RESPIRATORY CHECKLIST

1. O2 uptake and delivery

 Inspired oxygen from the environment moves across the alveolar-capillary

membrane into the blood.
 Most of the oxygen binds to hemoglobin in red blood cells, although a small
amount dissolves into the plasma.
 The oxygen is then transported from the lungs to the peripheral tissues, where it is
removed from the blood and used to fuel aerobic cellular metabolism. This
process can be conceptualized as three steps: oxygenation, oxygen delivery, and
oxygen consumption
 Oxygenation
 Blood returning to the heart from the tissues has a low PO2 (4.3kPa) and
travels to the lungs via the pulmonary arteries.
The pulmonary arteries form pulmonary capillaries, which surround alveoli.
Oxygen diffuses (moves through the membrane separating the air and the
blood) from the high partial pressure in the alveoli (13kPa) to the area of
lower partial pressure - the blood in the pulmonary capillaries (4.3kPa).
After oxygenation, blood moves into the pulmonary veins and returns to the
left side of the heart, to be pumped to the systemic tissues.
In a ‘perfect lung’, the PO2 of pulmonary venous blood would be equal to
the PO2 in the alveolus (the PaO2).
Two main factors cause the PO2 of pulmonary venous blood to be less than
the PaO2, that is, to increase the alveolar:arterial difference. These are
ventilation/perfusion mismatch (either increased deadspace or shunt) and
slow diffusion across the alveolar-capillary membrane.
 Ventilation/perfusion (V/Q) mismatch
 In a ‘perfect lung’ all alveoli would receive an equal share of alveolar
ventilation and the pulmonary capillaries that surround different alveoli
would receive an equal share of cardiac output – i.e. alveolar minute
ventilation and perfusion would be perfectly matched, V/Q = 1.
 Even in health this is not achieved and at almost all levels in a normal
lung there is a relative imbalance of perfusion and ventilation
 Perfusion is best at the base of the lung and gradually reduces towards the
top of the lung, largely due to the effects of gravity.
 The alveoli at the base of a normal lung are at a lower resting volume in
expiration (at functional residual capacity, FRC), but they are better
ventilated (they increase their volume proportionately more) during
inspiration
  Where blood flows past alveoli with no gas exchange taking place (shunt,
see Figure 3), well ventilated alveoli (with high PO2 in capillary blood)
cannot compensate for the lack of oxygen transfer in the under-perfused
alveoli with a low PO2 in the capillary blood. This is because there is a
maximum amount of oxygen that can combine with haemoglobin (this is
shown by the oxygen-haemoglobin dissociation curve, later). Arterial
oxygen, PaO2 is therefore lower than the alveolar oxygen, PaO2.
 Causes
 Lung pathology that exacerbates the physiological shunt includes
atelectasis, consolidation of the lung, pulmonary oedema or small
airway closure. Pulmonary embolism causes increased
physiological deadspace.

 Diffusion
 Pulmonary disease may cause an abnormality of the alveolar-capillary
membrane, thus impairing transfer of oxygen from the alveolus to the
capillary (diffusion abnormality)
 Causes
 Fluid : pulmonary oedema, pneumonia, infarction, blood
 Fibrosis

 Alveolar hypoventilation

Obstruction Restriction
 COPD  Decrease drive : CNS sedation, trauma, tumor
 Asthma  NM disease : cervical cord lesion, polio, Gullian
 Bronchiectasis Barre syndrome, Myasthenia Gravis
 Bronchiolitis  Chest : flail, kyphoscoliosis, obesity ,fluid and
 Intra and extra thoracic ( carcinoma, LN, epiglottis fibrosis

 Oxygen delivery
 Three factors need to be taken into account: haemoglobin concentration,
cardiac output and oxygenation.
 Oxygen consumption
 At rest, oxygen delivery to the cells of the body exceeds oxygen
consumption. During exercise, oxygen consumption increases. The
increased oxygen requirement is usually provided by an increased cardiac
output (as shown in the formula above). A low cardiac output, low
haemoglobin concentration (anaemia) or low oxygen saturation will result in
reduced tissue oxygen delivery, unless there is a compensatory change in
one of the other factors. 

 If oxygen delivery falls relative to oxygen consumption, the tissues extract
more oxygen from the haemoglobin and the saturation of mixed venous
blood falls below 70%. Below a certain point, decreased oxygen delivery
cannot be compensated for by an increased oxygen extraction, and this
results in anaerobic metabolism and lactic acidosis. This situation is known
as supply-dependent oxygenation.
 2. Pathophysiology of respiratory failure

Type 1 Type 2
 PaO2 of <8 kPa (60 mm Hg) with normal  PaCO2 >6 kPa (45 mm Hg) and PaO2 <8 kPa
or low arterial carbon dioxide tension  Alveolar hypoventilation +/- V/Q mismatch
(PaCO2).  Failure of ventilation (hypercapnia, type II failure)
 V/Q mismatch and diffusion failure Abnormalities of central respiratory drive
 Failure of oxygenation (hypoxaemia, Neuromuscular dysfunction
type I failure) Abnormalities of the chest wall
Low inspired oxygen partial pressure Abnormalities of the airways
Alveolar hypoventilation Abnormalities of the lungs
Diffusion impairment  Causes
Ventilation/perfusion (V/Q) mismatch
Right-to-left shunt
 Causes
Acute asthma Pulmonary Acute severe asthma
Acute respiratory distress syndrome Upper airways obstruction
(ARDS) Chronic obstructive pulmonary disease
Pneumonia (COPD)
Pulmonary embolus Bronchiectasis
Pulmonary fibrosis Obstructive sleep apnoea
Pulmonary oedema Thoracic Chest wall trauma (flail chest)
Chronic obstructive pulmonary disease wall Ruptured diaphragm
(COPD) Kyphoscoliosis
 Emphysema Abdominal distension (ascites, blood,
surgical packs)
Morbid obesity
CNS Coma
Raised intracranial pressure
Head injury
Opioid and sedative drugs
Neurom Cervical cord lesions (trauma, tumour)
Spinal cord (poliomyelitis)
Peripheral nerves (Guillain–Barré
syndrome, diphtheria, critical
illness polyneuropathy)
Neuromuscular junction (myasthenia gravis,
organophosphorus poisoning, muscle
relaxants, botulism)
Muscular dystrophy
 3. Respiratory failure presentation

Hypoxia Hypercapnoea
Acute Chronic
 Dyspnea  Polycythaemia  Headache
 Agitation  PHT  Flushing and peripheral vasodilation
 Confusion  Cor pulmonale  Bounding pulse
 Cyanosis  Flap
 Confusion  coma

4. Respiratory failure ix

Blood  Arterial blood gas analysis: confirmation of the diagnosis.

 FBC: anaemia can contribute to tissue hypoxia; polycythaemia may indicate chronic hypoxaemic
respiratory failure.
 Renal function tests and liver function tests: may provide clues to the aetiology or identify
complications associated with respiratory failure. Abnormalities in electrolytes such as
potassium, magnesium and phosphate may aggravate respiratory failure and other organ
dysfunction.
 Serum creatine kinase and troponin I: to help exclude recent myocardial infarction. Elevated
creatine kinase may also indicate myositis.
 TFTs (hypothyroidism may cause chronic hypercapnic respiratory failure).
Imaging  CXR: often identifies the cause of respiratory failure.
 Echocardiography: if a cardiac cause of acute respiratory failure is suspected.
Special  Spirometry: useful in the evaluation of chronic respiratory failure
 Pulmonary function tests are useful in the evaluation of chronic respiratory failure.
 ECG: to evaluate a cardiovascular cause; it may also detect dysrhythmias resulting from severe
hypoxaemia or acidosis.
 Right heart catheterisation: should be considered if there is uncertainty about cardiac function,
adequacy of volume replacement and systemic oxygen delivery.
 Pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from non-
cardiogenic oedema.

5. Mechanisms of hypoxemia

Ventilation – perfusion mismatch Right – left shunt Diffuse defects

 V/Q mismatch when :  Pulmonary venous blood  Increase alveolar –

Any reduction of inspiratory inflow bypasses ventilated alveoli and capillary membrane
Parenchymal infiltartion (pneumonia) is not oxygenated thickness
Obstruction of vessels (PE)  This shunted blood retains the  Pulmonary fibrosis
 Eg saturation of mixed venous O2
 Atelectasis (70–80% in healthy individuals).  Acute pulmonary
Pulmonary embolus It then mixes with and reduces oedema
Endobronchial intubation the O2 con- tent of the non-
shunted blood, causing a fall in
Patient position
PaO
Bronchospasm  Eg
Obstruction of the airways ASD / VSD
Pneumonia Pulmonary AV
ARDS. malformations
 Will respond to oxygen administration Hepatopulmonary syndrome
Acute atelectasis
 May not respond to oxygen
administration

6. Indications for respiratory support

 In acute respiratory failure, a PaO2 <8 kPa (60 mmHg) or an SaO2 <90%, is an
indication for oxygen therapy. Aim to maintain an SaO2 of >92%.

7. Principles of administering respiratory support

 There are a wide variety of devices to deliver O2 .

Nasal prongs Simple face mask / Non – rebreathing mask Venture mask
Hudson mask
 FIO2 25–50%  FIO2 30–50%  Reservoir bag allows  Provide precise oxygen
with flows of 1–6 with flows of 6– delivery of high concentration at high flow rate
l/minute 8 l/minute concentration if oxygen Yellow : 5%
 60 – 90% at 10 – 15 L White : 8%
Blue : 24%
Red :40%
Green:60%

 The patient should be monitored with pulse oximetry and blood gas analysis performed
within 20 minutes.
 If the SaO2 is <90% or the PaO2 is <7 kPa (53 mmHg) in a patient with previously
healthy lungs, the O2 concentration should be increased and further blood gases
checked. Meanwhile, the underlying condition should be treated.
 Patients with COPD and chronic type II respiratory failure who have lost their
hypercapnic drive and rely on hypoxic drive to stimulate ventilation, the inspired O2
concentration should be limited to 24–28% using Venturi-type fixed performance
oxygen masks whenever possible. The aim of treatment should be to maintain the PaO2
at 8–10 kPa (60–75 mmHg).
 If the hypoxemia does not improve with oxygen therapy, or the patient becomes
exhausted with a rising PaCO2, then transfer to an ICU and mechanical ventilation
should be considered.

8. Non – invasive ventilation

  Non – invasive ventilation is the use of airway support administered through a face
(nasal) mask instead of endotracheal tube
 Inhaled gases are given with positive – end expiratory pressure often with pressure
support or with assist control ventilation at a set of tidal volume and rate
 Indications

Primarily hypercapnea Primarily hypoxaemia

- Acute exacerbation of COPD; decrease work of
breathing and unload respiratory muscles
- Post extubation acute respiratory failure; planned
strategy in selected patients
- OSA / obesity hypoventilation syndrome
- Cystic fibrosis; bridge to transplant
- Patient awaiting for lung transplantation
- Acute asthma
- Cardiogenic pulmonary oedema; alveolar
recruitment, decreased
- Post – operative respiratory failure in selected
patients
- Post – traumatic respiratory failure rib fractures
- Respiratory failure in AIDS and other
immunosuppressed states
- Patient not candidates for intubation/treatment
limitation orders who may qualify for HDU
admission to respiratory care unit
- Pre – oxygenation prior to intubation

 Types

Negative pressure Positive pressure Positive pressure (cyclical) Positive and

(cyclical) (non – cyclical) negative pressure
(cyclical)
- Iron lung chest - Continous positive - Bilevel positive airway pressure - Cough assist
box airway pressure (CPAP) (BIPAP), inspiratory positive - Used for
- Used for - Used for acute airway pressure (IPAP), pressure neuromuscular
COPD, pulmonary oedema, support ventilation (PSV) and disease
neuromuscular asthma, OSA positive pressure ventilation (PPV)
disease - Used for COPD, weaning asthma,
neuromuscular disease

 Physiology
 Augmentation of alveolar ventilation, helps reverse acidosis and hypercapnoea
 Alveolar recruitment and increased FiO2, helps reverse hypoxia
 Reduction in work of breathing and respiratory effort/fatigue
 Stabilization of chest wall in the presence of chest trauma / surgery
 Reduction in LV afterload, improves LV function
 Counterbalances the respiratory workload and/or reduces respiratory muscle effort,
helps maintain alveolar ventilation and prevents exhaustion

 Contraindications
 Cardiac / respiratory arrest
 Inability to protect airway – poor cough, excessive/inability to clear secretions,
decreased conscious state/coma
 Upper airway obstruction
 Untreated pneumothorax
  Marked haemodynamic instability; eg shock, ventricular dysarrhthmias, severe acute
myocardial ischaemia, GI bleeding
 Follwoing upper GI surgery (debatable)
 Maxillofacial surgery
 Base of skull fracture (risk of pneumocephalus)
 Patient refusal
 Intractable vomitting

9. Invasive ventilation / mechanical ventilation

 The term “invasive” is used if it involves any instrument penetrating via the mouth (eg
endotracheal tube), nose or skin (eg tracheostomy tube through stoma, a surgically –
created hole in windpipe to serve as an artificial airway)
 Mechanical ventilation uses a breathing machine called a ventilator to help move air
into and out of the lungs.
 In order to connect a lungs to a ventilator, a doctor may insert a narrow plastic tube
through the mouth and into the windpipe through a process called intubation.
 The objective of mechanical ventilation are primarily to increase oxygen, remove carbon
dioxide and decrease the work of breathing
 Indications
 Life – threatening respiratory failure
 Failure of non - invasive ventilation
 Arterial blood gas abnormalities
 Can be used as a means to maintain a patient’s airway during a surgical procedure,
such as intubation done in ICU
 FiO2>50%
 PaO2<8.0kPa/ 60mmHg
 PaCO2> 6.0kPa/ 45mmHg
 GCS<8
 Facilitation of mechanical ventilation
 Protection from aspiration
 Facilitation of tracheobronchial suction
 Relief of upper airways obstruction
 Types

Standard endotracheal tube Tracheostomy tube

 Inserted via the nose or mouth
 Provides a secure airway when the balloon on the cuff
is inflated and sealed, and is mostly used in adult
patients with acute respiratory failure; pediatric
patients can benefit from uncuffed ET
 Inserted via stoma, a surgically – created opening in
trachea, the tracheostomy tube is used in patient who
need long – term mechanical ventilation, and exists
with cuffed and uncuffed options

 Complications
 Infections—The ET or trach tube allows germs (bacteria) to get into the lungs more
easily. This can cause an infection like pneumonia
 Collapsed lung (pneumothorax)—Sometimes, a part of the lung that is weak can
become too full of air and start to leak. The leak lets air get into the space between the
lung and the chest wall. Air in this space takes up room so the lung starts to collapse.
  Lung damage—The pressure of putting air into the lungs with a ventilator can damage
the lungs. Doctors try to keep this risk at a minimum by using the lowest amount of
pressure that is needed. Very high levels of oxygen may be harmful to the lungs as
well.

10. Long term oxygen therapy

 LTOT for more than 15 h/day improved mortality and morbidity in a well-defined group
of patients with chronic obstructive pulmonary disease
 Indications
 Chronic hypoxaemia
 Example
 Chronic obstructive pulmonary disease
 Severe chronic asthma
 Interstitial lung disease
 Cystic fibrosis
 Bronchiectasis
 Pulmonary vascular disease
 Primary pulmonary hypertension
 Pulmonary malignancy
 Chronic heart failure
 After appropriate assessment, when the PaO2 is consistently at or below 7.3 kPa
(55 mmHg), when breathing air during a period of clinical stability (defined as
the absence of exacerbation of chronic lung disease for the previous five weeks)
 Level of PaCO2 (which may be normal or elevated) does not influence the
need for LTOT prescription
 In chronic hypoxaemia patients when the clinically stable PaO2 is between 7.3
kPa and 8 kPa, together with the presence of one of the following:
 Secondary polycythaemia
 Clinical and or echocardiographic evidence of pulmonary hypertension
 LTOT should not be prescribed in patients with chronic hypoxaemia patients
with a PaO2 value above 8kPa
 Nocturnal hypoventilation
 Obesity Neuromuscular/spinal/chest wall disease*
 Obstructive sleep apnoea (with CPAP therapy)*
*assessment for LTOT requires referral to a physician with a specialist interest
in these disorders. LTOT will normally be used as an adjunct to ventilatory
support techniques (noninvasive ventilation (NIV) or continuous positive airway
pressure (CPAP)
 Palliative use
 Contraindication
 Smoking

11. Spirometry and the flow-volume loop.

 Spirometry measures how much air can be inhaled & exhaled.Also measures how fast air
can be emptied out of lung by measuring :
 Major : FVC, FEV1, FEV1:FVC, flow volume loop
 Minor : Peak expiratory flow, FEF values, forced inspiratory flow rate, maximal
voluntary ventilation, response to bronchodilator
 Forced expiratory volume in 1s (FEV1) – the volume exhaled in the first second after
deep inspiration and forced expiration, similar to PEFR (normal = 0.8)
 Forced vital capacity (FVC) – the total volume of air that the patient can forcibly exhale
in one breath (normal = 0.8)
 FEV1/FVC – the ratio of FEV1 to FVC expressed as a percentage (normal = 0.7)
 Flow – volume loop

 The flow-volume loop is a plot of inspiratory and expiratory flow (on the Y-axis) against
volume (on the X-axis) during the performance of maximally forced inspiratory and
expiratory maneuvers
 The normal expiratory portion of the flow-volume curve is characterized by a rapid rise to
the peak flow rate, followed by a nearly linear fall in flow as the patient exhales toward
RV
 The inspiratory curve, in contrast, is a relatively symmetrical, saddle-shaped curve
 Interpretating
12. Lung volumes.

13. Measurement of DLCO and clinical importance.

 A test of the diffusing capacity of the lungs
 Diffusing capacity (or transfer factor) is measured using small volume of CO and
measures the transfer of CO across alveolar – capillary membrane
 DLCO can assist in identification, assessment of severity and monitoring wide range
of disease affecting the lung parenchyma and pulmonary vascular bed
 CO is used because the uptake of the gas is diffusion limited
 Normal diffusion capacity ~ 25 mlmm-1mmHg-1
  Diffusing capacity increases on exercise : Recruitment & distension of pulmonary
capillaries
 Indications
 Differentiating emphysema from obstructive bronchitis and chronic asthma
 Assess COPD
 Differential diagnosis of volume restriction
 Detect pulmonary vascular disease
 Assessment of breathless patient
 Disability / impairment evaluation for ILD, COPD
 Follow up ILD
 Interpretations

Decreased DLCO Increased DLCO

 Emphysema  Pulmonary haemorrhage (eg pulmonary
 Interstitial lung disease vasculitis)
Interstitial pneumoniae (Eg idiopathic lung fibrosis)  Polycythemia
Hypersensitivity pneumonitis  Current smoker (in absence of emphysema)
Sarcoidosis  Pregnancy (if not anaemia)
Drug – induced lung disease (eg Amiodarone, bleomycin)
Collagen – vascular disease (eg. SLE, RA, slcleroderma)
Occupational lung disease
 Pulmonary vascular disease
Pulmonary arterial hypertension
PE
 Left – sided heart disease
Systolic and diastolic HF
Mitral valve disease
 Anaemia

14. Recognizing restrictive and obstructive patterns in PFT

Obstructive
- Characterized by reduction in
airflow
- Decrease in airflow  SOB 
problem exhaling air
- Air will remain inside the lungs
after full expiration
Restrictive
Pathology - Characterized by reduction in
lung volume
- Decrease in lung volume 
difficulty in taking in air into
lung due to stiffness inside the
lung tissue or chest wall
cavity

- COPD, asthma, bronchiectasis Examples - Interstitial lung disease, such as

idiopathic pulmonary fibrosis.
- Sarcoidosis, an autoimmune
disease
Normal / decrease Vital capacity Decrease
Normal / increase Total lung capacity Decrease
Below 80% predicted FEV1 Below 80% predicted
 Increase Residual volume Decrease
Decrease ; <0.7 FEV1 : FVC Normal; (>0.7) or increase
Decrease Maximum mid expiratory flow Normal
rate
Decrease Maximum breathing capacity Normal
Spirometry

15. Respiratory ix

Test Details
CXR  Provides information on lung fields, heart, mediastinum, vascular structures, thoracic
cage
 Important
Collapse & consolidation
Pleural effusion
Fibrosis
Round shadow
Military mothing : TB, pneumoconiosis, sarcoidosis, pulmonary fibrosis, pulmonary
oedema
ABG
Indications Contraindications
  Severe respiratory / metabolic disorder  Overlying infection / burn at insertion site
 Clinical features of hypoxia / hypercapnia  Absent collateral circulation
 Shock  Arteriovenous shunt, often radial / brachial
 Sepsis  Severe atherosclerosis
 Decreased cardiac output  Raynaud disease
 Renal failure  Coagulopathy

 Normal values
pH : 7.35 – 7.45
pO2 : 10 – 14kPa
pCO2 : 4.5 – 6 kPa
Base excess : -2 – 2 mmol/L
HCO3 : 22 – 26 mmol /L
Acid base disorders
Spirometry / peak  Performing the test
flow The patient should be sitting comfortably with both feet on the ground, and tight clothing
loosened
The patient begins by tidal breathing with their lips and teeth around the mouthpiece for
at least three breaths*
The patient should inspire maximally and rapidly and immediately blow out as hard and
as fast as possible
After a full and complete expiration the patient should inhale maximally again in a
relaxed manner
 Indications & contraindications

Indications Contraindications

 Detect respiratory disease in patient  Known or suspected respiratory infection

presenting with symptoms of
breathlessness and to distinguish
respiratory from cardiac disease as the
cause
 Measure bronchial responsiveness in
patients suspected of asthma
 Diagnose and differentiate between
COPD and restrictive lung disease
 Smokers
 COPD
 Asthma
 Chest tightness
 Unexplained chronic cough
 Neuromuscular disease
 Exertional dispneoa
 Systemic diseases
 Haemoptysis of unknown origin
 Pneumothorax
 Unstable cardiovascular status: recent
(within 1 month) myocardial infarction,
uncontrolled hypertension or pulmonary
embolism
 Uncontrolled hypertension or history of
haemorrhagic cerebrovascular event
 Recent thoracic, abdominal or eye surgery
 Nausea/vomiting/Pain
 Confusion/dementia


 Adv & disad

Advantages Disadvantages
Readily available Effort dependant
Useful tool in diagnosis and monitoring Poor compliance
of asthma False high readings
Quick to perform Possibility of manipulation of results
Cheap and portable
Bronchoscopy - A viewing tube used to evaluate patient’s lungs and airway including the voicebox, vocal
cord, trachea and many branches of bronchi
- Doesn’t allow direct viewing & inspection of lung tissues itself but lung tissue can be
biopsied
- Indications

Diagnosis Treatment
 Persistent / unexplained cough  Remove foreign bodies in airway
 Blood in sputum
  Abnormal CXR:mass, nodule,  To place a stent to open collapsed airway
inflammation due to pressure by mass / tumor
 Evaluation of possible lung infection  Remove mass /growth blocking airway

- Procedures
 Local anaesthetic spray to nose & throat during procedure
 Sedative  relax; awake but drowsy
 Oxygen is usually give, GA rarely needed
 Avoid eating drinking; up to 6 – 12 h before
 Ask doctors if ve to stop taking
 Aspirin, ibuprofen, warfarin, other blood thinners
 Insert into nose  mouth throat bronchi
 Brushes / needles may be attached to bronchoscope  collect lung tissue sample
 This involves spraying saline solution over surface of airways
 The cells that are washed off  collected looked under microscope
 May also do bronchial washing to collect cells
 May find blood, mucus, infection, swelling, blockage, tumor
 If blocked airway, insert stent to keep it open
- Potential complications
 Nose bleeding
 Vocal cord injury
 Irregular heart beats
 Lack of oxygen to body tissue
 Head injury due to medications or lack oxygen
 Bleeding from biopsy site
 If bleeding tumor; use cold saline / adrenaline
- Contraindications

Absolute Relative
 Untreatable life – threatening arrhythmias  Uncooperative patient
 Inability to adequately oxygenate patient during  Recent myocardial
procedure infarction
 Acute respiratory failure due to hypercapnia (unless  Uncorrectable coagulopathy
patient is intubated, ventilated)
 High grade tracheal obstruction
CT thorax - Examine abnormality found in other imaging tests
- Helps to diagnose the cause of unexplained cough, SOB, chest pain and fever
- Fast, painless, non – invasive , accurate
- Excellent images of lungs, mediastinal structures
- Essential in staging bronchial carcinoma; size, nodule involvement, metastases
- CT – guided needle biopsy
- Demonstrate
 Benign, malignant tumor
 Pneumonia, TB
 Bronchiectasis, CF
 Inflammation, other pleura disease
 Interstitial & chronic lung disease
 Congenital abnormality
6 minute walk - Assess aerobic capacity and endurance
test - The distance covered in 6 minutes issues as outcome by which to compare changes in
performance capacity
- Indications
 Pre & post treatment comparison
 Lung transplantation, lung resection, lung volume reduction surgery, pulmonary
rehabilation, COPD, pulmonary hypertension
 Functional status
 COPD, CF, HF, peripheral vascular disease, fibromyalgia, older patients
- Contraindications
 Absolute : unstable angina, myocardial infarction in previous month
 Relative
 Resting HR :127/min
 SBP : >180 mmHg
 DBP : >100 mmHg
- Stable angina is not a contraindication; but patient must take anti – angina medication
beforehand and the rescue nitrate medication should be readily available

16. Respiratory pharmacology

17. Asthma pathology
 Bronchial muscle contraction; triggered by variety of stimuli
 Mucosal swelling / inflammation caused by mast cell and basophil degranulation 
release inflammatory mediators
 Increase mucus production

18. Asthma Presentation

Symptoms Signs
 Intermittent dyspnea  Tachypnea
 Wheeze  Audible expiratory wheeze
 Cough (often norcturnal)  Prolonged expiratory phase
 Sputum  Hyperinflated chest
 Hyperesonant percussion
 Reduced air entry
 Harrison’s sulcus: a groove at the inferior border of the rib cage that may be
seen in children with chronic severe asthma. Also seen in rickets.

19. Asthma diagnosis

 Document FEV1/FVC is reduced (at least once, when FEV1 is low)
 Excessive bronchodilator reversibility (adults : increase in FEV1 >12% and > 200mL,
children >12% predicted)
 Excessive diurnal variability from 1 – 2 weeks twice daily PEF monitoring
 Significant increase in FEV1 or PEF after 4 weeks of controller treatment

Increased probability that symptoms is due to asthma
 More than 1 type of symptoms; wheeze, SOB, cough,
chest tightness
 Symptoms often worse in night / early morning
Decreased probability that symptoms is due to asthma
 Isolated cough with no other respiratory symptoms
 Chronic production of cough
 SOB associated with dizziness, light – headedness
or peripheral tingling
 Symptoms are triggered by viral infections, exercise,  Chest pain
allergen exposure, changes in weather, laughter,  Exercise – induced dyspnea with noisy inspiration
irritants such as car exhaust fumes, smoke or strong (stridor)
smell

20. Acute asthma severity

Severe Life - threatening

 Unable to complete 1 sentence  PEF : < 33%
 RR > 25/m  Silent chest, cyanosis, feeble respiratory effort
 Pulse rate ≥ 110/m  Bradycardia or hypotension
 PEF : 33 – 50%  Exhaustion , confusion or coma
 ABG
Normal / high PaCO2
PaCO2 should be low w hyperven; serious
PaO2 : <8kPa / SpO2 :< 92%
pH : < 7.35

21. Asthma acute mx

 Airway: Ensure patent airway
 Breathing: Give 100% Oxygen (15L) via non-rebreather mask
 Circulation: Insert two large-bore cannulae and start IV 0.9% Saline
 Access severity
 PEF, HR ,RR
 Ability to speak
 Oxygen saturation
 Warn ICU of severe / life – threatening
 Immediate treatment
 Salbutamol 5 mg ( or terbutaline 10 mg) nebulised with oxygen
 Hydrocortisone 100 mg iv or prednisolone 40 – 50 mg / both if very ill
 Start oxygen if saturation < 92% ( check abg ). Aim sat 94 – 98 %
 Inform ICU

 Life – threatening features

 Give salbutamol neb every 15 min or 10 m g continuously per hor. Monitor ECG
for arrhythmia
 Add ipratropium bromide 0.5 mg to nebuliser
 Give single bolus of magnesium sulphate 1.2 – 2 g iv over 20 m

 Further treatment
Not improving Improvement in 15 – 30 m
 ICU referral if  Neb salbutamol every 4 h
Deteriorating PEF  Prednisolone 40 – 50 mg PO OD for 5 -7 days
Persistent / worsening hypoxia  Monitor peak flow and oxyen sat, aim 94 –
Hypercapnia 98% with supplemental if needed
Low ph / high hydrogen ion – ABG
Exhaustion, feeble respiration
Drowsiness, confusion, altered conscious level
Respiratory arrest

22. Asthma severity scale

23. Asthma control

24. Asthma GINA strategy
  STEP 1
 Preferred controller: As-needed low dose ICS-formoterol (off-label)
 Step 1 recommendations are for patients with symptoms less than twice a month
and no exacerbation risk factors
 Other controller options at Step 1
 Low dose ICS taken whenever SABA is taken
 STEP 2
 Preferred controllers: Daily low dose ICS plus as-needed SABA, OR as-needed
low dose ICS-formoterol
 For this recommendation, the most important considerations were to prevent
severe exacerbations and to avoid the need for daily ICS in patients with mild
asthma.
 Other controller options at Step 2
 Low dose ICS taken whenever SABA is taken
 Leukotriene receptor antagonists (LTRA) are less effective than regular ICS,
particularly for preventing exacerbations.
 Daily low dose ICS-LABA as initial therapy leads to faster improvement in
symptoms and FEV1 than ICS alone but is more costly and the exacerbation
rate is similar.

25. Reviewing response and adjusting treatment

 How often should patients with asthma be reviewed?
 Patients should preferably be seen 1–3 months after starting treatment and every
3–12 months after that, but in pregnancy, asthma should be reviewed every 4–6
weeks.
 After an exacerbation, a review visit within 1 week should be scheduled.
 The frequency of review depends on the patient’s initial level of symptom
control, their risk factors, their response to initial treatment, and their ability and
willingness to engage in self-management with an action plan.

 Stepping up asthma treatment

 Sustained step-up (for at least 2–3 months): if symptoms and/or exacerbations
persist despite 2–3 months of controller treatment, assess the following common
issues before considering a step-up
 Incorrect inhaler technique
 Poor adherence
 Modifiable risk factors, e.g. smoking
 Short-term step-up (for 1–2 weeks) by clinician or by patient with written
asthma action plan (p29), e.g. during viral infection or allergen exposure
 Day-to-day adjustment by patient for patients prescribed as-needed low dose
ICS-formoterol for mild asthma, or low dose ICS-formoterol as maintenance and
reliever therapy.

 Stepping down treatment when asthma is well-controlled

 Consider stepping down treatment once good asthma control has been achieved
and maintained for 3 months, to find the lowest treatment that controls both
symptoms and exacerbations, and minimizes side-effects

26. The written asthma action plan should include:

  The patient’s usual asthma medications
 When and how to increase medications, and start OCS
 How to access medical care if symptoms fail to respond
 Action plans can be based on symptoms and/or (in adults) PEF. Patients who
deteriorate quickly should be advised to seek urgent care immediately.

27. Non-pharmacological strategies and interventions – asthma

 Smoking cessation advice: at every visit, strongly encourage smokers to quit. Provide
access to counselling and resources. Advise parents and carers to exclude smoking in
rooms/cars used by children with asthma
 Physical activity: encourage people with asthma to engage in regular physical
activity because of its general health benefits. Provide advice about management of
exercise-induced bronchoconstriction.
 Occupational asthma: ask all patients with adult-onset asthma about their work
history. Identify and remove occupational sensitizers as soon as possible. Refer
patients for expert advice, if available.
 NSAIDs including aspirin: always ask about asthma before prescribing.

28. COPD aetiology

 COPD is a progressive disorder characterized by airway obstruction (FEV1 < 80%,
FEV1:FVC<0.7) with little or no reversibility
Smoking Alpha-1 antitrypsin deficiency
 90% of  Alpha-1 antitrypsin deficiency is an autosomal codominant condition characterised by a
cases of deficiency in alpha-1 antitrypsin.
COPD  Alpha-1 antitrypsin is a protease inhibitor that is synthesised by the liver. It acts in the lung
parenchyma to oppose the action of elastase.
 Elastase is a protease that causes the breakdown of elastin, a protein important to the structural
integrity of the alveoli. This causes emphysema.

29. COPD pathophysiology

Airway  Chronic bronchitis refers to inflammation of the bronchi, defined as a chronic productive cough
for three (or more) months in two consecutive years where other causes are excluded.
 Chronic bronchitis leads to:
Goblet cell hyperplasia
Mucus hypersecretion
Chronic inflammation and fibrosis
Narrowing of small airways
Alveoli  Emphysema is the permanent enlargement of airspaces distal to the terminal bronchiole when
interstitial pneumonias are excluded.
 Inflammatory processes lead to the production of proteases by inflammatory cells such as
macrophages. The protease elastase causes the destruction of elastin, a protein important to the
structural integrity of the alveoli.
 Loss of elastin has two effects:
Collapse: the alveoli are prone to collapse.
Dilation and bullae formation: alveoli dilate and may eventually join with neighbouring
alveoli forming bullae.
Cor  Cor pulmonale refers to right ventricular impairment secondary to pulmonary disease. In the
pulmonale developed world COPD is the most common cause.
 Clinical features are those of right-sided heart failure

30. Emphysema vs chronic bronchitis

Emphysema; Pink puffer Chronic bronchitis; blue bloaters

 Pursed lips
 No problem getting air inside lung, but problem
with exhalation
 Increased alveolar ventilation
 Breathless but not cyanosed
 Normal or low PaCO2
 Progress  type 1 respiratory failure
 Decreased alveolar ventilation
 Cyanosed but not breathless
 Decreased PaO2 and increased PaCO2; rely on
hypoxic drive
 Progress  type 2 respiratory failure & cor
pulmonale

31. COPD presentation

Symptoms Signs
 Cough + sputum  Tachypnea
 Dyspnea  Prolonged expiratory phase
 Wheeze and chest tightness  Hyperinflation
 Others : fatigue, weight loss, anorexia, syncope,  Decreased cricosternoid distance
rib fractures, ankle swelling, depression, anxiety  Loss of cardiac dullness
 Displaced liver edge
 Wheeze
 May have early inspiratory crackles
 Cyanosis
 Signs of C02 retention
Drowsy
Asterixis
Confusion
 Cor pulmonale
Peripheral oedema
Left parasternal heave (caused by right
ventricular hypertrophy)
Raised JVP
Hepatomegaly
 Signs of steroid use

32. COPD severity

 MRC dyspnoea scale
  Spirometry may be used to categorise COPD. The table below is based on NICE clinical
guidance 101.

 Combined assessment

33. COPD ix

Bedside Blood Imaging

 Observations  FBC :  CXR
 BMI anaemia, Hyperexpanded
 Sputum culture (if purulent) polycythemia Flattened hemidiaphragms
 Pulse oximetry Hypodense
 Arterial blood gas (if hypoxia or
Saber-sheath trachea
hypercapnia is suspected)
 CT scan: if symptoms disproportionate to
 ECG (if cor pulmonale suspected)
spirometric assessment.
 Echocardiogram: if cor pulmonale suspected.

34. COPD pharmacology mx

 Group A
 All group A patients should be offered bronchodilator treatment based on effect on
breathlessness. This can be either short / long – acting bronchodilator
 This should be continued if symptomatic benefit is documented
 Saba – Ventolin
 Sama
 Group B
 Initial therapy should consists of long – acting bronchodilator
 Long – acting bronchodilators are superior to short – acting bronchodilators as
needed; and therefore recommended
 There is no evidence to recommend one class long – acting bronchodilators over
another for initial relief of symptoms in this group of patients. In the individual
patient, the should depends on the patient’s perception of symptom relief
 For patients with persistent breathlessness on monotherapy the use of two
bronchodilators is recommended
 For patients with severe breathlessness, initial therapy with 2 bronchodilators maybe
considered
 If the addition of second bronchodilator does not improve symptoms, we suggest the
treatment could be stepped down again to single bronchodilator
 Group B patients are likely to have comorbidities that may add to their
symptomatology and impact their prognosis, and these possibilities should be
investigated
- Group C
 Initial therapy should consists of a single long – acting bronchodilator. In 2 head –
to head comparisons the tested LAMA was superior to the LABA, therefore we
recommend starting therapy with LAMA
 Patients with persistent exacerbations may benefit from adding a second long –
acting bronchodilator (LABA /LAMA) or using a combination of long acting Beta
2 agonist and an inhale corticosteroid (LABA/ICS). As ICS increases the risk of
developing pneumonia in some patients, our primary choice is LABA / LAMA
- Group D
 Recommend starting the therapy with LABA / LAMA combination because
 LABA/LAMA show superior results compared to the single substances. If a
single bronchodilator is choosen as an initial treatment, a LAMA is preferred for
exacerbation
 A LABA/LAMA combination was superior to a LABA/ICS combination in
preventing exacerbations
 Group D patients are at higher risk of developing pneumonia when receiving
treatment with ICS
 In some patients initial therapy with LABA/ICS maybe the first choice
 These patients may have a history of asthma – COPD overlap
 High blood eosinophil counts may also be considered as a parameter to support
ICS use (still under debate)
- In patients who develop further exacerbations on LABA/LAMA therapy, we suggest 2
alternative pathways
 Escalation to LABA/LAMA/ICS
 Switch to LABA/ICS
- If patient treated with LABA/LAMA/ICS still have exacerbations the following options
may be considered
 Add roflumilast. This maybe considered in patients with an FEV1<50% predicted and
chronic bronchitis, 13 particularly if they have experienced at least 1 hospitalization
for an exacerbation in the previous year
 Add macrolide. The best available evidence exists for Azithromycin. Consideration
to the development of resistant organism should be factored into decision making
 Stopping ICS. A reported lack of efficacy an, elevated risk of adverse effects
including pneumonia) and evidence showing no significant harm from withdrawal
supports this recommendation

35. LTOT for COPD

 Long-term oxygen therapy (LTOT) is reserved for patient who when stable:
 Have Pa02 < 7.3 kPa. or
 Have Pa02 < 8 kPa with any of:
 Pulmonary hypertension
 Peripheral oedema
 Nocturnal hypoxaemia
 Secondary polycythaemia
 LTOT is required for at least 15 hours a day for a benefit to be seen. Patients who
smoke should be explained the dangers of mixing oxygen and cigarettes.

36. COPD non – pharmacology mx

 Smoking cessation
 Education, self – management, pulmonary rehab
 Light exercises; with increasing capacity
 Benefit to almost 2 years
 Vaccination
 Nutrition
 Interventional bronchoscopy and surgery
37. Acute exacerbation of COPD
 Presentation
 Increasing cough
 Breathlessness / wheeze
 Decreased exercise capacity
 Ix
 ABG
 CXR – exclude pneumothorax, infection
 FBC U&E CRP
 ECG
 Sputum culture
 Blood culture if pyrexial

 Mx
 Airway: Ensure patent airway
 Breathing
 Circulation: Insert two large-bore cannulae and start IV 0.9% Saline
 Nebulized bronchodilator
 Salbutamol 5mg / 4h and ipratropium 500 microgram / 6h
 Investigate : CXR, ABG
 Controlled oxygen therapy if SaO2 < 88 % or PaO2 < 7 kpa
 Start 22- 24 %; iam sat 88 – 92 % ( 94 – 98 % if no hypercapnia on ABG)
 Adjust according to ABG, aim PaO2 > 8 kpa with rise in PaCO2 < 1.5 kpa
Steroid
 IV hydrocortisone 200 mg and oral Prednisolone 30 mg OD ( continue for 7
– 14 d)
 Antibiotics
 Evidence of infection
 Eg amoxicillin 500 mg / 8h PO or clarithromycin / doxycycyline
 Physiotherapy to aid sputum expectoration
 If no response to nebuliser and steroid
 Consider IV aminophylline
 If no response
 Consider NIV if RR > 30 or pH < 7.35 or PaO2 rising despite best medical
treatment; BIPAP
 Consider respiratory stimulant drug; eg doxapram 1.5 – 4 mg / min
 Side effects : agitation, confusion, tachycardia, nausea
  Short term measure if NIV is unavailable

38. Bronchiectasis
 A disease in which there is permanent enlargement part of the airway

39. Bronchiectasis causes

Idiopathic  50 %
Congenital  Cystic fibrosis (mainly upper lobe infiltration)
 Kartegener’s / PCD
Primary ciliary dyskinesia / immobile ciliary problem
Rare, ciliopathic, autosomal recessive disorder that causes defect in action of cilia
lining respiratoy tract
Main consequence : decrease / absent mucus clearance from lung  susceptible to
infections
 Young’s syndrome ( azopomeia + bronchiectasis)
Rare condition that encompasses a combination of syndromes such as
bronchiectasis, rhinositis, decreased fertility
Post – infection  2 most common; childhood infection- rare now due to vaccination
nd

 Measles, Pertussis, Pneumonia, TB, Broncholitis

Immunodeficiency  Hypogammaglobulinaemia
X – linked agammaglobulinaemia : Burton;s
CVID
Ig E subclass deficiency
Ig A deficiency
Others  Bronchiole obstruction : LN, tumor, foreign body
 ABPA; allergic bronchopulmonary aspergillosis
 RA
 UC, Crohns (IBD)
 Yellow nail syndrome
Yellow nail discolouration & dystrophy
Lymphedema
Pleural effusion
Bronchiectasis

40. Bronchiectasis presentation

Signs Smptoms
 Clubbing  Persistent cough with purulent sputum
 Coarse inspiratory crackles  Haemoptsysis (maybe massive)
 Wheeze  Fever, weight loss
 Purulent sputum
 Cause :
Sinus inversus ( +PCD = kartegener’s syndrome)
Splenomegaly – immune deficiency

41. Bronchiectasis ix
Blood  Se Ig, Aspergillus precipitants, RF, alpha 1 anti-trypsin level, test Ig for pneumococcal
vaccine
Imaging  CXR : Thickened bronchial wall
 High resolution CT test : access extent and distribution of disease
Dilated, thickened airways
Saccular dilations in cluster with pool of mucus
Others  Spirometry (obstructive pattern)
 Bronchoscopy + mucosal biopsy : locate site of haemoptysis, exclude bstruction, obtain
biopsy
 CF sweat test
 Sputum culture
 Aspergillus precipitins or skin prick

42. Bronchiectasis mx
 Postural drainage 2X/d
 Chest physio  aid sputum expectoration and mucous drainage
 Antibiotics
 If 3 or more exacerbation in 1 y  consider long term antibiotics
 Usually high dose for 10-14 days
 Guided by sputum culture
 If poor response check sensitivities & consider IV antibiotics
 Pseudomonas frequently requires IVs for 10-14 days
 If Pseudomonas colonised consider nebulized aminoglycosides / polymixins
 Organisms
Common Uncommon
 Haemophilus Influenzae  Staph Aureus
 Pseudomonas Aeriginosa  NTM
 Strep Pneumonia  Fungi
 Moraxhella Catarrhalis  Coliforms

 Bronchodilator : neb salbutamol maybe useful in patients with asthma, COPD, CF,
ABPA
 Corticosteroid : ABPA – long-term prednisolone itraconazole
 Surgery maybe indicated in localised disease / control severe haemoptysis

43. Bronchiectasis complications

 Pneumonia, pleural effusion, pneumothorax, haemoptysis, cerebral abscess,
amyloidosis

44. Cystic fibrosis pathophysiology and aetiology

 Cystic fibrosis (CF) is an autosomal recessive disorder caused by a mutation in the
CFTR gene, which encodes for the cystic fibrosis transmembrane conductance
regulator protein.
 The mutation leads to the production of defective chloride channels in cell
membranes of the exocrine glands, and symptoms are caused by these glands
producing abnormally hyperviscous secretions
 Hereditary autosomal recessive disorder
  Defective CFTR (cystic fibrosis transmembrane conductance regulator) protein
due to mutation in CFTR gene
 The most common mutation is delta F508 on chromosome 7.
 Delta F508 (ΔF508 mutation) denotes the absence of the amino acid
phenylalanine (F) in position 508 of the protein (present in 70% of non-
Hispanic white patients with CF).

45. Cystic fibrosis presentation

GI  Meconium ileus in newborns

 Failure to thrive due to malabsorption
 Gastrointestinal symptoms are common in infancy.
 Pancreatic disease
Pancreatitis
Exocrine pancreatic insufficiency
 Foul-smelling steatorrhea (fatty stools) may occur.
 Malabsorption
 Abdominal distention
 Diarrhea
 Deficiency of fat-soluble vitamins (e.g., night blindness due to vitamin A deficiency,
rickets due to vitamin D deficiency)
CF-related diabetes mellitus (CFRD)
 Liver and bile duct abnormalities
Cholecystolithiasis, cholestasis
Fatty metamorphosis of the liver, eventually progressing to liver cirrhosis
Biliary cirrhosis with portal hypertension
 Intestinal obstruction: abdominal distention, pain, and a palpable mass
 Rectal prolapse (rare
Resp  Respiratory symptoms are common in adulthood.
 Obstructive lung disease with bronchiectasis
 Chronic sinusitis; nasal polyps may eventually develop
 Recurrent or chronic productive cough and pulmonary infections with characteristic
microorganisms
S. aureus is the most common cause of recurrent pulmonary infection in infancy and
childhood.
P. aeruginosa is the most common cause of recurrent pulmonary infections in adulthood.
Dangerous bacteria (especially Pseudomonas aeruginosa) are easily transmitted to patients
with CF → rapid decline in pulmonary function and increased risk of death (multiple
antibiotic courses in their lifetime → high resistance to commonly used antibiotics!)
Expiratory wheezing (obstruction), barrel chest , moist rales (indicate pneumonia),
hyperresonance to percussion
Signs of chronic respiratory insufficiency: digital clubbing associated with chronic hypoxia
 Airway hyperreactivity (e.g., wheezing)
Sweat gland  Especially salty-tasting sweat → electrolyte wasting
 Hyperhidrosis does not occur.
MSK  Frequent fractures because of osteopenia
 Kyphoscoliosis
Urogenital  Urinary
Nephrolithiasis, nephrocalcinosis
Frequent urinary tract infections
 Genital
Delayed secondary sexual development in both sexes
Male Female
Obstructive azoospermia is common. Viscous cervical mucus can obstruct
The vas deferens may also be absent. fertilization.
Undescended testicle Menstrual abnormalities (e.g., amenorrhea

46. Cystic fibrosis dx

 Diagnostic criteria
 Typical clinical manifestations of CF: chronic sinopulmonary disease,
gastrointestinal and nutritional irregularities, syndromes of salt loss, obstructive
azoospermia
 AND evidence of CFTR dysfunction
 Sweat chloride ≥ 60 mmol/L on two occasions
 OR CFTR gene mutation
 OR abnormal nasal potential difference test
 Supportive test
 Other blood tests
  Contraction alkalosis and hypokalemia may occur (due to excessive loss
of H2O and NaCl via the sweat glands and renal H+/K+ wasting)
 Stool: ↓ chymotrypsin and pancreatic elastase
 Chest x-ray/CT: hyperinflation
 Pulmonary function tests: ↓ FEV1:FVC ratio and ↑ residual volume (RV)
and total lung capacity (TLC) ratio
 Findings are consistent with an obstructive ventilatory disorder; see
spirometry.
 Ultrasound: increased liver echogenicity (fatty liver)

47. Cystic fibrosis mx – symptomatic

Resp  Physio : postural change, forced expiratory technique

 Antibiotics : acute infection prophylaxis
 Mucolytics :DNAs
 Bronchodilators
 Vaccine : flu, pneumonia
GI  Pancreatic enzyme replacement
 ADEK supplement
 Insulin
 Ursodeoxycholic acid for impaired hepatic function : stimulates bile secretion
 Additional sodium chloride intake
 High-energy diet to compensate for increased demand
Advanced  Diuretics (cor pulmonale)
lung  NIV
disease  Heart / lung tx
 LTOT
Others  Rx for complications : eg DM
 Fertility, genetic counselling
 DEXA osteoporosis screen
Preventive  Annual influenza vaccine for all CF patients > 6 months with inactivated influenza vaccine (IIV)
measures  Pneumococcal vaccine (see the immunization schedule)
 Palivizumab: antibody against respiratory syncytial virus (RSV) for infants < 24 months
 Long-term treatment with azithromycin may be used to prevent recurrent pulmonary infection

48. Chest wall disease

49. Obesity hypoventilation (Pickwickian syndrome)
 Defined as combination of obesity (BMI > 30), hypoxemia during sleep and
hypercapnia during the day resulting from hypoventilation
 It is a form of sleep disordered breathing
 Many suffer obstructive sleep apnea; resulting in many partial awakening during the
night which leads to continual sleepiness in the day
 The disease put strain on the heart, which eventually may lead to symptoms such
as heart failure, leg swelling and various related symptoms
 The most effective treatment is weight loss, but it is often possible to relieve the
symptoms by nocturnal ventilation with positive airway pressure (CPAP) or related
method
 Presentation
 Concurrent obstructive sleep apnea
  Snoring
 Episodes of apnea (cessation of breathing)
 Interrupted sleep
 Excessive daytime sleepiness
 Depression
 Hypertension difficult to be managed with medication
 Headache; which tend to be worse in the morning
 Low oxygen level  physiologic constriction of pulmonoray arteries to
correct ventilation – perfusion mechanism  excessive strain on right side of
heat  right HF (cor pulmonale)
 Heart has difficulty to pump blood through the lungs
 Fluid may accumulate in skin of legs in form of edema and in abdominal
cavity ; ascites
 Decreased exercise tolerance and exertional chest pain may occur
 Raised JVP
 Palpable parasternal heave
 Heart murmur due to blood leaking through tricuspid valve
 Hepatomegaly

 Dx
 BMI > 30
 Arterial carbon dioxide > 45mmHg / 6.0 kPa
 No alternative explaination for hypoventilation; such as narcotics,severe
obstructive or interstitial lung disease, severe chest wall disorders such as
kyphoscoliosis, severe hypothyroidism, neuromuscular or congenital central
hypoventilation syndrome

50. Neuromuscular disease

51. Lung fibrosis
 Interstitial diseases (ILDs) are a heterogeneous group of disorders marked by
inflammatory changes in the alveoli.
 ILDs may be idiopathic or due to secondary causes such as autoimmune disease,
pharmacotherapeutic changes, or exposure to toxic substances.
 These changes can cause irreversible fibrosis and impaired pulmonary function.

52. Lung fibrosis pathological subtypes and causes

Idiopathic  Most common

pulmonary  Risk factors : smoking, environmental or occupational exposures, chronic aspiration, genetic
fibrosis predisposition
Other  Desquamative interstitial pneumonia (DIP)
idiopathic  Nonspecific interstitial pneumonia (NSIP)
subtypes  Cryptogenic organizing pneumonia (COP)
 Acute interstitial pneumonia (AIP)
Occupational,  Pneumoconioses
environmental, Asbestosis
iatrogenic Silicosis
causes Rare pneumoconioses (e.g., berylliosis, anthracosis)
 Radiation pneumonitis
  Pharmacologic
Chemotherapeutic agents: bleomycin , methotrexate, busulfan
Other agents: amiodarone , nitrofurantoin, phenytoin, penicillamine, cocaine, and heroin
 Secondary to underlying disease
Granulomatous ILD:
 Sarcoidosis: noncaseating granulomas in multiple organs, including the lung
 Pulmonary Langerhans cell histiocytosis
 Granulomatosis with polyangiitis (formerly Wegener granulomatosis)
 Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome)
Infectious diseases (eg, tuberculosis, legionellosis)
Alveolar filling disease
Hypersensitivity reactions
Connective tissue disorders
Bronchoalveolar carcinoma

53. Lung fibrosis upper vs lower

54. Lung fibrosis presentation

 Exertional dyspnea that progresses to dyspnea at rest
 Persistent nonproductive cough
 Fatigue
 Other symptoms related to underlying primary disorder (eg, joint pain in connective
tissue disorder)
 Later stages of disease: digital clubbing due to chronic hypoxia
 IPF: The majority of patients (> 70%) do not respond to therapy and experience
progressive respiratory failure

55. Lung fibrosis dx

Auscultation  Bibasilar, inspiratory crackles or rales

 In advanced pulmonary fibrosis: loud inspiratory squeaks
 Signs of restriction: diaphragmatic elevation; sudden cessation of breathing on deep inhalation
PFT  Restrictive lung disease (e.g., low lung volumes, high/normal FEV1/FVC ratio)
 Decreased diffusing capacity for CO (DLCO) → highly sensitive parameter
CXR  Normal in approximately 10% of patients.
  Increase in reticular opacities (sign of fibrosis)
 Ground-glass opacities and honeycombing
CT / HRCT  Irregular thickening of the interlobular septa, honeycombing, and bronchiectasis
Biopsy  Indications: atypical or rapidly progressive symptoms
 In patients with minimal signs or symptoms and stable disease, close observation (e.g., PFTs,
HR-CTs over several months) may be sufficient.
Lab  Arterial blood samples show: elevated alveolar-arterial partial pressure of oxygen gradient,
decreased partial pressure of oxygen
 Screen for rheumatic and autoimmune diseases.

Increased reticular markings in middle lung field bilaterally

Dx : idiopathic pulmonary fibrosis

Irregular thickening of interlobular septa

Honeycombing
Accentuation of the peripheral / basal sections
Dx : idiopathic pulmonary fibrosis

56. Lung fibrosis treatment

 In secondary disease, the first step is tolimit exposure to the toxic substance, cease
therapy with the drug causing symptoms, or treat the underlying disease.
 Antibiotics if bacterial interstitial pneumonia is suspected
 Corticosteroids and immune modulators
 Oxygen for symptomatic or end-stage ILD
 Pulmonary rehabilition
 Physical exercise to improve endurance
 Breathing technique that improves lung efficiency
 Nutritional counselling
 Counselling and support
 Education about condition
  Lung transplantation in end-stage ILD
 Pirfenidone is a commonly used medication for ILD – slow progression

57. Lung fibrosis complications

 Pulmonary hypertension
 Right – sided heart failure
 Respiratory failure
 Lung cancer
 Lung complications ; blood clot in lung, collapsed lung or lung infection

58. Pneumoconioses
 An occupational lung disease and restriction lung disease caused by inhalation
of dusts, often in mines and agricultural
 Types

Types Details
Coalworker’s pneumoconiosis / - Leads to progressive massive fibrosis
miner’s lung - Presents as progressive dyspnea and chronic bronchiolitis
- CXR : upper zone fibrotic mass
Silicosis - Quarrying, sand blasting
- Upper zone reticular shadowing and egg shell calcification of hilar nodes 
progressive massive fibrosis
Asbestosis - Demolition and ship building
- Basal fibrosis, pelural plaques
- Increase risk of mesothelioma
 Chest pain, weight loss, clubbing, recurrent effusion, dyspnea
 CXR : pleural effusion, thickening
 Diagnosis by histology of pleural biopsy
 < 2 years survival

59. Extrinsic allergy alveolitis / hypersensitivity pneumonitis

 An inflammation of alveoli within the lung caused by hypersensitivity to inhaled
organic dust
 Acute allergen exposure in sensitized pt  T3HS
 Chronic exposure  granuloma formation and obliterative bronchiolitis (T4HS)
 Causes
 Bird fancier’s lung : protein in bird droppings
 Farmer;s / mushroom worker’s lungs
 Malt worker’s lung : Aspergillus clavatus
 Clinical features

2 – 6 h post exposure Chronic

 Fever, rigor, malaise  Increasing dyspnoea
 Dry cough, dyspnea  Weight loss
 Crackles (no wheeze)  Type 1 respiratory failure
 Cor pulmonale

 Investigations
Blood  Acute : neutrophilia, inceased ESR
 Positive se precipitants
CXR  Upper zone reticulonodular opacification or fibrosis  honeycomb lung
 BHL (rare)
Spirometry  Restrictive effect
 Decrease transfer factor during acute attacks
BAL  Increase lymphocytes and mast cells

 Mx
 Avoid exposure
 Steroid : acute / long term
 Compensation maybe payable
60. Sarcoidosis
 Sarcoidosis is a rare multisystem granulomatous disorder of unknown aetiology.
 It is thought to have a prevalence of around 1-2 per 10,000 though it more commonly
affects blacks who also tend to suffer from more severe disease. The condition
typically affects those aged between 20 and 50.
 The aetiology, though poorly understood, is thought to involve immune dysfunction
and T-cell overactivity. It most frequently affects the lungs causing a form of
interstitial lung disease.
 The condition features noncaseating granulomas, which may be defined as a
collection of epithelioid histiocytes that develops in response to a persistent stimulus.

61. Pulmonary sarcoidosis

 The lungs are affected in 90% of patients, though signs and symptoms may be absent
or subtle.
 Sarcoidosis causes an overactive cellular immune response. Advanced pulmonary
sarcoidosis involves the development of fibrosis causing thickening of the pulmonary
interstitium. Bilateral hilar lymphadenopathy is the hallmark finding on chest
radiograph.
 The main symptom (if indeed symptoms are present) is progressive breathlessness.
 If fibrosis develops a number of signs may be identified on examination:
 Fine inspiratory crackles
 Exertional desaturations
 Clubbing
 Additionally pulmonary disease may lead to a number of complications:
 Pulmonary artery hypertension
 Cor pulmonale

62. Other sarcoidosis manifestations

 Ocular sarcoidosis
 The eyes are affected in around 30-60% of cases most commonly in the form
of uveitis.
 Cutaneous sarcoidosis
 Skin manifestations are seen in around 25% of patients with sarcoidosis
 Papular sarcoidosis: multiple papules develop, generally on the head and neck
or areas of trauma.
  Erythema nodosum: a panniculitis (a condition with inflammation of
subcutaneous adipose tissue) characterised by red, painful nodules.
 Lupus pernio: a violaceous, nodular rash distributed over the nose and cheeks.
It is pathognomonic but rare.
 Hypercalcaemia is seen in around 15% of cases. This occurs due extra-renal
synthesis of calcitriol causing 1-α hydroxylation of 25-hydroxyvitamin D and so
increased levels activated vitamin D. This leads to increased levels of calcium.
 Renal disease may occur but is rarely clinically relevant. Significant renal disease
sometimes occurs secondary to hypercalcaemia which may cause nephrocalcinosis.
Granuloma formation can lead to interstitial nephritis but this is rarely of
significance.
 CNS disease is rare but may be severe. Arthralgia and bone cysts (particularly in the
digits) and hepatosplenomegaly may be seen. Cardiac involvement is rare, it
can present with arrhythmias, cardiomyopathy and heart failure.
 Heerfordt's syndrome, also termed uveoparotid fever, is a variant of sarcoidosis
characterised by uveitis, parotid swelling, fever and facial nerve palsy.
 Löfgren's syndrome is an acute variant of sarcoidosis characterised by bilateral hilar
lymphadenopathy, erythema nodosum, arthralgia and fever

63. Sarcoidosis – Spirometry

 In cases of pulmonary sarcoidosis with pulmonary infiltrates and fibrosis a restrictive
lung disease pattern is seen.
 FVC: reduced.
 FEV1: reduced.
 FEV1/FVC: > 80%.

64. Sarcoidosis investigations

Bedside  Observations
 Mantoux test - to rule out TB, another granulomatous disease that may cause erythema nodosum.
Blood  Full blood count (FBC)
 Urea & electrolytes (U&Es)
 ESR/PV
 Bone profile:
 Hypercalcaemia is seen in around 15%.
 Serum ACE:
Raised in around 70%, levels show a response to treatment. However, it is not accurate enough to
be used diagnostically and has limited prognostic value.

Imaging  A chest x-ray may reveal bilateral hilar lymphadenopathy and reticular opacities.
 Depending on disease progression high-resolution CT may demonstrate:
Lymphadenopathy
Diffuse nodularity
Ground glass opacification
Fibrosis typically affecting the upper lobes
Special  Brochoalveolar lavage ± transbronchial biopsy:
Inversion of CD4/CD8 ratio
Raised lymphocytes
 Biopsy demonstrating non-caseating granuloma

65. Sarcoidosis staging

 Pulmonary sarcoidosis may be staged based upon chest radiograph findings

66. Sarcoidosis mx
 Mild disease may not require treatment, steroids are used in advanced and
symptomatic disease.
 Pulmonary
 Sarcoidosis requires specialist management.
 Algorithm is based on BTS Interstitial lung disease guideline (August 2008).
 The dose of prednisolone is typically between 20-40mg a day.
 Steroids are generally continued for 4-6 weeks. At this time, CXR and lung
function tests may be repeated. If improvement is seen the dose may be tapered,
if not they are continued with reassessment.

 Extra – pulmonary
 Eye involvement, hypercalcaemia and other extrapulmonary involvement are
indications for steroids.
 Severe or persistent erythema nodosum is an indication for a short course of
steroids.

67. Pneumonia vs bronchitis

 Bronchitis affects the bronchial tubes that carry air to your lungs.
 Pneumonia affects the air sacs, called alveoli, where oxygen passes into your blood.
Pneumonia causes these air sacs to fill with fluid or pus

68. Pneumonia causes

69. Pneumonia classification
 Pneumonia may be divided into groups based on the location it was contracted,
comorbidities and the immune status of the patient. This helps to identify the likely
causative organism and guide management
  Anatomical

Bronchopneumonia Lobar pneumonia

 Patchy consolidation of different lobes  Fibrosuppuratuve consolidation of single lobe
 Extermities in age  Diffuse
 Secondary in sick  Congestion  red  grey  resolution
 Both genders  Middle age : 20 – 50
 Staph, Strep, H. Influenza  Primary in healthy adults
 Not limited to anatomical boundaries  Male more common
 Usually bilateral crackles  Limited by anatomical boundaries
 Usually unilateral
 Bronchial breathing

 Aetiological

Class Details Organisms

Community –  Typical
acquired These tend to present with
features 'typical' of
pneumonia; a productive cough,
fever and pleuritic chest pain
 Atypical
These tend to have a
more insidious, subacute onset.
They often present with a
combination of pulmonary and
extrapulmonary
symptoms. Likely infecting
organisms may be divided into
nonzoonotic and zoonotic causes
Hospital –  > 48 h after admission
acquired  2 weeks of discharge
Aspiration  Increase risk of : stroke, bulbar palsy,
decreased GCS, GORD, achalasia
 Primary swallow problems, reflux,
vomiting
 Oesophageal dysmotility
 Gastronnostomy feeding
Immunocompromised  Get sick quickly
/ opportunistic  Post chemo
 DMARSs
 Haem malignancy
 HIV
 At risk of infective organisms not
usually seen in other patient groups.
 Streptococcus pneumoniae (most
commonly)
 S. Aureus, Mycoplasma, Haemophilus,
Moraxella catarrhalis.
 Virus (15%)
 Nonzoonotic: Mycoplasma pneumoniae,
Legionella pneumophila, Chlamydophila
pneumoniae
 Zoonotic: Chlamydophila
psittaci (psittacosis), Coxiella burnetii (Q
fever), Francisella tularensis (tularemia).
 Gram negative enterobacteriae
Pseudomonas aeruginosa),
Staphylococcus aureus, Legionella
pneumophila.
 S. Aureus
 Streptococcus pneumoniae,
Staphylococcus aureus, Haemophilus
influenzae, and Enterobacteriaceae, in the
hospital Gram-negative bacilli (e.g.
Pseudomonas aeruginosa)
 The usual suspects + PCP, TB, fungi,
CMV/HSV
 Bacterial pathogens: as discussed as well as
the mycobacterium complex and non-
tuberculosis mycobacterium.
 Fungal pathogens: such as Pneumocystis
jirovecii, Aspergillus fumigatus and
Cryptococcus neoformans.
  Viral pathogens: such as varicella zoster
virus and cytomegalovirus should be
considered.
 Parasitic pathogens: parasitic pneumonias
are very rare and seen almost exclusively
in the immunocompromised.

70. Pneumonia presentation

 Pneumonia is often characterised by cough, SOB, and the signs of consolidation. In
atypical pneumonias extrapulmonary features may predominate.

Symptoms Signs
 Fever  Dull percussion note
 Malaise  Reduced breath sounds
 Cough  Bronchial breathing (transmission of bronchial sounds to peripheries due to consolidation)
(purulent  Coarse crepitations
sputum)  Increased vocal fremitus (increased transmission of ’99' through consolidated lung)
 Dyspnoea  Tachycardia
 Pleuritic pain  Hypotension
 Confusion
 Cyanosis

71. Pneumonia complications

Respiratory  Type 1 : PaO2<8kPa + PaCO2 < 6kPa

failure  Type 2 : PaO2<8kPa + PaCO2 > 6kPa
 Management : Oxygen therapy, ventilation
Hypotension  Cause : dehydration + septic vasodilation
 Management
SBP < 90 : 250 ml fluid challenge over 15 min
No improvement : central line + IV fluid
If refractory : ITU for inotropes
Atrial  Usually resolves with prescription
fibrillation  Management : Digoxin / beta blocker for rate control
Pleural  Exudate
effusion  Management : tap, send for microscopy & culture, cytology, chem
Empyema  Pus in pleura cavity
 Anaerobes, staph, gram negative
 Associated with recurrent aspiration
 Patient with resolving pneumonia develops recurrent fever
 Tap : turbid (cloudy), pH < 7.2, decreased glucose, increased lactate dehydrogenase
 Management : US guided chest drain, Abx
Lung  Causes
abscess Aspiration
Bronchial obstruction : tumor, foreign body
Septic emboli : sepsis, IVDU, RH, endocarditis
Pulmonary infarct
Subphrenic / hepatic abscess
  Features
Swinging fever
Cough, foul purulent sputum, haemoptysis
Malaise, weight loss
Pleuritic pain
Clubbing
Empyema
 Test
Blood : FBC, ESR, CRP, culture
Sputum : micro, culture, cytology
CXR : cavity with fluid level
CT, bronchoscopy
 Management
Abx according to sensitivities
Aspiration
Surgical excision
Others  Sepsis
 Pericarditis / myocarditis
 Jaundice
Usually cholestatic

72. Pneumonia investigations and diagnosis

 Investigations should not delay antibiotic treatment which should be administered
within 4 hours of admission or diagnosis.

Bedside  Observations
 Sputum sample
 Urinary sample
 ECG
Blood  Full blood count (FBC)
 Urea & electrolytes (U&Es)
 CRP
 Blood culture
 Sputum culture
Imaging  Chest x-ray: often diagnostic showing consolidation though findings may lag behind onset and
remain following resolution. May also show parapneumonic effusions, pneumothorax, abscess and
empyema.

73. Pneumonia severity

 CURB 65 for CAP
 74. Pneumonia mx
 ABC approach
 Oxygen titrated to saturations: Aim for saturation of 94-98% in patients without
underlying lung disease. In patients at risk of type II respiratory failure (e.g. COPD)
aim for saturations of 88-92%.
 IV fluids: patients may be dehydrated, correct any deficit and prescribe maintenance
fluids as appropriate.
 Appropriate analgesia: NSAIDs and paracetamol may be sufficient. In cases of more
severe painconsider opiate analgesics. Care should be taken due to respiratory
depressant effects.
 Antibiotics
 CAP

Infection 1st line Penicillin allergy : Penicillin allergy : Comment

delayed onset / not immediate / severe
severe
Mild CURB  Amoxicillin PO 1 g/ 8h  Doxycycline PO 200 mg day one, then 100  Duration 5
65 – score 0 –  In younger patient g every 24 h days (provided
1 Add atypical cover  Avoid in pregnancy, breast feeding afebrile and
with Clarithromycin clinically
PO 500 mg / 12 h stable for 48 h)
Moderate  Amoxicillin PO/IV 1 g/  Levofloxacin PO (IV if NPO) 500 mg / 12  Otherwise 7
CURB 65 – 8h h days
score 2 +  Avoid in pregnancy, breast feeding
Clarithromycin PO (IV if Caution if risk for QT prolongation
NPO 500 mg/12 h)
Severe – score  Co – amoxiclav !V 1.2 g /  Ceftriaxone IV  Levofloxacin PO (IV  Duration : 7
3 8h 2 g / 24 h if NPO) 500 mg / 12 h days
+ + +  May need to
Clarithromycin PO Clarithromycin Consider adding extend to 14 –
(IV if NPO 500 mg/12 h) PO Vancomycin infusion 21 days based
(IV if NPO if risk for S.Aureus on clinical
500 mg/12 h) judgement

 HAP
 Should be treated as hospital – acquired if onset from 5 days after hospital
admission or within 14 days of discharge
Infection 1st line Penicillin allergy Comment
Moderate  Piperacillin / Tazobactam IV 4.5 g /  Vancomycin IV infusion  Duration : 7 days
8h +  May need to extend to 14
Severe  Piperacillin / Tazobactam IV 4.5 g / Ciprofloxacin !V 400 mg / – 21 days based on
8h 12 h clinical judgemen
+  If possible aspiration
Vancomycin IV infusion +
 If haemodynamically unstable Metronidazole IV 500 mg /
+ Gentamicin IV 8h
 If haemodynamically
unstable
+ Gentamicin IV

75. TB

 Primary TB: the initial infection, often subclinical, suppressed in the majority of
individuals.
 Primary-progressive TB: primary infection is not suppressed, almost always
pulmonary in nature.
 Latent TB: the outcome in the majority of patients with Primary TB. Non-infectious
state.
 Post-primary TB: also termed reactivation TB. It occurs in patients with latent TB,
frequently due to immunocompromise (e.g. AIDs). May be pulmonary (55%) or extra-
pulmonary (45%)
 Natural history
 Inhaled bacilli find their way into alveoli, here they begin dividing. This initial
infection is termed primary TB. Once a critical mass is reached a host immune
response is elicited. The highly antigenic mycobacterium produces a strong
immune response. Alveolar macrophages phagocytose bacilli which continue to
proliferate.
 The Ghon complex, a pathognomonic lesion most commonly seen in children,
may develop. The complex has three components:
 Ghon focus (a small caseating granuloma)
 Lymphadenitis
 Lymphangitis
 After 2-10 weeks a sufficient cell-mediated response halts the proliferation of the
bacilli in the majority of individuals. These patients develop latent TB. They may
 have a Ranke complex - a healed Ghon’s complex. Patients with latent TB may go
on to develop reactivation with post-primary TB.
 A small proportion of patients (around 5%) will develop primary-progressive TB, this
is almost always pulmonary in nature. Primary-progressive TB has a number of
manifestations:
 Miliary TB (haematogenous spread of TB)
 Primary caseous pneumonia
 Tuberculous bronchopneumonia

76. TB presentation
 General signs : fever, chills, night sweat, appetite loss, weight loss, fatigue, significant
nail clubbin
 Active TB is frequently asymptomatic, when symptomatic fever, weight loss and
cough are most commonly seen.
 Active TB may be primary-progressive or post-primary TB.
 The features of TB are dependent on the organ system involved with the lungs most
frequently affected.
 Post-primary TB may be pulmonary (55%) or extra-pulmonary (45%).
 Primary-progressive disease almost always manifests itself with pulmonary disease.

77. Types of TB

Pulmonary  Pulmonary TB is the most common clinical manifestation of TB.

 It may be asymptomatic or present with the classic triad of:
Cough, Fever , Weight loss
 Shortness of breath and haemoptysis can also be present. Additional symptoms may be
seen with laryngeal and pleural involvement.
 Chest radiograph may demonstrate consolidation, cavitation (upper lobe) and effusion.
Lymph node  The lymph nodes are the most common extra-pulmonary site. Nodes are typically described
as: Enlarged, Firm, Non-tender
 It most commonly affects cervical and supraclavicular nodes. In chronic cases, suppuration
and formation of a sinus tract can occur.
Miliary  Miliary TB is the disseminated haematogenous spread of the bacilli.
 The term miliary comes from the characteristic chest radiograph finding - the appearance
of millet seeds throughout the lung fields.
 CNS TB is present in 20%. Multiple organ failure and organomegaly may develop.
 Occurs following hematogenous dissemination; goes everywhere – lung ,bone etc
 Signs maybe non – specific / over – whelming
 CXR : nodular opacities; military TB is characterized by widespread dissemination of
mycobacterium into human body and by the tiny size of lesion; 1 – 5mm
  Look for retinal TB too
 Biopsy of liver, lung, lymph node, marrow may held AFB /granuloma
CNS  CNS TB has numerous manifestations, the most common being TB meningitis.
 TB meningitis tends to present with fever, malaise and headache.
 In TB meningitis CSF sampling shows: High protein, Low glucose , Lymphocytosis.
Vertebral  TB affecting the spine is called Pott’s syndrome.
 Symptoms include: Fever , Weight loss, Back pain
 Neurological deficits are seen in 50% and the development of spinal deformities,
typically kyphosis, is common.
Adrenal  Tuberculosis is the leading cause of Addison’s disease worldwide.

78. TB investigation and diagnosis

 Latent : immunological testing.

Mantoux test  This is the first line test in the diagnosis of latent TB. It Involves an intradermal injection of
tuberculin, a purified protein derivative from M. tuberculosis.
 If a patient has had exposure to TB they exhibit a delayed (type IV)
hypersensitivity reaction. Diagnosis is based on the degree of the local epidermal reaction.
 Previous BCG vaccination affects results. Interpretation is somewhat variable and at times
the results inconclusive. The Mantoux test is also used prior to the administration of the
BCG vaccine.
Interferon  These assays detect the bodies cellular immune response to TB. It tests for the T-cell
gamma release interferon gamma response to M. tuberculosis antigens.
assay  Its indications are complex, typically used after a positive Mantoux.
 It is unaffected by previous BCG and non-tuberculous mycobacterium (NTM).

 Active : microbial tests & imaging

Stains and  Three early morning sputum samples are taken on consecutive days. These are sent for acid-
Cultures fast bacilli (AFB) smear and culture.
 The smear is stained with auramine O which has largely replaced Ziehl-Neelsen staining. A
negative smear result does not exclude TB. Around 30% of positive cultures will have
negative staining.
 Culture, utilising a medium such as Lowenstein-Jensen, is a highly specific test. However, it
does take 4-6 weeks to get results.
PCR  DNA PCR is a nucleic acid amplification technique. It allows for rapid and accurate testing.
 It is an expensive test and is not currently part of NICE recommend investigations for
standard practice

Imaging &  When active pulmonary TB is suspected we obtain a chest radiograph and CT to look for
biopsies effusion, cavitation, infiltrates and lymphadenopathy.
 When active extrapulmonary TB is suspected we must rule out pulmonary disease with
a chest radiograph and CT. Imaging of suspected affected area should be
obtained. Consider biopsy if applicable e.g. lymph node.
 In miliary TB consider the need for a lumbar puncture and CT/MRI head.

79. TB mx
 Well : home
 Unwell / MDR – TB : isolate / negative pressure, but cant force treatment
  If histological and clinical picture consistent with TB, Rx before culture result and
continue even with negative result
 Contact tracing, public health notification is essential
 DOT : vulnerable pt, no fixed abode, addicts
 Prednisolone : TB meningitis, appetite, serosits, genitourinary
 Pyridozine 10 mg od while on isoniazie
 Pulmonary : 6 m
 Cavitatory TB still sputum culture + at 2/12 : 9 months
 TB meningitis : 1 y treatment
 Monitor
 Review monthly
 If ALT / AST increase > 5 than baseline; stop drugs.If less, monitor 1 – 2 weeks
 CXR monthly
 Antibiotics

Before Rx  Stress on compliance

 Test colour vision and acuity before and during treatment; Ethambutol may cause reversible
ocular toxicity (baseline visual acuity)
 Check FBC, U&E, LFT
 If pre Rc creatinine clearance : 10 -50 mL/ min
Decrease rifampicin dose by 50%, Monitor U&E if ethambutol, No dose change for
ethionamide
Initial  8 weeks on 4 drugs ( depends on susceptibility)
phase  Daily adult dose ( >50kg)
Rifampicin (600mg), Isioniazid (300mg), Pyrazinamide (2g), Ethambutol (15mg/kg)
 Directly observed therapy (DOT) considered
Continued  16 weeks on 2 drugs
phase  Rifampicin, isoniazid on same dose
 Consider steroid if meningeal / pericardial TB

 Side effects
 Seek help in renal, hepatic failure, pregnancy

Rifampicin  Increase LFT ; small AST increase is ok but stop drug when there is increase in Bilirubin
 Decrease platelet
 Orange /red urine discolouration, tears and contact lens
 Inactivation of pill
 Flu symptoms
 Drug interactions : steroid, OCP, warfarin, anti – convulsants
Isoniazid  Increase LFT
 Decrease WCC
 Stop if neuropathy give pyrazinamide (50mg / 8h PO)
 Rash, hepatitis, flushing, gout
Ethambutol  Optic neuritis; colour vision is the first to deteriorate, rash
Pyrazinamide  Hepatic, arthralgia, rash
 CI : acute gout, porphyria

80. Latent TB mx / prophylaxis

  1 or 2 anti – TB drug for shorter period than symptomatic
 Rifampicin + isoniazide for 3 motnhs
 Isoniazide for 6 months

81. BCG
 BCG is a live attenuated vaccine. Its efficacy is dependent on a number of factors,
particularly age: it is more effective when administered at a younger age.
 It is also protective against leprosy (caused by a NTM) and is a treatment in bladder
cancer.

82. PE causes
 Usually arise from DVT from proximal leg or iliac veins
 Rarely
 Right ventricle post MI
 Septic emboli in right – sided endocarditis
 Pulmonary artery thrombosis (rare)
 Chest compression; dislodged from small bone marrow emboli
 Embolism
 Fat embolism; from fracture – Decreased platelets
 Air embolism
 Amniotic fluid embolism

83. PE risk factors

 Virchow’s triad
84. PE presentation
 Classic triad : SOB, pleuritic chest pain, haemoptysis

Signs Symptoms
 Fever  SOB / dyspnea
 Cyanosis  Pleuritic pain
 Tachycardia, tachypnea  Haemoptysis
 Pleural rub  Syncope / dizziness
 Elevated neck veins  Wheezing
 Loud P2
 R – sided gallop
 RV lift
 Cardiovascular collapse
 RHF : hypotension, rise JVP, loud P2
 Evidence of cause : DVT

85. PE differential
 86. PE investigation

Blood  FBC, U&E, clotting, D – dimer (byproduct of fibrin but no specific for PE)
 D – dimer
 ABG
Normal or hypoxaemia; decreased PaO2 and PaCO2, increased pH (PE leads to hypoxemia,
which leads to tachypnea, which leads to respiratory alkalosis)
Imaging  CXR
Usually normal
Oligemia/hypovolemia ( the Westermark sign is a sign that represents a focus of oligemia
leading to collapse of vessel seen distal to PE).While, CXR is normal in majority of PE cases,
the Westermark sign is seen in 2% of patients

Normal or small pleural effusion

May suggest alternative diagnosis
 CT pulmonary angiogram (CTPA) + venous phase of legs and pelvis
85 – 95% sensitivity

Other  Doppler US
Thigh and pelvis ( +ve in 60%)
 ECG
Sinus tachycardia (MOST COMMON), RBBB, right ventricular strain (inverted T in V1 –
V4)
S1 Q3 T3
P Pulmonale

87. Imaging studies

CT PA V/Q scanning Echo

- Good sensitivity and - Most likely to be dx in absence of
specificity especially cardiopulmonary disease
for detecting emboli in - A normal perfusion lung scan
the main, lobar or effectively riles out acute PE
segmental pulmonary - A scan suggesting high probability
arteries of acute PE should be considered
- The negative predictive dx, unless clinical suspicion is low
value of CTPA ~95% - However, if clinical story strongly
- Scan the thorax, pelvis suggests PE despite nondx VQ
- CT – RV dilation scan, futher dx should be pursued
further
- May reveal findings that strongly
support haaemodynamically significant
PE, offering the potential to guide
treatment
- Emboli moving through the lungs are
occasionally confirmed by this technique
- Deviation of interventricular spetum into
Left
- Right ventricular dilation
- Measure RV pressure w Doppler
- Screening & test for pulmonary HPTN
 88. PE diagnosis

 Assess probability using Wells score (pretest probability)

High probability Low probability

 Imaging test; CTPA  CTPA
Low  ok
High  CTPA
 89. PE mx

 Anti – coagulate with LMWH or standard unfractioned heparin (if want to use
fibrinolytics; its reversible) initiated unless CI
 Anticoagulation improve survival among pt with symptomatic PE
 Subcutaneous LMWH administered at least 3 – 5 days
 With standard heparin administration, the activated partial – thromboplastin time
should be measured at 6 h intervals until it is consistenly in therapeutic range (15 –
2.5 times control)
 Options for prolonged anticoag : Start warfarin / vitamin K anta / newer anti – coag
(NOAC) /LMWH
 Based on less bleeding w NOAC, and greater conveninece now NOAC preferred
than VKA for the initial and long term treatment of VTE in pt without cancer
 Stop Heparin when INR >2 and continue warfarin (min 3 months); aim INR 2 – 3
 Thrombolysis for massive PE
 Consider placement of vena cava filter in patient who develop emboli despite
adequate anticoagulation.Significant increased risk if placed without concomitant
anticoagulation
 ~ increase overall survival
 Duration of treatment usually 3 m
 Extended treatment
 If NB RF persists; eg cancer
 If unstable, start fibrinolytics
 If stable, go to LMWH,heparin, NOAC
 Stable, unstable is based on vital (BP); hypotension

90. LMWH

Advantages Caution
 Greater bioavailability  Morbidly obese (>150 kg) or very small (<40kg)
 More predictable dosing  Pregnancy
 Subcutaneous delivery (usually without the need  Severe renal insufficiency
for monitoring)
 Lower risk of heparin – induced  Monitor activity against activated factor X (anti – factor
thrombocytopenia Xa)

91. Large PE mx

 ABC
 Oxygen if hypoxic; 10 – 15L/min
 Morphine 5 – 10mg IV with anti – emetic if pain / very distressed
 If critically ill with massive PE (peri – arrest), consider immediate thrombolysis ( a
50 mg of alteplase)
 Iv access and start Heparin
 LMWH eg tinzaparin 175 U/kg/24h SC or
 Unfractioned heparin ~ 10,000 U IV bolus
 Then , 18u/kg/h IVI as guided by PTT
 Systolic BP
 <90
 Start rapid colloid infusion. Get ICU output
 If BP still low after 500ml colloid, dobutamine 2.5 – 10 microgram/kg/min IV
– aim SBP >90
 If BP still low, consider IV adrenaline infusion
 If SBP < 90 after 30 – 60 m of standard treatment, clinically definite PE, no
CI, consider thrombolysis unless already given
 >90
 Start warfarin loading regimen; eg 5 -10 mg PO
 Confirm diagnosis

92. Thrombolysis
 Indication : Proven PE with cardiogenic shock

Role in  Submassive PE
 Severe respiratory failure
 Massive clot burden
Complications  Bleeding
 Intracranial haemorrhage 1 – 3%
Contraindications  Intracranial, spinal or ocular surgery or disease
 Recent major surgery or other iinvasive procedures
 Active or recent major bleeding
 Pregnancy

93. Vasculitis
94. Pleural effusion classification

Exudate Transudate
 Involve an increase in capillary permeability and  Involve increased hydrostatic pressure or reduced
impaired pleural fluid resorption osmotic pressure in the microvascular circulation
 Effusion protein > 35g/L (commonly caused by organ failures)
 Causes  Effusion protein < 25g/L
Infection Parapneumonic  Causes
 TB
Empyema Failure LVF
Malignancy Liver failure
Rheumatological RA Nephrotic syndrome,
Connective tissue disease hypoalbuminaemia
(RA, SLE) Pulmonary PE
PE Can be transudate / exudate Atelectasis
Rare Post-MI, pancreatitis, Malignancy – 5 % transudate
meothelioma, sarcoidosis, Cardiac Constrictive pericarditis
asbestosis Others Hypothyroidism
Drug induced (methotrexate, Meig’s syndrome
amiodarone, bromocriptine,
phenytoin, nitrofurantoin)
Radiotherapy
Yellow-nail syndrome,
familial Mediterranean fever
Lymphangioleiomyomatosis

95. Light’s criteria

96. Pleural effusion presentation

 Clinical examination will usually pick up effusion >500ml
 SOB
 Cough
 Chest pain
 Reduced chest wall movement
 Mediastinal deviation away (if large)
 Stony dullness to percussion
 Decreased breath sounds
 Decreased Vocal resonance
 Bronchial breathing or aegophony (bleating vocal resonance) over top of effusion,
due to lung compression

97. Pleural effusion investigation

Blood  FBC, U&E, LFT, TFT, carcinoma, ESR

 Amylase, LDH, TFT
  RF and autoimmune profile
 ABG
Imaging  CXR : Sensitive to effusion >300ml (some places say 200)
 CT : Ideally scan before fluid removal as can improve images of pleural surfaces.
Others  USS
For assessing pleural effusion
For guiding aspiration
 Pleural tissue biopsy for histology and TB culture
 Aspiration
Must be USS guided
Percuss upper border and go 1 -2 ribs below
Infiltrate to pleura with ligocaine
Aspirate with 21G needle
Note appearance of fluid
 Sent for
 Biochem: protein, LDH, pH, glucose
 Cytology (at least 20ml sample)
 MCS and AFB
 pH
 Other: Amylase, cholesterol, RF and ANA

98. Aspiration
Differential cell
count (predominance of
white cells) (predominance
of white cells)
 Neutrophils – PTE, pancreatitis, pneumonia, empyema
 Lymphocytes – Cancer, TB pleuritis
 Eosinophila – Pneumothorax, haemothorax, asbestosis, Churg-Strauss
 Mononuclear cells – Chronic inflammatory process

Gram stain and culture  Use blood culture bottles and specimen jars – especially if chronic illness or
and cytology suspect TB or fungus
 Cytology useful in cases of suspected malignancy

Glucose (low)  Common: Infection (pneumonia) and malignancy

 Rare: TB, haemothorax, Churg-Strauss

LDH level (classically high  Repeated testing confirms continuation or cessation of process
in exudate) Increasing LDH (ongoing inflammation)
Decreasing LDH (cessation of process)

Pleural fluid pH  Low glucose and pH = infection or malignancy

Taken if suspect pneumonic or malignant process (Low glucose)
<7.20 with pneumonia…Drain the fluid
<7.20 with malignancy …Life expectancy 30 days

Amylase  Useful if suspect pancreatitis as cause

99. Empyema, carcinoma, RA, SLE features

  Increased protein
 Decreased glucose; <3.3 mM
 Decreased pH < 7.2
 Increased LDH >0.6* serum/ULN

100. Pleural effusion complications

 Respiratory failure
 Infection and empyema

101. Pleural effusion mx

 Treat the underlying cause : diuretics, antibiotics, immunosuppressants
 Aspiration (USS guided)
 Indications for chest drain:
 Empyema or parapneumonic effusion with purulent fluid or pH<7.2
 Malignant effusions which are candidates for pleurodesis
 Large effusions in acutely unwell patients
 Pleurodesis
 Medical or VATs

102. Procedure for Thoracocentesis

 Explain procedure to patient
 Obtain written consent
 Complications include pneumothorax, cough, bleeding, empyema, spleen or liver
puncture, malignant seeding (particularly in mesothelioma – my need prophylactic
radiotherapy to area later)
 Check clotting (INR <1.5)
 Must be done under USS Guidance (by a doctor trained in USS – see BTS
guidance)
 Aseptic technique
 Infiltrate site (skin, intercostals muscle and parietal pleura) with 10ml 1%
lidocaine.
 Aim above the upper border of the appropriate rib to avoid neurovascular bundle
that runs below each rib.
 For Diagnostic Thoracocentesis:
 Aspirate pleural fluid with a green (21G) needle and 50ml syringe
 If uncomplicated – no need for CXR post procedure
 For Therapeutic Thoracocentesis:
 Hospitals vary as to kit available
 Verify that insertion site is correct by aspirating fluid with a green (21G)
needle
 Advance a large bore cannula along the same track
 Remove needle and attach a 3 way tap
 Aspirate fluid with a 50ml syringe via the 3 way tap and flush the fluid out
into container through extension tubing connected to remaining port of 3 way
tap.
 Drain maximum of 1.5l in one go – risk of re-expansion pulmonary oedema
  Stop aspirating if any resistance felt or if patient experiences any discomfort
or severe coughing
 CXR post to document extent of improvement and to exclude pneumothorax
or trapped lung

103. Pneumothorax causes

 Spontaneous pneumothorax: spontaneously occurring pneumothorax
 Primary spontaneous pneumothorax: occurs in patients without clinically
apparent underlying lung disease
 Secondary spontaneous pneumothorax: pneumothorax occurs as a
complication of underlying lung disease
 Tension pneumothorax: life-threatening variant of pneumothorax characterized
by progressively increasing pressures within the chest and cardiorespiratory
compromise

Spontaneous Non - spontaneous
Primary (no underlying lung Secondary (with lung disease)
disease)

 Ruptured subpleural apical  Chronic lung disease : COPD,  Trauma

blebs asthma, CF, lung fibrosis, Penetrating
 Risk factors sarcoidosis Blunt ± rib fracture
Family history  Infection : TB, pneumonia  Iatrogenic
Male gender  Carcinoma Subclavian CVP line
Asthenic body habitus  Connective tissue disorder : insertion
(slim, tall stature) (e.g., in Marfan’s, Ehler’s Danlos (a group
Positive pressure ventilation
Marfan syndrome) of disorders that affect connective
tissues Transbronchial biopsy
Smoking Liver biopsy
 Pulmonary fibrosis, sarcoidosis
Homocystinuria

104. Pneumothorax pathophysiology

 Increased intrapleural pressure → alveolar collapse → decreased V/Q ratio and
increased right-to-left shunting
 Spontaneous pneumothorax: rupture of blebs and bullae → air moves into pleural
space with increasing positive pressure → ipsilateral lung is compressed and
collapses
 Traumatic pneumothorax
 Closed pneumothorax: air enters through a hole in the lung (e.g., following
blunt trauma)
 Open pneumothorax: air enters through a lesion in the chest wall (e.g.,
following penetrating trauma)
 Air enters the pleural space on inspiration and leaks to the exterior on
expiration
 Air shifts between the lungs
 Tension pneumothorax: disrupted visceral pleura, parietal pleura, or
tracheobronchial tree → air enters the pleural space on inspiration but cannot
exit → progressive accumulation of air in the pleural space and increasing
 positive pressure within the chest → collapse of ipsilateral lung and
compression of contralateral lung, trachea, heart, and superior vena cava →
impaired respiratory function, reduced venous return to the heart and
reduced cardiac output → hypoxia and hemodynamic instability

105. Pneumothorax classification

Closed  Break in lung parenchyma causing air to escape into pleural space
 The lung collapse and air builds up in the pleural space
 Pleura still intact and holding the air that leaked from the lungs
 Pleural cavity pressure < atmospheric pressure
 Trachea deviated toward pneumothorax
Open  Penetrating injury causes a break in parietal pleura
 Defect in chest wall allows communication between patient and exterior; maybe sucking
 Pleural cavity pressure = atmospheric pressure
 Trachea in neutral position
Tension  Break in parietal pleural exposing pleural space to inflow of air from the outside.The torn segment of
parietal pleura acts as a valve – like structure that allows air flow from outside into pleural space
during inspiration
 This valve structure does not let air exit the pleural space during expiration  mediastinal
compression
 Pleural cavity pressure >atmospheric pressure
 Trachea deviates away from pneumothorax

106. Pneumothorax presentation

 P-THORAX: Pleuritic pain, Tracheal deviation, Hyperresonance, Onset sudden,
Reduced breath sounds (and dyspnea), Absent fremitus, X-rays show collapse.

Symptoms Signs
 Sudden onset  Chest : decreased expansion, resonant percussion, decrease breath
 Dyspnea sounds, decreaee vocal resonance (increase over solid tissue)
 Pleuritic chest pain  Tension : increase JVP, mediastinal shift, increase HR, decrease BP
 Tension : respiratory distress,  Crepitus : surgical emphysema.seen in pt
cardiac arrest

107. Pneumothorax ix
 Suspected pneumothorax is confirmed by chest x-ray.
 Immediate x-ray or an extended focused assessment with sonography for trauma
(eFAST) in adults with severe respiratory compromise and children
 CT may provide detailed information about the underlying cause (e.g., bullae in
spontaneous pneumothorax).
 Tension pneumothorax is primarily a clinical diagnosis and prolonged diagnostic
studies should be avoided to initiate immediate treatment.
  CXR should not be performed if tension pneumothorax is suspected
(delay treatment), instead request an expiratory film and look for area devoid
of lungs marking, peripheral to the edge of collapsed lung
 In cases of tension pneumothorax, immediate decompression is a priority and
should not be delayed by imaging!
 Ensure the suspected pneumothorax is not a large emphysematous bulla
 Arterial blood gas analysis (ABG) to detect respiratory acidosis
 Chest x-ray (confirmatory test)
 Ideally in two projections (PA and lateral), in supine and upright position
 Ipsilateral pleural line with reduced/absent lung markings
 Sudden change in radiolucency
 Deep sulcus sign: dark and deep costophrenic angle on the affected side
 If pulmonary disease is present: airway or parenchymal lesions
 Additional features in tension pneumothorax:
 Ipsilateral diaphragmatic flattening/inversion and widened intercostal spaces
 Tracheal deviation towards the contralateral side
 CT: In stable adults without severe respiratory compromise and responsive to
resuscitation.
 Other indications:
 Presurgical workup
 Suspected underlying lung disease, to determine the likelihood of recurrent
disease
 Uncertain diagnosis despite chest x-ray
 ECG: for all patients with anterior chest trauma
 Reduced QRS amplitude in leads V2–V6 in left-sided pneumothorax
 Increased QRS amplitude in leads V5–V6 in right-sided pneumothorax
 ST elevation or depression

108. Pneumothorax mx

Simple  If small (≤ 2 to 3 cm between the lung and chest wall on a chest x-ray) and asymptomatic
Usually resolve spontaneously within a few days (∼ 10 days)
Supplemental oxygen (4-6 L/min) via nasal cannula or mask with reservoir
Serial follow-up with repeat CXR
 If small and symptomatic (but hemodynamically stable) or large (> 3 cm between
the lung and chest wall on chest x-ray) primary pneumothorax, iatrogenic, traumatic, or secondary
pneumothorax
Immediate supplemental oxygen (4-6 L/min) via nasal cannula or mask with reservoir
Upright positioning
Symptomatic treatment
Tube thoracostomy
Open  Simple partially occlusive dressings taped at 3 out of 4 sides of the lesion
 Followed by thoracostomy
 Observe for development of tension pneumothorax
Tension  Emergency chest decompression via chest tube placement if immediately available
 Otherwise perform emergency needle thoracostomy, followed by chest tube placement
Chest tube placement
  Bülau drain: 4th intercostal space (nipple line) in between anterior and median axillary
line (safe triangle; midaxillary line)
Needle thoracostomy
 Immediate insertion of a large-bore needle into the 2nd intercostal space along the
midclavicular line (followed by insertion of a chest tube)

109. Pneumothorax complications

 Complete pulmonary collapse → respiratory failure
 Tension pneumothorax → cardiac failure
 Mediastinal flutter in case of open pneumothorax → hemodynamic shock
 Hemothorax in cases of trauma
 Pneumomediastinum
 Pneumoperitoneum
 Recurrence
 Post-surgical/-procedural complications
 Persistent fistula with continuous air leak
 Injury to intercostal nerves and vessels
 Infection

110. Epidemiology of lung cancer including trends and mortality rates

 3rd most common cancer, 19% of all cancer,27% of cancer deaths (most common)
 Mainly occur in older population; more difficult to manage due to comorbidies
 Major cause : smoking, 2nd hand smoking, Radon, workplace exposure (asbestos,
arsenic, silica, open fires), diesel fumes, radiation therapy to chest, previous lung
cancer, air pollution
 80% present w advanced disease
 Stage 3b/4 disease
 Extensive stage SCLC
 84% NSCLC, 16% SCLC

111. Aetiology of lung cancer

 Smoking
 Cause of lung cancer in 80-90% of cases.
 The effects of smoking remain long after cessation. The relative risk remains
around two times that of a non-smoker at 30 years post cessation.
 Exposure
 Asbestos, a fibrous building material, is perhaps the best-known carcinogen aside
from tobacco. Though more strongly associated with mesothelioma, asbestos is
linked with adenocarcinoma of the lung. Tobacco and asbestos exposure act
synergistically increasing the risk of cancer multiple times.
 Radon gas, released from naturally occurring uranium, is a recognised cause of
lung cancer

112. Lung cancer risk factors

 Smoking
 Radiation therapy
 Environmental toxins
  Scar tissues in lung : pulmonary fibrosis, history of TB
 HIV infection
 Genetic factors
 Idiopathic : particularly adenocarcinoma

113. Major histological types with clinical correlation

 Lung cancer is classified into small cell lung cancer (SCLC) and non-small cell
lung cancer (NSCLC).
 SCLC is characterized by its central location, rapid tumor growth, early
metastases, and association with numerous paraneoplastic syndromes.
 NSCLC comprises a number of cancer types, including peripheral
adenocarcinoma and central squamous cell carcinoma.

Type Freq Location Characteristics

(%)
SCLC  Strongly correlates with smoking
~ 15 Central
 Pulmonary neuroendocrine tumours; associated with several
paraneoplastic syndromes
 Very aggressive; early metastases
 Associated with mutation : I – myc
NSCLC Adenocarcinoma ~ 40 Peripheral  Most common type of cancer overall and in women
 Most common lung cancer in non – smoker
 More often found peripherally – therefore present late
because they less likely to cause obstruction symptoms
 Arises from mucous cells in the bronchial epithelium
 Commonly invades the mediastinal lymph nodes and the
pleura, and spreads to the brain and bones
 Does not usually cavitate
 Can cause excessive mucous secretion
 Associated mutation : EGFR, ALK, KRAS
 Distant metastases = common
 May sometimes be confused with mesothelioma
 Most likely to cause pleural effusion (as are mesotheliomas)
 Non – invasive subtype : bronchioloalveolar carcinoma
These are very rare
It is a variation of adenocarcinoma
they account for 1-2% of all lung carcinoma
they will present as a single nodule, or many small nodular lesions
occasionally they cause production of huge amounts of mucous
(which will be coughed up as sputum)
may appear like consolidation on the CXR
Causes ‘bronchorrhoea’ – diarrhoea of the bronchus – produces huge
amounts of white sputum!

Squamous cell 20 – Central  Strong association with smoking

carcinoma 25 airways  Cavitary lesion = common
 Direct spread to hilar lymph noses
 Increased parathyroid – related protein  hyperCa
 By bone destruction / increased PTH
Large cell 5– Peripheral  Late metastases
carcinoma 10  Poor px

114. Lung cancer presentation

Pulmonary Extra – pulmonary

 Cough (chronic or  Constitutional symptoms (weight loss, fever, weakness)
recently developed)  Clubbing
 Hemoptysis  Signs or symptoms of tumor infiltration or compression of neighboring structures
 Progressive dyspnea SVC syndrome: Compression of the superior vena cava impairs the venous
 Chest pain backflow to the right atrium, resulting in venous congestion in the head, neck,
 Recurring common and upper extremities.
colds in patients ≥  Feeling of fullness in the head
40 years should  Dyspnea
always raise the  Edema of the upper extremities and face
suspicion  Prominent venous pattern on the chest, face, and upper extremities
of lung cancer!
Paralysis of the recurrent laryngeal nerve: hoarseness
Paralysis of the phrenic nerve: results in diaphragmatic elevation and dyspnea
Malignant pleural effusion: dullness on percussion, reduced breath sounds on the
affected side
Dysphagia
Postobstructive pneumonia

115. Paraneoplastic syndrome

 Paraneoplastic syndromes are rare disorders that are triggered by an altered
immune system response to a neoplasm.
 They are defined as clinical syndromes involving nonmetastatic systemic effects
that accompany malignant disease. ...
 Paraneoplastic syndromes may be the first or most prominent manifestation of a
cancer.

NSCLC SCLC
 General paraneoplastic manifestations: cachexia, increased risk of thrombosis (and lung embolism!)
 Dermatomyositis
 Acanthosis nigricans
 Endocrine  Endocrine
Hypercalcemia of malignancy (squamous cell carcinoma) Cushing syndrome
Gynecomastia (large cell carcinoma)
 Others
 Hypertrophic osteoarthropathy (also known as Pierre-Marie- Syndrome of inappropriate
Bamberger disease) antidiuretic hormone secretion
 Clubbing of the fingers and toes (Hippocratic fingers) (SIADH)
 Swelling and pain in joints and long bones  Neuro
Hypercoagulability and thrombophlebitis migrans Lambert-Eaton syndrome (similar
(adenocarcinoma) clinical features as myasthenia gravis)
Nonbacterial verrucous endocarditis (adenocarcinoma) Paraneoplastic cerebellar
degeneration
Peripheral neuropathy

116. Symptoms of metastatic disease

 Early lymphogenic and hematogenic metastasis (particularly in SCLC)
 Brain: headaches, behavioral changes, seizures, focal motoric deficits
 Liver: nausea, jaundice, ascites
 Adrenal gland: usually asymptomatic
 Bones: bone pain

117. Approach to diagnosing suspected lung cancer

Blood 
FBC – for detection of anaemia

LFT’s – to check for liver involvement

Coagulation

Biochemistry – hypercalcaemia, hyponatraemia

Increased Ca2+ – this will occur as a result of bone metastasis. May also be a result of secretion of
parathyroid hormone.
 Decreased sodium – this will occur as a result of adrenal involvement (Addisonianism).
Imaging  CXR
Symptomatic tumours will usually be visible on x-ray
Asymptomatic tumours can be seen on x-ray if they are greater than 1cm in diameter.
Lateral views may be useful to assess areas of the lung behind the heart and in the hilar region.
A small number of tumours are confined to central airways and not visible on x-ray because of
the heart. These tumours however will be seen on bronchoscopy and CT.
Coin lesion
 Coin lesion differential diagnosis
 Foreign body
 Abscess : Staph, TB, Klebsiella, mycetoma
 Neoplasia : primary / secondary
 Granuloma : RA, Wegener’s, TB, sarcoid
 Structural : AVM
Hilar enlargement
Consolidation
Collapse
Bony secondaries
 CT thorax
This is particularly useful for looking at disease in the mediastinum.
It can also detect masses that are too small to be seen on CXR (<1cm diameter)
A normal CT of nodes before surgery excludes the need for mediastinoscopy and node biopsy.
 Staging CT should include the liver, adrenals and brain to check for mets
A staging CT of the chest:
 Looks at the chin to the kidneys (so includes adrenals and liver)
 Must do one with contrast and without – contrast shows whether it is a lesion or just a blood
vessel.
This is only about 60% accurate for mets – it doesn’t always pick up nodes if they are less than
10mm
 PET CT
It is also useful for staging – where the f-deoxyglucose PET scan is employed.
No point in doing a PET if you don’t plan to operate! Basically it just tells you if it has spread –
thus if it is suitable for surgery.
You would normally do a staging CT first – if this is clear, then you use a PET to look for more
distant spread. If it all looks clear, then you can operate.
This is about 90% accurate for mets
On the PET results you look at the SUV value – the higher this is, the more likely the lesion is to
be metastatic spread (scale is about 1-9)

Others  Bronchoscopy
This is most useful to obtain cytology and biopsy. Tumours that involve the first 2cm on either
main bronchus are inoperable. You may also see:
 Widening of the angle of the carina – this suggests involvement of the mediastinal lymph
nodes; either due to metastasis or they may be reactive. You can biopsy them on bronchoscopy
by passing a needle through the bronchial wall.
 Cytology – this is the study of cells that are no longer in their natural environmental structure –
e.g. cell obtained from a bronchial washing. Histology is the study of both the cells, and the
natural structure in which they are found.
Only really useful for tumours in an area about 10cm square around the hilum:
 Percutaneous aspiration and biopsy – CT guided biopsy
This is useful for peripheral lesions that cannot be seen by bronchoscopy. It is done through the
chest wall and usually guided by x-ray or CT.
This is able to reach 75% of peripheral lesions that cannot be reached by bronchoscopy.
The chance of pneumothorax is very high (anywhere between 1-25% – thus the patient has to be fit
enough to survive one of these if you are going to do this on them. Twice as many patients will
require a chest drain as receive a pneumothorax)
Haemoptysis will also occur in about 5% of patients
This is useful if positive, but if negative is pretty useless (i.e. it could just means you missed the
part of the lesion you wanted)
 Other cytology
Sputum and pleural fluid – you need to make sure you send at least 20ml of each
Cytology is generally not very accurate – because there is a very high false negative rate.
 Mediastinoscopy

118. Approach to staging lung cancer

 The staging of NSCLC is based on the UICC TNM staging system.
  This classification defines four stages from I to IV, corresponding to cancer spread.
 As soon as distant metastases are detected, the cancer is classified
as UICC stage IV!
UICC stage TNM Description
Stage IA T1  Tumor size ≤ 7 cm
Stage IB T2a  No lymph node involvement beyond the ipsilateral hilar
Stage IIA T2b, N0 or T1, N1 nodes
Stage IIB T3, N0 or T2b, N1  No mediastinal invasion
 No metastases
Stage IIIA Up to T4. N1 or T3, N2  Tumor size > 7 cm
 Mediastinal lymph node involvement and/or regional spread
 No mediastinal invasion or metastases
Stage IIIB T4, N2 or N3  Mediastinal invasion
Stage IV M1  Distant metastases / node

 The SCLC staging mostly depends on whether the tumor is limited to one hemithorax or
has spread beyond the hemithorax. Alternatively, the TNM classification may be used.

Classification Cancer spread TNM Cancer stage ( % )

Very limited  Confined to 1 hemithorax  T1-2, N0-1  5
Limited  T3-4, N0-1 or  20
T1-4, N2-3
Extensive  Beyond 1 hemithorax  M1  75
Contralateral supraclavicular or hilar lymph node
involvement
Malignant pericardial or pleural effusion
Distant metastasis
 
119. Evaluation of solid tumour
 CXR – compare
 In patients aged > 40 years, any pulmonary nodule detected on CXR is
considered lung cancer unless proven otherwise!
 CT for further evaluation
 New lesion detected on chest x-ray
 Changes (e.g., enlargement) compared to previous chest x-ray
 No previous CXR is available
 Assessment of lesion size and probability of malignancy (based on CT findings and
patient characteristics)
 Increased probability of malignancy
 History of smoking
 Patient age > 40 years
 Other known risk factors (e.g., positive family history, asbestos exposure)

Solid lesion size (mm) Probability of malignancy Next step

<4 Low No follow-up needed
High Follow-up CT at 12 months
4–6 Low Follow-up CT at 12 months
High Follow-up CT at 6 – 12 months
6–8 Low Follow-up CT at 6 – 12 months
High Follow-up CT at 3 – 6
≥8 Low or high PET +/- bopsy
 120. Principles of treatment options for lung cancer
 While early stages of lung cancer are treated with a curative approach, the majority of
cases are diagnosed in advanced stages and can therefore only be treated palliatively.
 Surgery is often not possible due to distant metastases or because the patient has poor
pulmonary reserve.
 In such cases, chemotherapy is the mainstay of treatment; radiation therapy is also
frequently necessary.
 An individual treatment approach is usually determined by an interdisciplinary tumor
board and discussed with the patient.

Stage Treat Regimen

NSLC Stage I Curative  Surgical resection ± adjuvant chemotherapy (radiation therapy is only
and II required if the resection margins are not tumor free)
 If surgery is not possible: radiation therapy + polychemotherapy
Stage  Polychemotherapy + radiation therapy
IIIA  Consider surgery if tumor size decreases significantly after initial treatment
 Prophylactic cranial irradiation does not improve survival
Stage Palliative  Polychemotherapy ± targeted therapy
IIIB and  Alternative: symptom-oriented palliative support
IV  Radiation therapy may be considered for management of metastases and
complications (e.g., bone pain, brain metastasis, SVC syndrome)
Pancoast Curative  Neoadjuvant radiation therapy + polychemotherapy
tumour  Surgery
up to
 stage
IIIB
SCLC Limited Curative  Polychemotherapy + radiation therapy
disease  Usually unresectable; consider surgery in patients with very small,
(20%) resectable lesions
 Prophylactic cranial irradiation in patients who respond to initial
chemotherapy treatment
Extensive Palliative  Polychemotherapy
disease  Radiation therapy if the patient responds well to initial chemotherapy
(75%)  Prophylactic cranial irradiation if the patient responds to the initial
chemotherapy treatment

 Therapeutic option

Medical  Polychemotherapy (mainstay of treatment),

SCC: cisplatin and vinorelbine
SCLC: cisplatin and etoposide
 Targeted therapy
EGFR inhibitors (e.g., gefitinib) in advanced-stage NSCLC that is EGFR-positive
ALK tyrosine kinase inhibitors (e.g., crizotinib) in advanced-stage NSCLC that is ALK-
positive
 Management of concurrent symptoms/conditions (e.g., pain, electrolyte imbalances due to
paraneoplastic syndromes, dysphagia, cachexia, COPD)
Radiation  Includes prophylactic cranial irradiation
Surgical  Approx. 65% of lung cancer cases are inoperable at the time of diagnosis!
 Procedures: open surgery or video-assisted thoracoscopic surgery
Lobectomy (standard approach): resection of one lobe
 If FEV1 > 1.5 L and DLCO > 60%: lobectomy can be tolerated
Sublobar resection: wedge resection or segmentectomy for patients who cannot tolerate
lobectomy
 Advantages: lower perioperative mortality than lobectomy; preserved lung function
 Disadvantages: only possible for small, localized tumors
Pneumonectomy: complete lung resection in the case of a central tumor
Systematic lymph node dissection
 Complications
Displacement of the heart towards the operated side
Bronchial stump insufficiency
Severe complication of lung resection
Invariably leads to effusions; risk of pleural empyema
Pneumothorax (possibly tension pneumothorax)
Postoperative hemorrhage → hemothorax
Chylothorax (damage to the thoracic duct)
Atelectasis
Pneumonia
Acute cor pulmonale

121. Lung cancer prognosis

 Overall 5‑ year survival rate: approx. 17%
 SCLC
 Limited disease 5-year survival: 12–15%
 Extended disease 5-year survival: 2% (median survival 8–13 months)
 NSCLC: better prognosis, depends primarily on extent of disease and lymph node status
 Locally confined stages (no lymph node involvement, no metastasis) have a survival
rate of up to 60–70%.

122. OSA
 Obstructive sleep apnea (OSA): breathing-related sleep disorder in which airflow
significantly decreases or ceases because of upper airway obstruction (typically the
oropharynx)
 Apnea: respiratory arrests of ≥ 10 seconds
 Hypopnea: reduction of airflow by ≥ 50% for ≥ 10 seconds in combination with reduction
of blood oxygenation by ≥ 3% or EEG arousal

123. OSA causes and risk factors

 Obstruction of the upper airways due to the collapse of the pharyngeal muscles
during sleep
 Risk factors
 Obesity, especially around the neck (short, wide “bull neck”)
 Structural abnormalities that impair respiratory flow: tonsillar hyperplasia, nasal
septum deviation, previous upper airway surgery, enlarged uvula, tongue, or soft
palate, overbite with a small chin, hypertrophied pharyngeal muscles, nasal polyps
 Alcohol consumption before sleep
 Intake of sedatives and/or beta-blockers before sleep
 Smoking
 Family history
 Acromegaly
 Hypothyroidism

124. OSA pathophysiology

 Obstruction of the upper airways → apnea → ↓ partial pressure of oxygen in
arterial blood (PaO2), ↑ partial pressure of carbon dioxide in arterial blood
(PaCO2, also known as hypercapnia)
 → ↑ Hypoxic pulmonary vasoconstriction → ↑ pulmonary hypertension → cor
pulmonale
 → ↑ Sympathetic activity → secondary hypertension
 → Respiratory acidosis → renal compensation → increased HCO3 retention
and decreased chloride reabsorption

125. OSA presentation

 Restless sleep with waking, gasping, or choking
 Loud, irregular snoring with apneic episodes (third-party reports)
 Excessive daytime sleepiness (e.g., patient falls asleep, microsleep during
meetings or while watching TV)
 Impaired cognitive function (e.g., impaired concentration, memory loss)
 Depression, decreased libido
126. OSA diagnosis
 Initial assessment: standardized questionnaires and third-party reports (interview
sleeping partner regarding snoring and respiratory interruptions)
 Laboratory tests are not usually considered useful in the diagnosis of OSA, but
may help identify underlying conditions or physiological consequences of OSA.
 Polycythemia occurs because hypoxia induces erythropoietin secretion by the
kidneys, which stimulate the blood marrow, leading to increased RBC
production.
 TSH (thyroid-stimulating hormone) may be considered in patients with
possible hypothyroidism.
 Sleep studies
 Polysomnography
 Apnea and hypopnea events; cease on arousal
 Oxygen desaturation
 Arousal events on EEG
 ↑ Pulse pressure
 Bradycardia
 Fragmentation of sleep with pathological reduction of REM-sleep phases
and slow-wave sleep

127. OSA ddx

 Central sleep apnea
 Breathing-related sleep disorder characterized by repetitive cessation or
decrease of respiratory effort during sleep due to impaired function of the
respiratory center. Airway obstruction is absent.
 Etiology: idiopathic or caused by an underlying disorder
 Risk factors : age > 65 years, male sex , heart failure , central nervous system
disease (e.g., brainstem tumor, stroke)
 Pathophysiology: lack of stimulation to the respiratory center with patent upper
airways → periodic lack of respiratory muscle innervation → interruption of
thoracic and/or abdominal respiratory movements
 Clinical features
 Morning headaches
 Repeated waking at night
 Daytime sleepiness
 Snoring
 Association with OSA is very common
 Diagnosis
 Based on clinical history (e.g., underlying conditions such as heart failure
or stroke)
 Polysomnography
 Treatment
 Treat underlying disorder (if present)
 CPAP

 Obesity hypoventilation syndrome (Pickwickian syndrome)

128. OSA treatment
Mild –  Mild symptoms and < 20 apneic episodes
mod  Weight loss
 Reduce and/or avoid risk factors: alcohol, nicotine, sedatives (e.g., benzodiazepines)
 Sleep hygiene: regular and sufficient sleep
 Lateral as opposed to supine sleeping position
 Blood pressure control
 Oral appliances
Severe  > 20 apneic episodes and alterations in arterial oxygen saturation)
 Surgery (uvulopalatopharyngoplasty)
Resection of the uvula and redundant retrolingual, soft palate, and tonsillar tissue
This procedure should only be considered as a supplementary treatment.
 Bilevel positive airway pressure (BPAP)
 Continuous positive airway pressure (CPAP)

129. OSA complications

 Hypertension
 Hypoxia-induced cardiac arrhythmia
 Pulmonary hypertension and cor pulmonale
 Global respiratory insufficiency
 Cardiac infarction, stroke, and sudden cardiac death (the risk of sudden death is
high in infants and the elderly)
 Risk of accidents (e.g., car crashes, occupational accidents) due to microsleep
 Increased risk of developing vascular dementia
 Poor sleep leads to increased appetite and obesity

130. OSA px
 The mortality rate is higher in patients with severe OSA who do not receive
adequate treatment.
 CPAP ventilation can significantly lower the risk of mortality in OSA.
131. ARDS
132. Atelectasis