Respiratory Presentations Flashcards
What are the basics of adult life support?
-30:2 compression rate
-Chest compressions are continued while defibrillator charges
What are the types of rhythms in cardiac arrest (2 types)
- shockable (VT/ pulseless VT)
- non-shockable (asystole/ PEA)
what is meant by non-shockable rhythms?
- organised cardiac electrical activity in the absence of any palpable pulses
- caused by issues which don’t allow the heart to pump properly.
what are some causes of PEA (6)
- Tension pathologies
(PE, Cardiac tamponade, tension pneumothorax) - ischaemia/ hypoxia
- hypovalemia
- acidosis
- hyperthermia
- hyperkalemia
Managment of Non- shockable rhythms?
- 30:2 compression and breath rate.
- continue compressions while the AED charges up.
- 1mg of adrenaline which is given every 3-5 minutes
amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
Managment of non- shockable rhythms?
30:2 compressions to resuce breaths.
Alteplase
Tissue plasminogen activator
thrombolytic agent
encourages thrombolysis
CPR should be continued for an extended period of 60-90 minutes
anitbodies associated with Churg Strauss Syndrome
- MPO-ANCA
- P-ANCA positive antibodies
Churg-Strauss syndrome
Eosinophilic granulomatosis with polyangiitis (EGPA), is a rare autoimmune condition characterized by inflammation of blood vessels (vasculitis)
various organs affected, but mostly affects small and medium- sized blood vessels
causes of Churg-strauss
Believed to involve an abnormal immune response, possibly triggered by an allergic reaction.
Eosinophils, a type of white blood cell, play a significant role in the inflammation process in this condition.
Symptoms assoicated with Churg-Strauss
- asthma
- sinusitis
- allergic rhinitis
- skin rashes
- peripheral neuropathy
- gastrointestinal problems,
- symptoms related to kidney or heart involvement.
Myocardial infarction (description and patient likely to have)
Cardiac-sounding pain
heavy, central chest pain they may radiate to the neck and left arm
nausea, sweating
elderly patients and diabetics may experience no pain
Pneumothorax: when to suspect
History of asthma, Marfan’s etc
Sudden dyspnoea and pleuritic chest pain
Pulmonary embolism- when to suspect
Sudden dyspnoea and pleuritic chest pain
Calf pain/swelling
Current combined pill user, malignancy
Pericarditis- when to suspect?
Sharp pain relieved by sitting forwards
May be pleuritic in nature
Dissecting aortic aneurysm
‘Tearing’ chest pain radiating through to the back
Unequal upper limb blood pressure
Gastro-oesophageal reflux disease- when to suspect
Burning retrosternal pain
Other possible symptoms include regurgitation and dysphagia
Musculoskeletal chest pain
One of the most common diagnoses made in the Emergency Department. The pain is often worse on movement or palpation.
May be precipitated by trauma or coughing
shingles
pain oftern preceeded by rash
what is aortic dissection ?
Flap or filling defect within the aortic intima.
Blood tracks into the medial layer and splits the tissues with the subsequent creation of a false lumen. ascending aorta or just distal to the left subclavian artery (less common).
Afro-carribean males aged 50-70 years.
Presentation of aortic dissection
Patients usually present with a tearing intrascapular pain, which may be similar to the pain of a myocardial infarct.
The dissection may spread either proximally or distally with subsequent disruption to the arterial branches that are encountered.
Type A and Type B aortic dissection
- Stanford classification system
- (Type A)-ascending aorta
- (Type B)- descending aorta, typically beyond the left subclavian artery.
- Type A lesions are usually treated surgically
- Type B lesions are usually managed non operatively.
PE ECG findings
Diagnosis may be suggested by various ECG findings including
* S waves in lead I, Q waves in lead III
* inverted T waves in lead III.
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* Confirmation of the diagnosis is usually CTPA
treatment of PE
Treatment is with anticoagulation, in those patients who develop a cardiac arrest or severe compromise from their PE, consideration may be given to thrombolysis.
- altepase
- rivoraxiban
Diagnosis of MI
ECG changes (and cardiac enzyme changes). Inferior and anterior infarcts may be distinguished by the presence of specific ECG changes (usually II, III and aVF for inferior, leads V1-V5 for anterior).
treatment of MI
PCI in 120 mins of presentation
oral antiplatelet agents, primary coronary angioplasty and/ or thrombolysis.
perforated peptic ulcer presentation
Patients usually develop sudden onset of epigastric abdominal pain, it may be soon followed by generalised abdominal pain.
pain of gastric ulcer is typically worse immediately after eating.
Diagnosis of perforated peptic ulcer
erect chest x-ray which may show a small amount of free intra-abdominal air (very large amounts of air are more typically associated with colonic perforation).
Managment of perforated peptic ulcer
laparotomy, small defects may be excised and overlaid with an omental patch, larger defects are best managed with a partial gastrectomy.
Boerhaaves syndrome
Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.
Rupture is usually distally sited and on the left side.
presentation of Bohaaves syndrome
Patients usually give a history of sudden onset of severe chest pain that may complicate severe vomiting.
Severe sepsis occurs secondary to mediastinitis.
Bohavees syndrome diagnosis
Diagnosis is CT contrast swallow.
Bohavees syndrome managment
thoracotomy and lavage,
Less than 12 hours after onset then primary
repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin.
Delays beyond 24 hours are associated with a very high mortality rate.
Anteroseptal
V1-V4 Left anterior descending
Inferior
II, III, aVF Right coronary
anterior lateral region
V1-6, I, aVL Proximal left anterior descending
lateral region
I, aVL +/- V5-6 Left circumflex
posterior region
Changes in V1-3
Reciprocal changes of STEMI are typically seen:
horizontal ST depression
tall, broad R waves
upright T waves
dominant R wave in V2
Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9) Usually left circumflex, also right coronary
features of lung cancer (9)
persistent cough
haemoptysis
dyspnoea
chest pain
weight loss and anorexia
hoarseness
seen with Pancoast tumours pressing on the recurrent laryngeal nerve
superior vena cava syndrome
3 exam findings of lung cancer
- a fixed, monophonic wheeze may be noted
- supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
- clubbing
paraneoplastic features of SCLC
ADH
ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
Lambert-Eaton syndrome
Paraneoplastic squamous cell cancer
- parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
- clubbing
- hypertrophic pulmonary osteoarthropathy (HPOA)
- hyperthyroidism due to ectopic TSH
Paraneoplastic adenocarcinoma side effects
gynaecomastia
hypertrophic pulmonary osteoarthropathy (HPOA)
presentation of acute brochitits
cough: may or may not be productive
sore throat
rhinorrhoea
wheeze
usually normal chest exaination, however some patients will also have
Low-grade fever
Wheeze
bronchitis vs pneumonia
History: Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze. Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.
Investigations of bronchitits
acute bronchitis is typically a clinical diagnosis
however, if CRP testing is available this may be used to guide whether antibiotic therapy is indicated
Managment of bronchitits
analgesia
good fluid intake
consider antibiotic therapy if patients:
are systemically very unwell
have pre-existing co-morbidities
have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
NICE Clinical Knowledge Summaries/BNF currently recommend doxycycline first-line
doxycycline cannot be used in children or pregnant women
alternatives include amoxicillin
acute bronchitis
Result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.
The disease course usually resolves before 3 weeks, however, 25% of patients will still have a cough beyond this time
viral URTI (aka cold/ coryzal symptoms)
Upper respiratory tract infections involve the mucosa of the nasal cavity, sinuses, nasopharynx, oropharynx and larynx.
Most commonly caused by rhinovirus
Other viruses include adenoviruses, influenza, parainfluenza, respiratory syncytial virus and enteroviruses.
epidemiology of URTI
Adults may be affected by URTIs 2-3 times per year on average, but children may average up to 5-6 infections
coryzal symptoms
The most common symptoms are nasal discharge, nasal obstruction, sore throat, headache, cough, tiredness and general malaise. Other symptoms include facial pain, earache, hoarseness and nausea.
signs of colds
Erythema or injection of the back of the throat
Nasal discharge
Tender cervical lymphadenopathy
Mild fever
assessment of coryzal symptoms
Examination of throat, ears and cervical lymph nodes
Respiratory examination to exclude pneumonia, significant wheeze etc
Assess hydration status, especially in young children and the elderly
Basic observations (heart rate, blood pressure, respiratory rate, temperature, oxygen saturations) - if significantly abnormal may need to consider other causes e.g. sepsis
useful features of assessments for coryzal symptoms (2 scales)
Children under 5 - NICE fever traffic light system
FeverPAIN score - used to assess likelihood of Strep infection in adult with sore throat and guide decision making re antibiotic usage
Investigations for coryzal symptoms
Generally not needed in healthy adults
May be required in less straightforward cases where more serious infections may present with similar symptoms e.g. baby/infant with fever, immunocompromised adult
Viral throat swabs may be needed in certain cases e.g. adult with suspected influenza being admitted to hospital for infection control purposes
Managment of coryzal symptoms
Supportive management only is usually sufficient
Admission for supportive care may be required in frail or elderly patients with low physiological reserve or multiple comorbidities
An uncomplicated cold in a healthy adult usually resolves in 7-10 days but may last up to 3 weeks
Provide reassurance that condition is self-limiting and recovery will not be aided by antibiotics
Advise paracetamol, fluids, rest and over the counter remedies if appropriate
Complications of coryzal symptoms
Sinusitis
Otitis media
Secondary bacterial infection e.g. pneumonia
Exacerbations of pre-existing respiratory conditions such as asthma, or COPD
Viral wheeze, bronchiolitis and croup in infants and young children
types of lung function tests
- spirometry
- peak expiratory flow (PEF)
-PEC
obstructive lung function finding
FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced
examples of obstructive diseases
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans
restrictive lung function finding
FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased
restriction lung disease examples
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity
pleural plaques
Pleural plaques are benign and do not undergo malignant change. They, therefore don’t require any follow-up. They are the most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.
Asbestosis
The severity of asbestosis is related to the length of exposure.
This is in contrast to mesothelioma where even very limited exposure can cause disease.
The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis.
Features of asbestosis
dyspnoea and reduced exercise tolerance
clubbing
bilateral end-inspiratory crackles
lung function tests show a restrictive pattern with reduced gas transfer
Treatment of asbestosis
- convervative mangament
Mesothelioma
Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form.
Features of mesothelioma
progressive shortness-of-breath
chest pain
pleural effusion
Managment of mesothelioma
Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy.
Unfortunately, the prognosis is very poor, with a median survival from diagnosis of 8-14 months.
Symptomatic
Industrial compensation
Chemotherapy, Surgery if operable
Prognosis poor, median survival 12 months
Investigations of mesothelioma
suspicion is normally raised by a chest x-ray showing either a pleural effusion or pleural thickening
the next step is normally a pleural CT
if a pleural effusion is present fluid should be sent for MC&S, biochemistry and cytology (but cytology is only helpful in 20-30% of cases)
local anaesthetic thoracoscopy is increasingly used to investigate cytology negative exudative effusions as it has a high diagnostic yield (around 95%)
if an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used
Pathophys of mesothelioma
Malignancy of mesothelial cells of pleura
Metastases to contralateral lung and peritoneum
Right lung affected more often than left
features of mesothelioma
Dyspnoea, weight loss, chest wall pain
Clubbing
30% present as painless pleural effusion
Only 20% have pre-existing asbestosis
History of asbestos exposure in 85-90%, latent period of 30-40 years
2 categories (causes) of pleural effusion
- exudative causes
- transudative causes
transudate causes of pleural effusion
(< 30g/L protein)
heart failure (most common transudate cause)
hypoalbuminaemia
liver disease
nephrotic syndrome
malabsorption
hypothyroidism
Meigs’ syndrome
exudative causes of pleural effusion
(> 30g/L protein)
infection
pneumonia (most common exudate cause),
tuberculosis
subphrenic abscess
connective tissue disease
rheumatoid arthritis
systemic lupus erythematosus
neoplasia
lung cancer
mesothelioma
metastases
pancreatitis
pulmonary embolism
Dressler’s syndrome
yellow nail syndrome
features of pleural effusion
dyspnoea, non-productive cough or chest pain are possible presenting symptoms
classic examination findings include dullness to percussion, reduced breath sounds and reduced chest expansion
imaging of pleural effusion
posterioranterior (PA) chest x-rays should be performed in all patients
ultrasound is recommended: it increases the likelihood of successful pleural aspiration and is sensitive for detecting pleural fluid septations
contrast CT is now increasingly performed to investigate the underlying cause, particularly for exudative effusions
pleural effusion aspiration approach
ultrasound is recommended to reduce the complication rate
a 21G needle and 50ml syringe should be used
fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
Light’s criteria for pleural effusion
Exudates typically have higher protein concentration and LD activity and lower pH and glucose values than transudates
BTS criteria for borderline cases
exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L
if the protein level is between 25-35 g/L, Light’s criteria should be applied. An exudate is likely if at least one of the following criteria are met:
pleural fluid protein divided by serum protein >0.5
pleural fluid LDH divided by serum LDH >0.6
pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
other characteristics for pleural effusion
low glucose: rheumatoid arthritis, tuberculosis
raised amylase: pancreatitis, oesophageal perforation
heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis
Managment of pleural effusion
recurrent aspiration
pleurodesis
indwelling pleural catheter
drug management to alleviate symptoms e.g. opioids to relieve dyspnoea
Well’s criteria
Objectifies risk of pulmonary embolism.
- PE likely diagnosis
- clinical signs of DVT
-HR greater than 100
-Hemoptysis
-Immobilization at least 3 days OR surgery in the previous 4 weeks
Previous, objectively diagnosed PE or DVT
Malignancy w/ treatment within 6 months or palliative
Spontaneous pneumothorax
-primary spontaneous pneumothorax (PSP):
Occurs without underlying lung disease, often in tall, thin, young individuals. PSP is associated with the rupture of subpleural blebs or bullae.
-secondary spontaneous pneumothorax (SSP):
Occurs in patients with pre-existing lung disease, such as COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia. Certain connective tissue diseases such as Marfan’s syndrome are also a risk factor
traumatic pneumothorax
results from penetrating or blunt chest trauma, leading to lung injury and pleural air accumulation.
Iatrogenic causes of pneumothorax
occurs as a complication of medical procedures, such as thoracentesis, central venous catheter placement, ventilation, including non-invasive ventilation or lung biopsy.
tension pneumothorax
severe pneumothorax resulting in the displacement of mediastinal structures that may result in severe respiratory distress and haemodynamic collapse.
Catamenial pneumothora
- 3-6% of spontaneous pneumothoraces occurring in menstruating women.
- It is thought to be caused by endometriosis within the thorax.
Signs and symptoms of pneumothorax
Symptoms tend to come on suddenly:
dyspnoea
chest pain: often pleuritic
Signs
hyper-resonant lung percussion
reduced breath sounds
reduced lung expansion
tachypnoea
tachycardia
signs and symptoms of tension pneumothorax
respiratory distress
tracheal deviation away from the side of the pneumothorax
hypotension
Bronchiectasis
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation. There are a wide variety of causes are listed below:
features of bronchoectasis
persistent productive cough. Large volumes of sputum may be expectorated
dyspnoea
haemoptysis
Signs and symptoms of bronchectasis
abnormal chest auscultation
coarse crackles
wheeze
clubbing may be present
Investigations for bronchectasis
High-resolution computed tomography (HRCT) scan of the chest
Chest X-ray
Pulmonary function tests (spirometry)
Sputum culture and analysis
Bronchoscopy
causes of bronchectasis
Post-infectious (resulting from severe or recurrent respiratory infections)
Cystic fibrosis
Immunodeficiency disorders
Inhalation of toxic gases or fumes
Autoimmune conditions
Managment of bronchectasis
Antibiotics to treat infections
Chest physiotherapy to help clear mucus from the airways
Bronchodilators to improve airflow
Inhaled corticosteroids to reduce inflammation
Surgical intervention in severe cases (such as lung resection or bronchial artery embolization)
complications of bronchectasis
Respiratory failure
Recurrent pneumonia
Atelectasis (lung collapse)
Hemoptysis
Cor pulmonale (right-sided heart failure)
Managment of bronchectasis
Regular monitoring by a pulmonologist
Pulmonary rehabilitation
Vaccinations (such as influenza and pneumococcal vaccines)
Smoking cessation
Avoidance of respiratory irritants and pollutants
COPD
COPD is an umbrella term encompassing the older terms chronic bronchitis and emphysema. In the vast majority of cases, COPD is caused by smoking
Risk factors of COPD
Smoking (primary cause)
Environmental exposure to pollutants (such as air pollution, secondhand smoke, and occupational dust or chemicals)
Genetic factors
Respiratory infections
Aging
Types of COPD
- Chronic bronchitis: Involves inflammation and narrowing of the bronchial tubes, leading to excessive mucus production and cough.
- Emphysema: Involves damage to the alveoli (air sacs) in the lungs, impairing their ability to exchange oxygen and carbon dioxide.
Investigations in COPD
post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
chest x-ray
hyperinflation
bullae: if large, may sometimes mimic a pneumothorax
flat hemidiaphragm
also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation
Risk factors of COPD
Smoking (primary cause)
Environmental exposure to pollutants (such as air pollution, secondhand smoke, and occupational dust or chemicals)
Genetic factors
Respiratory infections
Aging
What is this CT showing?
CT scan showing small cell lung cancer with multiple pulmonary nodules and extensive mediastinal nodal metastases.
what is this?
silicosis.
Note the bilateral diffuse upper lobe reticular shadowing superimposed with occasional scattered mass like opacities. These features are in keeping with silicosis and progressive massive fibrosis (PMF)
What is this?
** silicosis**
showing upper zone predominant mass-like scarring with calcification and volume loss. Hilar and mediastinal lymph node calcification also noted. No cavitary changes are seen. There is a left pleural effusion.
