Respiratory - Pleural and Pulmonary Vascular Diseases Flashcards
The structure of the pleura
The pleural space is bounded by the parietal and visceral membranes covered by a continuous layer of mesothelial cells
What can result in the accumulation of excess pleural fluid
Disturbances in either formation or absorption
When can we determine pleural fluid is an exudate - Light’s criteria
Pleural fluid proteins divided by serum proteins is >0.5
Pleural fluid LDH divided by serum LSD > 0.6
Pleural fluid LDH > 2/3 the upper limits of labs normal value for serum LDH
Determining transudates vs exudates
Hx
Examinations
Ix
Ix to help determine transudates vs exudates
Radiology Bloods - clotting screen, FBC, LFTs etc Light's criteria CT, PET Bx
Most important examples of condns causing transudates
Usually caused by failures
HF
Liver cirrhosis
Nephrotic syndorme
Hypoalbuminaemic status
Other condns causing transudates
Mitral stenosis
Meigs syndrome
Constrictive pericarditis
Features of transudates
Slower time scale
Usually bilateral but R side may be larger - may find fluid in other areas e.g. ascites, pitting oedema
Treatment of transudates
Treat the case- if pt fails to respond will need to reconsider dx
Causes of pleural exudates
Parapenumonic effusions and empyema Malignancy Pulmonary infarction TB Drugs RhA
Clinical assessment of pleural exudates
Risk factors (smoking, asbestos)
Red flag symptoms
A/c and subacute symtoms - timescale
Look for systemic signs (should be minimal) and effusion is often unilateral
Examination findings of pleural exudates
Reduced chest expansion
Percussion - stony dullness
Absent breath sounds
Use of ultrasound when determining between transudates and exudates
Fluid vs thickening - darker fluid. is usually transudate
Loculations
Guided thoracocentesis (Light’s criteria)
What do we send pleural aspiration for
Cytology Protein LDH pH/ glucose Gram stain Culture & sensitivity Optional extras depending on likely cause
Thoracoscopy
Placing camera in pleural space under anaesthetic
Can also take fluid from parietal pleura during this procedure
Why should an ultrasound be done before a thoracospy
To guide needle placement
Should be above rib to avoid neurovasc bundle
Ddx for complete white-out on CXR w/ trachea deviation
Complete lung collapse
Massive pleural effusion
Pneumonectomy
Pleural plaques
Benign condn
Sign of asbestos exposure
When might a pt develop diffuse pleural thickening
Heavy exposure to asbestos ** Previous haemothorax TB Chest surgery Radiation Infection drugs
What can diffuse pleural thickening lead to
SOB, restricted lung function - requires follow up
What are the majority of pleural effusions. (90%) caused by
Infection - treat w/ abx, CXR in 6-8 weeks (exudate)
HF - treat cause, don’t drain (transudate)
Malignancy (exudate)
PE (exudate)
Clinical px of PTX pts
Hx - cigarette, cannabis smoking
PMH - lung disease
A/c onset symptoms - pleuritic chest pain, breathlessness
Examination findings in PTX pts
Trachea/ mediastinum - pushed Reduced/ absent expansion Percussion - hyper resonant Reduced/ absent breath sounds Hypoxamia esp if underlying lung disease
Hypoxaemia
Low levels of oxygen in blood nOT tissues
Causes of PTX
Primary spontaneous
Secondary spontaneous
Iatrogenic
Trauma
Which group of people do we tend to see primary sponatanoues PTX in
Taller pts
Alveoli at the lung apex in tall individuals are subject to significantly greater distending pressure than those at the base of the lung
What are apical pleural blebs associated with
High risk of PTX
What should you ask spontaneous PTX pts about
Smoker - 12% risk of developing PTX
Lung disease
Causes of secondary spontaneous PTX
COPD PJP CF TB Others - incl Marfan
PJP
Pnemoctitis jiroveci pneumonia
Tension PTX
Air trapped in between parietal and visceral pleura resulting in lung collapse, displacement of mediastinal structure and compromised cardiopulmonary function
Medical emergency - Tension PTX
Low BP and low HR
Emergency needle decompression
Anterior border of safe triangle for chest drain
Lateral border of Pec Major
Superior border of safe triangle for chest drain
Base of axilla
Inferior border of safe triangle for chest drain
Line of 5th ICS
Lateral border of safe triangle for chest drain
Lateral edge of Lat Dor
Complications of Chest Drain
Infection/ pain Drain dislodgement Drain blockage Visceral injury Death
Methods of chest drain insertion
Seldinger technique
Surgical blunt dissection approach
Suction recommendations for chest drain
High volume low-pressure suction systems
Wall suction or digital suction system
Conservative mx of PTX
Shouldn’t dive until definitive prevention strategy
Avoid air travel until 7/7 post PTX resolution
Smoking cessation
Organise follow up CXR to ,omit resolution
Manage comorbidities
Definitive prevention strategy for ptx
Surgical pleurectomy
Why do PTX pts need to stop smoking
Reoccurrence risk for smokers is 32%
8% in non-smokers
When should a follow up CXR be organised for a PTX
2 - 4 weeks
Risk factors for recurrence of SSP
Age
Pulmonary fibrosis
Emphysema
Surgical intervention to prevent recurrence of PTX
Medical Chemical Pleurodesis (Talc)
Done for recurrent pneumothoraces and non-resolving PTX
When is melatonin secreted
As a result of darkness, from the pineal gland
Retinal hyper thalamic pathway
Stages of sleep
REM (dream sleep)
Non-REM - light sleep, slightly deeper, deep sleep
When do we experience non-REM sleep
First half of sleep
Which sleep refreshes cells
Deep sleep
Breathing in NREM sleep
Normal
Regular muscle tone
Breathing in REM sleep
Breathing is erratic
Muscles are atonic except diaphragm
Which stage of sleep generally exacerbates sleep apnoea
REM sleep
Sleep Disordered Breathing Classification
OSA
Central Sleep Apnoea
Mixed obstructive/ central apnoea
Obesity hypoventilation Syndrome
Most common pattern seen in Sleep disordered breathing
OSA
2nd most common pattern seen in sleep disordered breathing
Obesity Hypoventilation Syndrome
Hx and clinical px of OSA pts
Snoring Witnessed apnoea Excessive daytime sleepiness (EDS) Nocturia Unrefreshed sleep Morning headaches
Witnessed apnoea in OSA
Bed partner will note pt stopped breathing and then took a v loud breath on inspiration
Nocturia
Urinating <4 a night
Things to ask about in hx of OSA pts
Occupation and riving Medications PMH Trisomy 21 Past surgical hx
What medication can be a ppts factor in OSA
Opiod analgesics
What diseases should be screened for in PMH of OSA pts
Thyroid disease
DM
Systemic hTN
CDV and CBV disease
Why do we ask about trisomy 21 in OSA pts
High risk for OSA (reduced muscle tone)
What is relevant in the past surgical hx of OSA pts
Tonsillectomy
Measuring EDS
Epworth Sleepiness Scale
Scores of 11/24 = EDS
Epworth Sleepiness Scale
Looks at high likely a pt is to fall asleep during following situations e.g sitting, watching TV, talking to someone, in a car
Rated from 0 (would never dose) - 3 (high chance)
Limitations of ESS
Pt may be worried to accurately report lapse in judgement e.g. driving
Timescale - values may may change by the time the pt is seen
Possible sleep questionnaires
Pittsburgh sleep quality index index (PSQ1)
ESS
STOP BANG (pre-op screening)
4 variable screening tool used in Norfolk
Examination for OSA
Obesity - BMI >30kg/m2, measure waist circumference
Upper airways -
Look for signs of acromegaly, hypothyroidism, Cushing’s syndrome
Look for cranial abnormalities
What do you look for in upper airways when examining OSA pts
Enlarged tonsils esp in younger pts
Which craniofacial abnormalities should you look for in OSA pts
Micrognathia (small jawline)
Retrognathia (receding jawline)
These can cause smaller airways
Mallampati Score
Class I (Complete visualisation of soft palate) to Class IV (soft palate is covered)
Desaturation in apnoea
Cessation of breathing for 10s or more
Usually scored w/ >4% desaturation (SpO2)
Hypoapnoea
Reduction in the airflow (nasal flow) by 50% or more
Does hypoapnoea always cause O2 desaturations
No - may not cause O2 desaturation
Apnoea Hypoapnoea Index scores for OSA
2-15 - mild OSA
15 - 30 - moderate OSA
>30 severe OSA
Desaturation index criteria fro OSA
> 4%
OSAS
OSA syndrome
OSA vs OSAS
Abnormal Sleep study and EDS - OSAS
Abnormal Sleep Study and no EDS - OSA
Measurements in sleep disordered breathings
Nocturnal oximetry Resp Polygraphy (Home Sleep Test) Polysomnography - Gold standard
Treatment of sleep disordered breathing
Lifestyle modifications - mild OSA/ OSAS
Wt reduction
Sleep Hygiene - excessive caffeine
Positional training
Mandibular advancement devices
Used in mild OSA(S)
Boil and bite devices - pushes lower jaw forward creating more room at back of throat
CPAP
Continuous Positive Airway Pressure
When is CPAP given for OSAS
Definitive treatment - moderate/ severe disease
Given after attempting lifestyle modification and mandibular advancement devices
Relieves symptoms majorly
Driving and sleep apnoea
Pts have to declare dx to DVLA
CPAP compliance > 4hrs/ night
HGV/ public transport drivers need to inform employers and occupational health - asked not to drive unless established in treatment
Obesity Hyperventilation Syndrome
Morbid obesity BMI > 35kg/m2
Mean SpO2 < 90% in sleep study
Need to measure time spent <90% SpO3 - shallow breathing, reduced TV
ABG of pts w/ obesity Hypoventilation Syndrome
Day time CO2 retention and/or elevated HCO3 (.27mmol/L)
Mx of Obesity Hypoventilation Syndrome
Wt loss
NIV (+ve pressure)
Co-existent lung disease in sleep disordered breathing
Asthma and OSA
COPD/ emphysema: overlap syndrome of OSA/COPD
Consequences of SDB (sleep disordered breathing)
Systemic HTN
AF
MI, CVA
Pulmonary arterial hypertension
Ventilation
Rate at which air enters or leaves the lungs
Minute ventilation
Volume of air moving in and out per unit time
Alveolar ventilation
Amount of air utilised for gas exchange (VT - dead space) x RR
Perfusion (Q)
Movement of blood in to lungs through pulmonary capillaries
V/Q ratio
Alveolar ventilation/ pulmonary blood flow
When do we see hypoxaemia
Reduction in altitude Hypoventilation Diffusion Shunts VQ mismatch
When are V and Q matched
When pulmonary blood flow is proportionally matched to the pulmonary ventilation
Results in greatest efficiency for gas exchange
VQ ratio for single alveolus
Alveolar ventilation/ capillary blood flow
How many zones are there for perfusion and ventilation in the lungs
3
Pressures in zone I (apex) for perfusion and ventilation
PA > Pa > Pv
A - systemic arteries
a - alveoli
v - pulmonary vein
Pressure in zone II for V & Q
Pa > PA > Pv
A - systemic arteries
a - alveoli
v - pulmonary vein
Pressures in zone III
Pa > Pv > PA
A - systemic arteries
a - alveoli
v - pulmonary vein
How does V/Q vary in diff zones of the lung
Highest in apex and lowest in base (but has higher O2 content)
Clinical rel - certain infections attack apex as less aerobic than base
Shunt
Physiological phenomena where deoxygenated blood mixes w/ oxygenated blood
Occurs when there’s an intracardiac defect - doesn’t participate in gas exchange
Pulmonary shunt
Mixing of blood without participating in the gas exchange at level of pulmonary capillaries
When do we see a pulmonary shunt
Occurs when alveoli are perfused like normal but ventilation fails to supply perfused region - pathological condn (VQ = 0)
Examples of intrapulmonary shunting
Fluid in alveoli e.g. pulmonary oedema & pneumonia
Shunt fraction
% of blood pumped by heart that is not ventilated (oxygenated)
When is the shunt fraction increased
Greater in pulm contusion or haemorrhage even at breathing 100% oxygen
What can minimise shunt fraction
Vasoconstriction - compensatory mechanisms of hypoxaemia
What can cause a VQ mismatch
Dead space (physiological) - ventilation of poorly perfused alveoli (V > Q) Shunts; perfusion of poorly ventilated alveoli (V < Q)
Pathologies resulting in VQ mismatch - low VQ ratio
Pneumonia Pulmonary oedema ILD/ pulm fibrosis Asthma Mucous plugging Airway obstruction
Pathologies resulting in AQ mismatch - high VQ
PE
Emphysema
What does a VQ mismatch respond to
100% oxygen
Normal VQ in healthy lung
0.8
Aa gradient
Alveolar to capillary oxygen gradient
Mechanisms of hypoxaemia
Shunt Diffusion impairment VQ mismatch Hypoventilation Low ambient oxygen
Aetiology of primary pleural malignancy
Mesothelioma
Aetiology of secondary pleural malignancies
Lung - 1st most common
Breast - 2nd most common
Lymphoma - 3rd most common
But almost any cancer can metastasise to the pleura
What do pleural malignancies commonly cause
Malignant pleura effusions and/or pleural thickening
Pathology of exudative effusion caused by pleural malignancy
Tumour dissemination
Angiogenesis - w/ vasc hyperpermeability
Tumour secreted vasoactive mediators (VEGF)
Asbetsos-related resp disease
Asbestosis Malignant pleural mesothelioma Pleural plaques Benign pleural thickening Benign pleural effusion
Why is asbestos considered an ILD
Asbestos in lung tissue –> fibrosis and scarring
When can pts get compensation for benign pleural thickening after asbestosis exposure
If disabled by SOB
Epidemiology of pleural malignancy
Common - incidence about 30,000/ yr
Breast cancer commonest in women and lung cancer commonest cause in men
Increasing incidence w/ age (max at 80-85)
Ddx of pleural effusion
Transudative pleural effusion - cardiac, renal or hepatic failure Pleural infection PE CTD Benign asbestos pleural disease
What should be asked in the hx of a pt w/ pleural malignancy
Symptoms spp to effusion Constitutional symptoms Symptoms of other malignancy PMH - previous malignancies SH
Symptoms spp to effusion in pts w/ pleural malignancy
Breathlessness, cough, dull chest pain
Time course: months - weeks
Constitutional symptoms seen in pts w/ pleural malignancy
Wt loss
Loss of appetite
Fatigue
Symptoms of the malignancies that may be seen in pts w/ pleural malignancy
Dysphagia
Change in bowel habits
Lumps
Relevant SH in pts w. pleural malignancy
Smoking
Asbestos exposure
Perfomance status
ECOG performance status
Looks at effects of malignancy on pts lifestyle From 0 (fully active, able to carry on pre-disease performance) to 4 (completely disabled, cannot cary on self-care)
Why is ECOG performance status important for pleural malignancy
Helps determining what ix the pt is fit for e.g <2 fit for thoracoscopy
Helps determine mx, 4 is usually disseminated and not fit for treatment
Examination of pts w/ pleural malignancy
Increased RR
Cachexic
not usually hypoxic
Decreased air entry, decreased lung expansion, dull percussion note, decreased vocal resonance
Other signs of malignancy e.g. breast lumps, testiuclar lumps, lymphadenopathy
Main ix for pleural malignancy
Bloods - U&Es, FBC, CRP, clotting, PSA
CXR
Addn ix for pleural malignancy
Thoracic ultrasound
CT
Pleural aspiration
Thoracoscopy
What might you see in a thoracic ultrasound in pleural malignancy
Pleural effusion
Pleural thickening
Pleural modularity
Difference in CT scan for men and women for suspected pleural malignancy
CT scans in men of chest and upper abdomen
For women also do pelvis
What do you send pleural aspiration for in suspected pleural malignancy
Biochem: total protein, LDH (malignant effusions typical transudative)
MC&S - excl infection
Cytology - +ve in 90% MPE, only 20% in mesothelioma
MPE
Malignant Pleural effusion
Main procedures done in thoracoscopy
Fluid drainage and pleural biopsy
After procedure can perform pleurodesis (using sterile talc), IPC insertion
IPC
indwelling pleural catheter
Complication of thoracosocpy
Re explosion pulmonary oedema
Making a dx of pleural malignancy - role of MDT
Team reviews hx and ix
Make a dx - radiological or definitive
Mx plan
Possible mx plans for pleural malignancy
Further biopsies
Cancer treatment
Watch and wait
Palliative care
Treatment for pleural malignancy
Treat underlying malignancy - lymphoma, small cell lung cancer, breast cancer Therapeutic aspiration Chest drain and pleurodesis IPC insertion Pleurectomy
Chest drain and pleurodesis for pleural malignancy
Inpt 2-5 days
Seldinger chest drain and underwater seal
~75% success rate
Why is talc used in pleurodesis
4g talc creates infl causing pleura to fuse together
What can pts be left w/ after chest drain and pleurodesis
Residual pleural thickening –> breathlessness
IPC for pleural malignancy treatment
Day case
intermittent drainage at home using vacuum bags, 3x/ week initially
Definitive treatment
Can give talc to perform pleurodesis
What IPC the treatment of choice for
Trapped lung
Failed pleurodesis
Risk associated w/ IPC
Blockage
Infection
Trapped lung
Thickened visceral pleura so unable to expand fully
Pulmonary HTN
Pathophysiological disorder that may involve multiple clinical condns, where mPAP > 20 mmHg
mPAP
Mean pulmonary artery pressure
What can pulmonary HTN complicate
Majority of CDV and resp diseases
What kind of symptoms are seen in pulm HTN
Non-spp
What does pulmonary HTN dx and classification require
R heart catheterisation
Calculating PVR
80(mPAP - PAWP)/ CO
PAWP
Pulm artery wedge pressure
Normal pulmonary artery pressure
14 mmHg +/- 3.3 mmHg at rest
Criteria for Pulm HTN
Precapillary PH mPAP > 20mmHg, PVR > 3 WU and PAWP < 15mmHg
Combined pre and post capillary PH - mPAP > 20mmHg, PVR > 3 WU, PAWP > 15
WU
Wood units
Classification of pulm HTN
Pulm arterial HTN (PAH) Left heart disease - PAWP > 15 Lung disease CTEPH Unclear/ multifactorial
Epidemiology of pulmonary HTN
Global PH incidence data is poor
In the UK, prevalence of 97/1,000,000
F:M ratio of 1.8
L heart disease believed to be most common cause
How is clinical presentation of Pulm HTN classed
By functional class From Class I (nob symptoms w/ exercise or rest) to Class IV (symptomatic at rest, syncope and fatigue)
Determinants of prognosis in pulmonary HTN
Clinical signs of R heart failure
Progression of symptoms
Syncope
WHO functional class
Cardiopulmonary exercise testing
NT-proBNP plasma levels - higher is worse
Imaging - increased RA area, pericardial effusion
General mx of pulmonary HTN
Avoid pregnancy Influenza and pneumococcal vaccinations Psychosocial support Pulm/ cardiac rehab Diuresis if evidence of volume overload LTOT if pO2 consistently less than 8kPa Correct anaemia
Spp mx for pulm HTN
Group I - depends on functional class, assess severity
Group 2 - targeted therapy not currently licensed
Group 3 - no targeted therapy
Group 5 - v difficult to mx
CTEPH
C/c thromboembolic pulmonary HTN
What is CTEPH
Fibrotic transformation of a pulmonary arterial thrombosis, causing fixed mechanical obstruction of pulmonary arteries
Microvascular remodelling causing a progressive increase in PVR
What % of CTEPH pts lack a hx of a/c PE
~25%
Treatment for CTEPH
PEA (pulmonary endarterectomy) surgery - removing central obstructing lesions
BPA (Balloon pulmonary angioplasty)
CTEPH prognosis
In operable pts, treated w/ drugs, 3 yrs survival varies from 41-805
3-yr survival of 89% in operated PEA pts and 70% in non operated pts
Drugs given for CTEPH
IV prostacyclin analogues or oral PAH targeted drugs
What does BPA in non-operable CTEPH pts show significant improvement in
Functional status QoL Pulm pressure Exercise capacity PVR
Causes of cardiac chest pain
MI/ infarction
Pericarditis
Aortic dissection (pleurite chest pain)
Resp causes of chest pain
PE
PTX
Pneumonia
Pleural infl (pain happens even at rest)
GI causes of chest pain
Oesophageal spasm
Dysmotility/ reflux
Oesophageal rupture (Boerhavve’s)
MSK causes of chest pain
Rib frature/ metastasis
Muscle spasm/ strain
Costochondritis (localised pain - can be elicited)
Psychological states causing chest pain
Panic attack
Hyperventilation
Ix for differentiating between causes of chest pain
Bloods - FBC, CRP/ESR, LFT, D-dimer etc
ECG - cardiac causes, arrhythmia
CXR +/- further imaging
What is a PE
Occlusion of a segment of pulmonary arterial circulation through embolism from a distant source - lower limbs
Embolic material that can cause a PE
Commonly blood clots
May be fat embolism - following major trauma
Air embolism following invasive procedures e.g. central line insertion
Causes of a PE
Virchow’s triad
Hypercoagulable stae
Stasis (local/ systemic) - VV, immobilisation
Endothelial damage - c/c infl
What can cause a hyper coagulable state –> PE
Factor V Leiden, Protein S/C deficiency
Malignancy
Loss of proteins incl clotting factors - myeloma
Major risk factors for a PE
Recent immobility Major surgery incl obstetric Leg fracture Previous DVT/ PE Thrombotic disorder Metastatic cancer
Minor risk factors for PE
Oestrogen Travel Known thrombophilia Obesity Minor surgery
Presentation of a PE
SOB Pleuritic chest pain Cough Leg swelling/ pain Haemoptysis
Well’s score for PE - criteria
Previous VTE Tachycardia Recent surgery/ immobilisation Clinical signs of DVT - 3 point Haemoptysis Cancer
Bloods for a PE
ABG
D-dimer
FBC/ clotting profile
ECG for PE
Sinus tachycardia
Fast AF
S1Q3T3
May also be normal
Ix for PE
Bloods ECG CXR - doesn't excl/ confirm dx CTPA V/Q
D-dimer for PE
Highly sensitive
High -ve predictive value
Used in combo w/ probability score
What is D-dimer commonly elevated in
Pts w/ infl states, infection, ACS, malignancy recent surgery
What might you see on a CXR for for PE
Pulmonary infarct
Pleural effusion
CTPA
CT pulmonary angio
Gold standard for PE
Involves higher dose of ionising radiation and risk of nephrotoxicity w/ contrast
Embolus is dark grey - found in white area
VQ scan for a PE
Compares radioactive material uptake in lungs via inhalation and iV injection
Reported as probability risk
Pulmonary angio for PE
Invasive
Superseded in a/c setting by CTPA
Relevat in dx CTEPH
Echo for PE
Looks for evidence of R heart dilatation/ strain
Relevant in a/c setting/ peri-arrest situation
To screen for 2’ pulmonary HTN
Treatment of a/c PE
Heparin - LMWH, unfractionated heparin (IV)
Warfarin
Anticoagulants for 3/12
Massive PE
PE w/ evidence of systemic compromise - central/ proximal/ multiple clots
Hypotension, R heart strain
Thrombolysis of a massive PE
Dissolution of a clot
Improvement of physiological parameter
Reduce risk of death
Follow up for PE
Echo
Consider VTE risk factors and their modification
Consider lifelong anticoagulants
Who gets lifelong treatment after a PE
Idiopathic PE - cause unknown
First episode and ongoing risk factors
2 or more VTE events - IVC filter
Canonball metastases on CXR
Discrete lesion, multiple opacities
Mx of tension PTX
Urgent needle decompression
Chest drain and admission
Ddx of whole lung field white out
Collapse
Large pleural effusion
Pneumonectomy
Consolidation
Pneumonectomy
Surgical removal of lung or part of lung
What direction does the trachea move in lung collapse
Pulls trachea towards it
What direction does a large pleural effusion push the mediastinum
Away
Why might you see a white out on a CXR following a pneumonectomy
Fluid fills up space where lung has been taken out
What direction does a pneumonectomy move the mediastinum
Moves in or may be normal
When do you see a meniscus sign on a CXR
Pleural effusion
What do we see in hydro PTX on CXR
Fluid line
What side do you normally see surgical emphysema in
The side of the chest drain
Pancoasts tumour
Apical lung tumour
May cause denervation
Signs in Horner’s syndrome
Anhydrosis
Ptosis
Miosis
What does it mean if the cricothyroid distance is <3 fingers
Hyperinflation of the chest
What types of crackles do we hear
Coarse (infection and bronchiectasis) and fine end inspiratory (pulm fibrosis)
Features of vesicular breathing
Normal breathing
Longer inspiratory phase (2:1)
Gentle sound
Features of bronchial breathing
Seen in infections
Longer espiratrxy phase (1:3)
Break in between inspiratory and expiratory phases
Louder sound
Features of rhonci
Sounds similar to snoring
Can be cleared by coughing
Combination of wheeze and crackles - low pitched
Cause of rhonci
Build up of secretions
Features of a wheeze
Heard in expiratory
High pitched
Whistling/ musical tone
When do we hear a pleural rub
Pleurisy
Added breath sounds
Crackles Bronchial breathing Wheeze Stridor Rhonci Pleural rub
Signs of anaphylaxis
V quick onset
Stridor (inspiratory wheeze)
Angiodema
Urticarial rash
Crash call should be put out
Where do we aspirate PTXs from
2nd IC space, mid clavicular
Where do we insert a chest drain for PTX
5th IC space mid axillary
How do we measure a PTX
From edge of lung to hilum
Mx of PSP
If >2cm and/or breathless - aspirate
If no success, insert chest drain and admit
Mx of SSP
Insert chest drain if >2cm and/or breathless
Aspirate if 1-2cm
Which hilum is higher
L
What can a cavitating mass be caused by
Carcinoma of bronchus
SCC metastasis
Pulm infarct
Bacterial abscess
Definition of apnoea
Cessation of breathing for 10 seconds, causing 4% destauration
Ideal V/Q ratio
1 for maximally efficient pulmonary function
Usual VQ ratio
0.84 overall
Diff ratios for diff areas due to where area lies in relation to heart
How does VQ ratio change at the apex and base of lung
When standing up straight, ratio is 3.3 in apex and only 0.63 in base
V > Q in apex
V < Q in base
Examples of diseases causing Class I PHTN
Idiopathic/ heritable PAH - pts usually px quite young
PAH 2’ to drugs of CTD
Examples of diseases causing Class II PHTN
LV systolic/ diastolic dysfunction
Valvular disease e.g. MS, MR
Examples of diseases causing Class III PHTN
COPD
ILD
Examples of disease causing Class V PHTN
Sarcoidosis
Sickle cell anaemia
What mutation causes familial PAH
BMPR2
PAH
Pulm arterial HTN
Symptoms of Pulm HTN
(Non-spp) Progressive exertion dyspnoea Syncope Fatigue Limb swelling Chest pain Haemoptysis
Examination findings for pulm HTN
Looking for associations w/ CTD e.g. Raynaud’s, calcinosis, telangiectasia, sclerodactyly
Main ix for pulm HTN
R heart catheterisation
Echo
ECG
Bloods - NTproBNP, FBC (anaemic pts have worse prognoses)
Cardiac MRI
6 in walking test (stamina and desaturations)
Why do we measure glucose in pleural aspirate
To rule out Rh effusion when glucose is low
What is the pleural effusion most likely to be if the pH of the aspirate is below 7.2
Acidotic fluid implies parapneumonic effusion or empyema
Chest drain must be inserted ASAP (5th IC space)
What can be done for a PTX pt if a chest drain has not worked
Insert large bore cannula
Surgery
Talc pleurodesis
Key mechanism of hypoxaemia in pE
Physiological dead space - no gas supply to alveoli
Key mechanism of hypoxaemia in pleural effusion
Physiological shunting
What must HGV and public transport drivers do after a dx of OSA is made
Declare to DVLA and stop driving ASAP
Once established on treatment for 2-3/52, and assessed, they can resume
Indications for CPAP
ESS 11/24 and moderat/severe apnoea
Mild apnoea but CDV risk factors
Which CTD is most likely to cause heart failure
SScl
Specifically R heart
h
Example of a drug that may cause PAH
Fenfluramine - anti-epileptic
Drug therapy for PAH
Sildenafil
Bosentan
Both venodilators
Absolute contraindications for thrombolysis in PE
Haemorrhage stroke Ischaemic stroke within 3/12 Recent head injury Recent surgery Current active bleeding Bleeding disorder
Mechanism of tension PTX
The opening in the pleura creates a flap that acts as a one-way valve
This allows air to enter the cavity during inspiration but stops it from leaving during expiration
Mechanism of a spontaneous PTX
Small bleb/ weakness ruptures - more common in tall pts
Air in pleural space can results in pain - variable in intensity
Feeling breathless - dependent on air leak
Air in pleural space may result in the lung collapsing
Key landmark for insertion of a needle in a tension PTX
2nd IC space in the mid-clavicular line (urgent needle decompression)
