Shortness of Breath

Question 1

What could the 4 broad causes of SOB be?

Answer 1

1. Insufficient O2 getting into lungs
2. Insufficient O2 getting into blood
3. Insufficient O2 getting around the body
4. Increased respiratory drive

Question 2

What may cause insufficient O2 to get into the lungs?

Answer 2

1. Obstructed airways - COPD, airway oedema (anaphylaxis), obstructing tumour
2. Decreased lung volume - intrathoracic (pneumothorax, pleural effusion) or extra thoracic (kyphoscoliosis)
3. Decreased volume of functioning lung - bullous disease, fibroses lungs in interstitial disease)
4. Inability to inflate lungs - due to increased work to do (obesity/increased lung stiffness), weak respiratory muscles (e.g. Guillain-barre / myasthenia gravis), or already hyper inflated (COPD)

Question 3

What may cause insufficient oxygen getting into bloodstream?

Answer 3

1. Damage to alveolar membrane - e.g. emphysema / fibrosis (ILD)
2. Fluid between alveolar wall and capillary - oedema (HF) / inflammatory (pneumonia)
3. Disrupted blood supply (e.g. pulmonary embolus)

Question 4

What may cause insufficient oxygen getting around the body?

Answer 4

1. Shock
2. Reduced cardiac output (e.g. HF, aortic stenosis)
3. Anaemia

Question 5

What may cause increased respiratory drive?

Answer 5

1. Hysterical hyperventilation

2. Acidaemia (e.g. DKA)

Question 6

Why does the timing of onset of SOB matter?

Answer 6

Vascular (PE, etc) and mechanical (pneumothorax, foreign body, etc) - present suddenly

Lung cancer / pulmonary fibrosis = present over weeks/months

Question 7

What alleviating / exacerbating factors regarding shortness of breath must you ask?

Answer 7

1. Worse on exertion? - (?HF)
2. Worse when lying flat? (HF)
3. Time of year - if allergy/asthma?
4. Anxiety/stress related? - psychogenic hyperventilation

Question 8

What risk factors must you ask about for SOB?

Answer 8

1. Smoking
2. Occupational history - asbestos? silica? dust/coal? Puts them at risk of pneumoconioses
3. Medications? - drugs like nitrofuarantoin, amiodarone, methotrexate, bleomycin can cause hypersensitivity pneumonitis (a type of ILD)
4. PMH - autoimmune conditions e.g. rheumatoid arthritis/SLE can cause ILD and Pleural effusions
5. Pets

Question 9

What associated symptoms must you enquire about?

Answer 9

1. Cough - indicates respiratory pathology
2. Chest pain - pleuritic (PE/pneumonia/pneumothorax) vs non-pleuritic (CVS pathology)
3. Muscular weakness / fatigue - ?neuromuscular diseases
4. Tender limbs - ?PE. Patients will notice DVT as inflammation is present
5. FLAWS - red flag symptoms - ?metabolic pathology e.g. cancer
6. Blood loss - ?anaemia. Ask about menstrual bleeding / rectal bleeding / melaena

Question 10

Describe the information that can be gathered by asking the patient about their cough in relation to SOB

Answer 10

Cough - indicates respiratory pathology.
Persistent productive cough over past few days = ?pneumonia.

Persistent, productive cough over past 3 months over a few years = ?chronic bronchitis.

Dry cough w/ SOB or at night time = ?Asthma/LVF.

Question 11

Why may pleuritic chest pain indicate PE/pneumothorax/pneumonia?

Answer 11

Because these conditions often involve parietal pleura

Question 12

If SOB presents within seconds to minutes, what Ddx must you exclude?

Answer 12

1. Bronchospasm (acute asthma/COPD)
2. Anaphylaxis
3. Laryngeal oedema
4. PE
5. Pneumothorax
6. Inhaled foreign body
7. Tension pneumothorax
8. Acute epiglottitis/supraglottitis

Question 13

If SOB presents within hours to days, what ddx must you exclude?

Answer 13

1. Pneumonia
2. HF
3. Pleural effusion
4. ARDS (Acute Respiratory Distress Syndrome)

Question 14

If SOB presents within weeks to months, what ddx must you exclude?

Answer 14

1. COPD
2. Chronic asthma
3. HF
4. Pulmonary fibrosis
5. Anaemia
6. Bronchiectasis

Question 15

Which 2 conditions does COPD encompass

Answer 15

Emphysema and chronic bronchitis

Question 16

What may be the risk factors for COPD

Answer 16

1. Smoking (usually >20 pack years)
2. Occupational exposure
3. a1 - antitrypsin deficiency

Question 17

What are the signs of COPD?

Answer 17

1. Hyperexpanded chest
2. Hyperresonant percussion
3. Breathing through pursed lips
4. Reduced air entry/chest expansion
5. Prolonged expiratory phase

Question 18

In chronic asthma, what may a typical history include?

Answer 18

History of wheeze (audible on lung auscultation), breathlessness, chest tightness/cough. Often worse at night / early morning, during exercise, or when exposed to cold/allergens

Family hx - presence of atopic conditions in the family e.g. eczema, hay fever, allergies, nasal polyps

Question 19

Which drugs may exacerbate symptoms of asthma?

Answer 19

NSAIDS, aspirin, B-blockers

Question 20

What may be a typical history of ILD?

Answer 20

Exposure to asbestos, silica, coal: all 3 are pneumoconioses that cause ILD

Exposure to drugs (e.g. methotrexate, amiodarone)

Question 21

What signs on examination may be present in someone with ILD?

Answer 21

Clubbing
Reduced air entry/chest expansion
Late inspiratory fine crackles

Question 22

What may a typical history of someone with HF be?

Answer 22

History of SOB on exertion, orthopnoea, PND (waking up short of breath), swollen ankles

NB swollen ankles if RHF as well as LHF

Question 23

What RFs can cause HF?

Answer 23

IHD (smoking, DM, hypercholesterolaemia, HTN, south asian, family history)
Atherosclerotic disease e.g. Stroke, TIA, limb claudication
HTN on its own can cause HF
Valvular diseases (Eg Aortic stenosis)
Cardiomyopathy

Question 24

What signs may be present on examination in someone with HF

Answer 24

1. Displaced apex beat
2. HS 3 + 4
3. Crackles in both lung bases
4. Raised JVP, hepatomegaly, peripheral oedema (ankles, sacrum)

Question 25

What may a typical history of someone with anaemia be?

Answer 25

History of bleeding (Eg menorrhagia, melaena), fatigue and SOB on exertion

Question 26

What signs may be present on examination in someone with anaemia

Answer 26

Peripheral (fingers) / central (tongue) cyanosis Koilonychia, glossitis, angular stomatitis. Check for conjunctival pallor but it is unreliable

Question 27

What history may suggest chronic bronchiectasis is occurring?

Answer 27

History of productive cough and recurrent chest infections

Question 28

Name 3 conditions that cause SOB that can be excluded on inspection

Answer 28

Obesity, kyphoscoliosis, ankylosing spondylitis

Question 29

What investigations should be arranged for suspected SOB?

Answer 29

1. FBC - checking for anaemia 2. Blood cholesterol, glucose, HbA1c - abnormal cholesterol/glucose = ?IHD 3. TFTs - hyperthyroidism --> tachyarrhythmia/high output cardiac failure 4. Urea & electrolytes - determine baseline levels if starting diuretics later 5. BNP - released by ventricular cells in HF.

Question 30

What imaging investigations are done and why?

Answer 30

CXR - ?HF, pneumonia, pleural effusion, bronchiectasis, fibrosis, pneumothorax, lung collapse ECG - abnormal ECG in HF (e.g. MI can cause HF). Pathological Q waves or BBB indicates previous MI

Question 31

What investigations would you do if you suspected respiratory cause of SOB?

Answer 31

1. PEFR - helps identify severity of asthma attack in severe asthma 2. Spirometry - obstructive (mucus causes narrowing of bronchi) vs restrictive (reduced functional lung volume) In obstructive (asthma, COPD, bronchiectasis), FEV1<70% but FVC > 70%. Hence FEV1/FVC ratio <0.7. In restrictive (pulmonary fibrosis), FVC reduced (<70%) but FEV1 preserved (>70%)

Question 32

In HF, differentiate the signs of LVF and RVF

Answer 32

LHF: bibasal crackles due to pulmonary oedema, displaced apex beat, CXR showing bilateral pulmonary oedema) RVF: peripheral oedema, raised JVP

Question 33

What is the most common cause of HF?

Answer 33

IHD

Question 34

How does HF cause SOB?

Answer 34

Heart can't pump enough blood OUT. Esp if venous return (i.e. blood IN) increases when lying down/exercising or if heart has to work harder (e.g. exertion) ---> back pressure forces fluid out from pulmonary vessels into alveoli ---> causes feeling of SOB (patients may report feeling of drowning) In LVF patients, dyspnoea commonly driven by decreased lung compliance, decreased gas exchange, airway obstruction

Question 35

How does HF cause orthopnoea

Answer 35

Lying down increases venous return to heart (heart already struggling to output enough blood). This causes congestion in pulmonary vessels --> forcing out more fluid into lungs. HF patients often sleep with pillows to prevent SOB feeling

Question 36

How does HF cause displaced apex beat

Answer 36

Heart dilates as it can't pump out all the blood --> leads to displaced and weak apex beat. Dilation is NOT the same as hypertrophy (caused by HTN/aortic stenosis). In hypertrophied heart, the concentric growth doesn't displace the heart but the apex beat is heaving. Dilated heart = volume overload Hypertrophied heart = pressure overload Pressure overloaded hearts may also dilate and fail later on in disease process

Question 37

How does HF cause crackles in lungs

Answer 37

The surfactant that keeps the alveoli open is diluted by increased interstitial fluid --> increases surface tension of the alveoli and leads to alveolar collapse. When patients breathe in deeply, the alveoli pop open - which is the crackling that is heard with the stethoscope

Question 38

How does HF cause peripheral oedema

Answer 38

Failing heart can't pump entire venous return --> back pressure in venous system. Furthermore, decreased CO activates RAAS --> salt and water retention. Consequently, the raises pressure of venous system manifests as raised JVP and/or hepatomegaly. Also forces fluid out into surrounding tissues (esp in areas of highest venous pressure i.e. ankles (standing). sacrum (lying)). Raised JVP and hepatomegaly not always clinically apparent

Question 39

If HF is suspected, what second line investigations should be done

Answer 39

1. Echocardiography - assess LV function to confirm low CO and HF, assess valve patency, check for areas of dyskinesia 2. Coronary angiography - if HF due to coronary artery disease suspected; may be likely if patient has previous MI and RFs for atherosclerotic disease. Coronary arteries may be revascularised through angioplasty/stenting or bypass grafting - will improve Ventricular function

Question 40

What drug treatments would you offer someone who has HF?

Answer 40

1. Symptomatic relief - vasodilators (nitrates/furosemide) to decrease cardiac preload, give O2, sit upright - if pt has acute pulmonary oedema. ?Morphine. Consider haemofiltration and CPAP 2. Pathophysiological treatment - need to stop 1) RAAS and 2) SNS as both worsen HF; B-blocker to reduce O2 demand of heart (but NEVER use B-blockers if pt has acute LVF), and ACEi to limit RAAS activation, or ARBs instead of ACEi. Give Spironolactone (aldosterone antagonists) in those with moderate to severe HF. 3. Treat underlying cause - treat atherosclerosis of coronary arteries - revascularise if possible. Give statins, aspirin to reduce risk of thrombosis, and DM treatment. If advanced HF, consider: Digoxin, cardiac resynchronisation therapy (biventricular pacemaker), ICDs, mechanical assist devices, or heart transplantation Also always give conservative measures e.g. minimise smoking, low salt diet, stop drinking, exercise regularly

Question 41

What causes activation of RAAS

Answer 41

Hypoperfusion of kidneys

Question 42

What may be the signs of lung cancer causing SOB?

Answer 42

Dry cough, haemoptysis, hoarse voice, weight/appetite loss, night sweats, Horner's syndrome, lymphadenopathy

Question 43

What may be the causes of postoperative breathlessness? "Rattling cough" = mucus trapped in lungs

Answer 43

1. Atelectasis (alveolar collapse) - pain means patients don't expectorate any mucus from lungs --> mucus buildup plugs bronchioles --> prevents air entry --> parts of lung collapse as trapped air is absorbed into surrounding tissues 2. Pneumonia - weakened immune response due to physiological stress of surgery and poor mucus clearance due to pain 3. Pulmonary oedema - due to HF or perioperative excess fluid 4. PE - ?DVT (classically occurs 10 days after operation). Prevent large DVTs by using anticoagulants (LMWH, factor 10a inhibitors), mobilise patients and use compression stockings 5. Anaemia - blood loss during surgery 6. Pneumothorax - always consider this if patient has interventions near chest --> e.g. insertion of central venous line, intercostal anaesthetic block

Question 44

What may crackles, reduced chest expansion, and dull percussion suggest postoperatively? How can this condition be prevented

Answer 44

Atelectasis (lung segment collapse) Atelectasis can be prevented with adequate analgesia, incentive spirometry and early mobilisation.

Question 45

How is postoperative atelectasis treated?

Answer 45

Physiotherapy, analgesia, oxygen

Question 46

Describe the ABG picture for Type 2 respiratory failure (2 things wrong)

Answer 46

Pa O2 <8kPa | Pa CO2 >6.5kPa

Question 47

Type 2 respiratory failure (T2RF) is a medical emergency. How is T2RF treated (If untreated CO2 narcoses patient and irreversible coma and death follows).

Answer 47

1. Controlled oxygen therapy - high CO2 means that CO2 no longer stimulates breathing. Hence 100% O2 is bad because you depress breathing and can cause respiratory arrest. So give controlled oxygen (24-35% using Venturi connector). Aim for O2 saturations of 88-92%. Redo ABG and check for decreased PaCO2. 2. Improve ventilation - if PaCO2 doesn't improve with oxygen therapy ensure fully patent airway and NIV. 3. Treat underlying cause - e.g. PE, pneumonia, pulmonary oedema, etc

Question 48

Which condition is a contraindication for Non-Invasive Ventilation (NIV)

Answer 48

Pneumothorax

Question 49

If a patient has dry cough, SOB, low O2 saturation/desaturation on exertion, diffuse interstitial shadowing and a travel history in Africa - what is the main ddx?

Answer 49

Pneumocystis jiroveci PNEUMONIA ( commonly causes pneumonia in immunosuppressed patients). Can be a common complication of patients with AIDS. Pneumocystis jiroveci pneumonia diagnosed via microscopy, sputum culture, bronchoalveolar lavage.

Question 50

If you suspect pneumocystis jiroveci, which 2 infections must you test for?

Answer 50

1. HIV - if positive, check CD4+ lymphocyte levels and viral load ---> then give anti-retroviral therapy 2. TB - frequent cause of pulmonary pathology

Question 51

Fine crackles + flow spirometry of a normal FEV1/FVC ratio indicates + absence of other obvious diagnoses indicates?

Answer 51

ILD - a restrictive lung pathology

Question 52

Which systemic inflammatory diseases can cause ILD? Which drugs can cause ILD?

Answer 52

Rheumatoid arthritis, ankylosing spondylitis, sarcoidosis Methotrexate, amiodarone

Question 53

What is the best way to confirm ILD as a diagnosis?

Answer 53

High resolution chest CT scan - look for characteristic linear reticular opacities and ground glass appearance of lung

Question 54

In heavy menorrhagia, what type of anaemia is expected?

Answer 54

Microcytic, hypo chromic anaemia - compatible with iron deficiency anaemia. If anaemia suspected, order FBC and clotting studies. NICE recommends levonorgestrel-releasing intrauterine device (LNG-IUD) or COCP to treat anaemia if no other abnormal cause.

Question 55

Wasting of hand muscles and fasciculations in the leg indicate upper/lower motor neurone pathology?

Answer 55

Lower

Question 56

Upgoing plantar reflex indicates what upper/lower motor neurone pathology?

Answer 56

Upper

Question 57

Diaphragmatic weakness combined with signs of upper and lower motor neurone pathology indicates what condition?

Answer 57

Motor neuron disease

Question 58

If suspecting a (malignant) pleural effusion, you should order what?

Answer 58

A CXR. Once pleural effusion is confirmed, do thoracocentesis and lymph node fine needle aspiration (FNA). Thoracocentesis is sampling the fluid to see if it is transudate or exudate. Transudate = protein <25g/L. Caused by changes in osmotic forces. Exudate = protein >35g/L. Caused by metastatic cancer cells, infectious agents or inflammatory proteins.

Question 59

If you get a fluid reading that has protein between 25-35g/L (i.e. neither transudate nor exudate) this is considered indeterminate and Light's criteria must be used.

Answer 59

Y

Question 60

Binucleated lymphocytes (Reed-Sternberg cells) are diagnostic of what?

Answer 60

Hodgkin's lymphoma

Question 61

Differentiate asthma and COPD

Answer 61

Asthma: reversible and transient obstruction of airways caused by excessive mucus production, airway inflammation and bronchoconstriction. Improves with bronchodilators COPD: irreversible and progressive obstruction of airways. Obstructive changes irreversible with bronchodilators. Patients tend to be older.

Question 62

What are the different classes of drugs used to treat asthma and/or COPD

Answer 62

1. Short acting bronchodilators:- Salbutamol (ventolin) - selective B2 agonist. G-protein coupled, activates adenylate cyclase and increases cAMP formation --> SMC relaxation Ipratropium (atrovent) - antimuscarinic/cholinergic. Antagonises MACh receptors in airways --> prevents PNS mediated SMC contraction. Used often in COPD, not frequently in asthma (salbutamol + ipratropium = combivent) 2. Inhaled steroids - e.g. beclametasone, budesonide (brown inhalers), fluticasone (orange inhaler). These work by reducing inflammation by affecting intracellular transcription of various proteins. Second line treatment in asthma and COPD treatment 3. Long acting bronchodilators:- Salmeterol, formoterol, vilanterol (these are all LABAs). Tiotropium - LAMA. Used in COPD but not asthma Can combine long acting bronchodilators with steroids (Symbicort = budesonide + formoterol), (Seretide = fluticasone + salmeterol) 4. Oxygen Can also give oral drugs - e.g. oral steroids, xanthine derivatives, leukotriene antagonists, biologics, phosphodiesterase inhibitors

Question 63

Differentiate bronchitis and pneumonia

Answer 63

``` Bronchitis = disease of airways (excess mucus causing partial airway obstruction --> cough present but not usually breathlessness) Pneumonia = disease of alveoli (pus accumulation in alveoli impairs gas exchange and shows as consolidation on CXR) ``` Pneumonia classified as bronchopneumonia (focal areas affected in patchy distribution - may involve 1/more lobes) or lobar pneumonia (involves most/all of a single lobe)

Question 64

Why do we get SOB at altitude?

Answer 64

1. Less PaO2 in high altitude 2. Hence decreased conc gradient between oxygen in alveoli and oxygen in blood 3. Hence less gas exchange ---> hypoxia 4. Hypoxia causes breathlessness and compensatory hyperventilation (hyperventilation can cause respiratory alkalosis) Hypoxia makes people feel breathless Respiratory alkalosis due to hyperventilation causes light-headedness

Question 65

How does the altitude sickness drug Acetazolamide work?

Answer 65

Acetazolamide inhibits carbonic anhydrase 1. Causes buildup of CO2 --> increased ventilatory drive 2. Increased bicarbonaturia (loss of bicarbonate in urine) --> causing a metabolic acidosis (as loss of HCO3- shifts eqm to produce more HCO3-, which also produces H+). The metabolic acidosis offsets the respiratory alkalosis caused by hyperventilation. Therefore hypoxia and alkalosis solved.

Question 66

Differentiate T1RF and T2RF

Answer 66

``` Hypoxaemia = PaO2 < 8kPa Hypercapnia = PaCO2 >6.5kPa ``` T1RF: - 1 gas wrong (oxygen) --> "hypoxaemic respiratory failure" - caused by asthma, COPD, pneumonia, fibrosis, pulmonary oedema T2RF: - 2 gases wrong (oxygen and CO2) - "hypercapnia respiratory failure" - caused by ventilatory failure due to decreased respiratory drive (e.g. opiates, CNS damage) or impaired lung movements (e.g. reduced compliance and hyper inflated lungs, chest wall deformity, obesity, neuromuscular impairment)

Question 67

What is cor pulmonale

Answer 67

RHF secondary to lung problems

Question 68

What is Eisenmengers syndrome and how can it cause heart failure

Answer 68

Eisenmengers syndrome is when a right to left cardiac shunt has emerged (initially from a left to right cardiac shunt) Patient initially has left to right cardiac shunt due to ASD/VSD or patent ductus arteriosus. This then causes pulmonary hypertension as pulmonary vasculature is subject to greater pressures from left ventricle. Eventually pulmonary hypertension provides enough resistance to reverse the direction of the shunt (i.e. shunt is now Right to Left). This can cause HF and only curable by lung-heart transplant

Question 69

If you hear bibasal crepitations, what are the 4 ddx and what signs would confirm them?

Answer 69

1. Pulmonary oedema - displaced apex, raised JVP, ankle oedema, orthopnoea, IHD 2. ILD - reduced expansion, clubbing, crepitations that don't vary with cough 3. Bronchiectasis - chronic productive cough, wheeze, crepitations that vary with cough, clubbing 4. Pneumonia - acute productive cough, fever, chest pain, bronchial breathing, dull percussion

Question 70

How do you manage a PE?

Answer 70

LMWH, start warfarin, anti-embolism stockings