Respiratory clinical conditions Flashcards
What is decompression sickness?
Increased partial pressure at below sea level leads to diffusion of nitrogen from lungs into blood so if the diver ascends too quickly the rapid change in pressure causes bubble formation leading to tissue damage and pain.
What is respiratory distress syndrome?
Loss of surfactant upsets Laplace’s law and surface tension of small alveoli isn’t kept low so there is alveolar collapse due to pressure differences in different sized alveoli. Less surface area for gas exchange and respiratory failure.
How is respiratory distress syndrome in premature babies managed?
Mum is given steroid injections to stimulate surfactant generation if anticipated.
How is carbon monoxide poisonous?
CO binds to haemoglobin and forms carboxyhaemoglobin so haemoglobin has less space to bind to O2 and also has greater affinity so won’t deliver O2.
What are the results of acute and chronic carbon monoxide poisoning?
Acute - death.
Chronic - headaches, confusion, nausea etc.
How is carbon monoxide treated?
Hyperbaric O2 therapy - O2 concentration high enough to displace CO and restore haemoglobin function.
What is pulmonary embolism?
Thrombus from a site other than the lungs lodges in one of the arteries of the pulmonary tree.
What are the effects of pulmonary embolism?
V/Q mismatch in the section of lung the artery supplies so pO2 of the blood leaving that section is normal but pCO2 is low as no new blood enters so has longer to equilibrate with alveolar air. The health lung is overloaded due to blood being redirected there. Too much blood means inefficient exchange of pO2 - blood has low pO2 and normal pCO2. Overall, there is type I respiratory respiratory failure.
What is the fatal danger of a pulmonary embolism?
Sudden pulmonary hypertension causes mechanical shock from RV failure in the heart.
How is hypercapnia from V/Q mismatch in pulmonary emboli corrected?
Increased respiratory rate.
What are the types of respiratory failure?
Type I - pO2 low, pCO2 normal or low.
Type II - pO2 low, pCO2 high.
What is type I respiratory failure caused by?
Diffusion defect or V/Q mismatch.
What diffusion defects can cause type I respiratory failure?
Pulmonary oedema - fluid in alveoli so increased diffusion distance.
Emphysema - decreased compliance of lungs causing hyperexpansion and reduced surface area for gas exchange.
Pulmonary fibrosis - fibrous deposits between alveolus and capillary basement membrane so increased diffusion distance.
What is type II respiratory failure caused by?
Decreased respiratory effort, chest wall defects, decreased compliance, extremely high airway resistance.
What can decrease respiratory effort and hence cause type II respiratory failure?
Narcotics/head injuries/neurological deficits impact ability of respiratory centre. Muscular dysfunction anywhere from the brain to the NMJ (MS, Duchenne’s muscular dystrophy etc).
What chest wall defects can cause type II respiratory failure?
Rigid structure means it’s harder to move and inflate the lungs. Severe scoliosis/kyphosis, severe pectum excavatum/carranatum, flail chest (multi-rib fracture), tension pneumothorax.
What can cause decreased compliance that causes type II respiratory failure?
Severe pulmonary fibrosis.
What causes increased airway resistance that leads to type II respiratory failure?
Severe life threatening asthma attack, acute exacerbation of late-stage COPD.
What is asthma?
A reversible airway obstruction.
What is the pathophysiology of asthma?
Airway remodelling: increased airway smooth muscle thickness; damaged epithelia/basement membrane from chronic inflammation from reaction to allergens. Contraction of smooth muscles, due to histamine and prostaglandin release in response to stimuli, increase airway resistance so less air is expired initially.
What is a hypothesis that could explain why asthma is so prevalent in the Western world?
Hygiene hypothesis - overuse of cleaning chemicals means immune system is less trained for harmless bacteria so hyperactive.
What are the types of asthma?
Allergic, viral - disappears by 5 years, occupational asthma.
What are the features of a history leading to an asthma diagnosis?
Expiratory, polyphonic wheeze; dry cough with diurnal variation (worse at night) - induced by exercise; breathlessness; chest tightness; reversed with B2 agonists.
What are the features of examination leading to an asthma diagnosis?
Eczema; lethargy and uncomfortable at rest; below heigh for age and underweight; laboured breathing signs - Harrison’s sulcus (indrawing of costal cartilages), tracheal tug, subcostal recession, obvious use of accessory muscles of inspiration.
What are the features of investigation leading to an asthma diagnosis?
Primary - PEFR reduces, single breath spirometry FEV1:FVC >70% but reversed with salbutamol.
Supportive (optional) - FENO high levels of NO, skin prick sensitivity to allergens, chest X ray excludes other causes.
What is the long term treatment for asthma?
Lifestyle - minimise exposure to allergens, exercise, fresh air.
Pharmacological - relievers: B2 agonists salbutamol and M3 antagonists ipratropium, preventers: low dose corticosteroids to suppress local immune function.
How is an asthma attack recognised?
Poor respiratory effort/loud wheeze/silent chest; panicked, agitated, sympathetic features - sweating, dry mouth, dilated pupils, nausea; altered GCS (cerebral hypoxia); O2 saturation <92% with peripheral cyanosis; pO2 low and pCO2 normal or rising.
How is an asthma attack managed?
High flow 100% O2, nebulised salbutamol and ipratropium continuously, IV salbutamol, aminophylline (smooth muscle relaxation in airways), and magnesium sulphate (no smooth muscle contraction in airways).
What is chronic obstructive pulmonary disease?
Progressive, worsening airway obstruction. An umbrella for chronic bronchitis and emphysema.
What is chronic bronchitis?
Mucus hypersecretion and inflammation due to cigarette smoke and reduced cilia
What are the features of chronic bronchitis?
Cough chronically productive with frequent infections. Airway remodelling to increase arterial smooth muscle.
What is emphysema?
Pathological destruction of terminal bronchioles and walls between alveoli.
lose elastic tissue
What is the pathophysiology of emphysema?
Inflammatory response to chronic irritation from cigarette smoke causes macrophages to release elastase and other proteolytic enzymes so breaks down elastin. Higher compliance, lower recoil and more air trapped inside the alveoli = hyper inflated chest (barrels chest), harder to breath as there is a reduced pressure gradient
What are the features of emphysema?
Fick’s law - less surface area for diffusion so impaired gas exchange. Less elastin lowers compliance so there is hyperinflation of lungs, causing barrel chest.
What are the causes of COPD?
Smoking mainly, a1-antitrypsin deficiency (hereditary leading to overactivity of elastase causing emphysema), pollution, occupational.
How do the stages of COPD present?
Early - productive cough, dyspnoea, tachypnea.
Middle - purse lip breathing, use of accessory muscles to inspire, barrel chesting.
Late - compensated respiratory acidosis (CO2 retention), wheeze, peripheral and central cyanosis, flapping tremor, pulmonary hypertension.
How is COPD diagnosed?
History used primarily but single breath spirometry and other tests can support diagnosis.
What single breath spirometry results support COPD diagnoses?
FEV1:FVC ratio affected without reversibility.
Mild 50-80%
Moderate 30-49%
Severe <30%
What tests support diagnosis of COPD?
CXR excludes other differential, CT assesses bullae in emphysema, ABG checks acid/base status, a1-antitrypsin blood test in young non-smoker.
What assesses COPD prognosis?
MRC dyspnoea score assesses amount of exertion that causes breathlessness:
1 - strenuous exercise
2 - hurrying or walking up hill
3 - walking at own pace
4 - 100m walking
5 - getting dressed
What lifestyle modifications are made to manage COPD?
Stop smoking (KEY), moderate exercise if MRC allows it, manage other co-morbidities.
What are the pharmacological interventions that are used to manage COPD?
B2 agonists, e.g. salbutamol, for bronchodilation but also causes systemic effects like tachycardia.
M3 antagonists, e.g. ipratropium, for bronchodilation but side effects like dry mouth and nausea.
Aminophylline for bronchodilation from inhibits phosphodiesterase so more cAMP and PKA so MLCK phosphorylated. Also increases respiratory drive and power.
Oral corticosteroids to reduce inflammation to improve chronic bronchitis.
Mucolytics thin the mucus so easier airway clearance.
What are some non-pharmacological interventions used in COPD management?
Pulmonary rehab - breaks cycle of breathlessness.
Long term O2 therapy - need 16 hours a day, no smoking around it due to flamability.
Pneumonectomy - remove damaged lung lobe so FEV1 increased and V/Q mismatch is corrected but less surface area for gas exchange.
What are the investigation performed in acute exacerbations of COPD?
Pulse oximetry, ABG, sputum culture, CRP, U&Es, FBC, CXR.
What is the management of acute exacerbations of COPD?
Titrated O2 therapy to get O2 sats above 88%.
Salbutamol, atrovent, aminophylline.
High dose steroids if non-infectious.
Non-invasive ventilation if conscious.
What are upper respiratory tract infections?
Acute inflammation of the middle airways, nothing sinister in most cases and usually viral.
What is the presentation of URTIs?
Dyspnoea, productive cough, fever, malaise. Associated with sinusitis and otitis media due to connections to nasal cavity.
What is the CXR of URTIs?
Clear as only middle airways affected.
