoconstriction
pathophysiology of respiratory failure
thrombus lodged in pulmonary artery
→ reduced blood flow to area of lung supplied by artery
→ ventilation-perfusion mismatch and inflammation → impaired gas exchange - LUNG INFARCTION
→ compensatory hyperventilation
→ persistent hypoxia and hypocapnia causing ALVEOLAR COLLAPSE, RESPIRATORY ALKALOSIS
hypotension and respiratory failure can cause?
respiratory or cardiac arrest
clinical manifestation of right ventricular failure and decreased CO
Hypotension
syncope
dizziness
breathlessness
clinical manifestation of ventilation perfusion mismatch
breathlessness - inc RR
palpitations - inc HR
hypoxia, hypocapnia
clinical manifestation of lung infarction
chest pain
haemoptysis
clinical manifestation of bronchostriction
chest pain
wheeze
cough
clinical manifestation of original thrombus
calf pain/swelling
calf redness
investigations for suspected PE (wells score dependant )
determined by Well’s score:
<4 - d dimer blood test
>4 definitive diagnostic imaging - CT pulmonary angiogram, non conclusive then v/q nuclear medicine scan
other investigations for suspected PE
- blood tests - BNP and troponin
- arterial blood gas
- ECG
- CXR
- bedside echo
wells score criteria
symptoms of DVT
PE most likely diagnosis
tachycardia more than 100bpm
immobilization or surgery in last month
prior dvt/pe
hemoptysis
active malignancy
management of PE for hemodynamically stable
anticoagulation treatment + discharged with follow up
