Shortness of Breath Flashcards
What could the 4 broad causes of SOB be?
- Insufficient O2 getting into lungs
- Insufficient O2 getting into blood
- Insufficient O2 getting around the body
- Increased respiratory drive
What may cause insufficient O2 to get into the lungs?
- Obstructed airways - COPD, airway oedema (anaphylaxis), obstructing tumour
- Decreased lung volume - intrathoracic (pneumothorax, pleural effusion) or extra thoracic (kyphoscoliosis)
- Decreased volume of functioning lung - bullous disease, fibroses lungs in interstitial disease)
- 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)
What may cause insufficient oxygen getting into bloodstream?
- Damage to alveolar membrane - e.g. emphysema / fibrosis (ILD)
- Fluid between alveolar wall and capillary - oedema (HF) / inflammatory (pneumonia)
- Disrupted blood supply (e.g. pulmonary embolus)
What may cause insufficient oxygen getting around the body?
- Shock
- Reduced cardiac output (e.g. HF, aortic stenosis)
- Anaemia
What may cause increased respiratory drive?
- Hysterical hyperventilation
2. Acidaemia (e.g. DKA)
Why does the timing of onset of SOB matter?
Vascular (PE, etc) and mechanical (pneumothorax, foreign body, etc) - present suddenly
Lung cancer / pulmonary fibrosis = present over weeks/months
What alleviating / exacerbating factors regarding shortness of breath must you ask?
- Worse on exertion? - (?HF)
- Worse when lying flat? (HF)
- Time of year - if allergy/asthma?
- Anxiety/stress related? - psychogenic hyperventilation
What risk factors must you ask about for SOB?
- Smoking
- Occupational history - asbestos? silica? dust/coal? Puts them at risk of pneumoconioses
- Medications? - drugs like nitrofuarantoin, amiodarone, methotrexate, bleomycin can cause hypersensitivity pneumonitis (a type of ILD)
- PMH - autoimmune conditions e.g. rheumatoid arthritis/SLE can cause ILD and Pleural effusions
- Pets
What associated symptoms must you enquire about?
- Cough - indicates respiratory pathology
- Chest pain - pleuritic (PE/pneumonia/pneumothorax) vs non-pleuritic (CVS pathology)
- Muscular weakness / fatigue - ?neuromuscular diseases
- Tender limbs - ?PE. Patients will notice DVT as inflammation is present
- FLAWS - red flag symptoms - ?metabolic pathology e.g. cancer
- Blood loss - ?anaemia. Ask about menstrual bleeding / rectal bleeding / melaena
Describe the information that can be gathered by asking the patient about their cough in relation to SOB
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.
Why may pleuritic chest pain indicate PE/pneumothorax/pneumonia?
Because these conditions often involve parietal pleura
If SOB presents within seconds to minutes, what Ddx must you exclude?
- Bronchospasm (acute asthma/COPD)
- Anaphylaxis
- Laryngeal oedema
- PE
- Pneumothorax
- Inhaled foreign body
- Tension pneumothorax
- Acute epiglottitis/supraglottitis
If SOB presents within hours to days, what ddx must you exclude?
- Pneumonia
- HF
- Pleural effusion
- ARDS (Acute Respiratory Distress Syndrome)
If SOB presents within weeks to months, what ddx must you exclude?
- COPD
- Chronic asthma
- HF
- Pulmonary fibrosis
- Anaemia
- Bronchiectasis
Which 2 conditions does COPD encompass
Emphysema and chronic bronchitis
What may be the risk factors for COPD
- Smoking (usually >20 pack years)
- Occupational exposure
- a1 - antitrypsin deficiency
What are the signs of COPD?
- Hyperexpanded chest
- Hyperresonant percussion
- Breathing through pursed lips
- Reduced air entry/chest expansion
- Prolonged expiratory phase
In chronic asthma, what may a typical history include?
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
Which drugs may exacerbate symptoms of asthma?
NSAIDS, aspirin, B-blockers
What may be a typical history of ILD?
Exposure to asbestos, silica, coal: all 3 are pneumoconioses that cause ILD
Exposure to drugs (e.g. methotrexate, amiodarone)
What signs on examination may be present in someone with ILD?
Clubbing
Reduced air entry/chest expansion
Late inspiratory fine crackles
What may a typical history of someone with HF be?
History of SOB on exertion, orthopnoea, PND (waking up short of breath), swollen ankles
NB swollen ankles if RHF as well as LHF
What RFs can cause HF?
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
What signs may be present on examination in someone with HF
- Displaced apex beat
- HS 3 + 4
- Crackles in both lung bases
- Raised JVP, hepatomegaly, peripheral oedema (ankles, sacrum)
What may a typical history of someone with anaemia be?
History of bleeding (Eg menorrhagia, melaena), fatigue and SOB on exertion
What signs may be present on examination in someone with anaemia
Peripheral (fingers) / central (tongue) cyanosis
Koilonychia, glossitis, angular stomatitis.
Check for conjunctival pallor but it is unreliable
What history may suggest chronic bronchiectasis is occurring?
History of productive cough and recurrent chest infections
Name 3 conditions that cause SOB that can be excluded on inspection
Obesity, kyphoscoliosis, ankylosing spondylitis
What investigations should be arranged for suspected SOB?
- FBC - checking for anaemia
- Blood cholesterol, glucose, HbA1c - abnormal cholesterol/glucose = ?IHD
- TFTs - hyperthyroidism –> tachyarrhythmia/high output cardiac failure
- Urea & electrolytes - determine baseline levels if starting diuretics later
- BNP - released by ventricular cells in HF.
What imaging investigations are done and why?
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
What investigations would you do if you suspected respiratory cause of SOB?
- PEFR - helps identify severity of asthma attack in severe asthma
- 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%)
In HF, differentiate the signs of LVF and RVF
LHF: bibasal crackles due to pulmonary oedema, displaced apex beat, CXR showing bilateral pulmonary oedema)
RVF: peripheral oedema, raised JVP
What is the most common cause of HF?
IHD
How does HF cause SOB?
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
How does HF cause orthopnoea
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
How does HF cause displaced apex beat
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
How does HF cause crackles in lungs
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
How does HF cause peripheral oedema
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
If HF is suspected, what second line investigations should be done
- Echocardiography - assess LV function to confirm low CO and HF, assess valve patency, check for areas of dyskinesia
- 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
What drug treatments would you offer someone who has HF?
- Symptomatic relief - vasodilators (nitrates/furosemide) to decrease cardiac preload, give O2, sit upright - if pt has acute pulmonary oedema. ?Morphine. Consider haemofiltration and CPAP
- 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.
- 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
What causes activation of RAAS
Hypoperfusion of kidneys
What may be the signs of lung cancer causing SOB?
Dry cough, haemoptysis, hoarse voice, weight/appetite loss, night sweats, Horner’s syndrome, lymphadenopathy
What may be the causes of postoperative breathlessness?
“Rattling cough” = mucus trapped in lungs
- 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
- Pneumonia - weakened immune response due to physiological stress of surgery and poor mucus clearance due to pain
- Pulmonary oedema - due to HF or perioperative excess fluid
- PE - ?DVT (classically occurs 10 days after operation). Prevent large DVTs by using anticoagulants (LMWH, factor 10a inhibitors), mobilise patients and use compression stockings
- Anaemia - blood loss during surgery
- Pneumothorax - always consider this if patient has interventions near chest –> e.g. insertion of central venous line, intercostal anaesthetic block
What may crackles, reduced chest expansion, and dull percussion suggest postoperatively?
How can this condition be prevented
Atelectasis (lung segment collapse)
Atelectasis can be prevented with adequate analgesia, incentive spirometry and early mobilisation.
How is postoperative atelectasis treated?
Physiotherapy, analgesia, oxygen
Describe the ABG picture for Type 2 respiratory failure (2 things wrong)
Pa O2 <8kPa
Pa CO2 >6.5kPa
Type 2 respiratory failure (T2RF) is a medical emergency. How is T2RF treated
(If untreated CO2 narcoses patient and irreversible coma and death follows).
- 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.
- Improve ventilation - if PaCO2 doesn’t improve with oxygen therapy ensure fully patent airway and NIV.
- Treat underlying cause - e.g. PE, pneumonia, pulmonary oedema, etc
Which condition is a contraindication for Non-Invasive Ventilation (NIV)
Pneumothorax
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?
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.
If you suspect pneumocystis jiroveci, which 2 infections must you test for?
- HIV - if positive, check CD4+ lymphocyte levels and viral load —> then give anti-retroviral therapy
- TB - frequent cause of pulmonary pathology
Fine crackles + flow spirometry of a normal FEV1/FVC ratio indicates + absence of other obvious diagnoses indicates?
ILD - a restrictive lung pathology
Which systemic inflammatory diseases can cause ILD?
Which drugs can cause ILD?
Rheumatoid arthritis, ankylosing spondylitis, sarcoidosis
Methotrexate, amiodarone
What is the best way to confirm ILD as a diagnosis?
High resolution chest CT scan - look for characteristic linear reticular opacities and ground glass appearance of lung
In heavy menorrhagia, what type of anaemia is expected?
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.
Wasting of hand muscles and fasciculations in the leg indicate upper/lower motor neurone pathology?
Lower
Upgoing plantar reflex indicates what upper/lower motor neurone pathology?
Upper
Diaphragmatic weakness combined with signs of upper and lower motor neurone pathology indicates what condition?
Motor neuron disease
If suspecting a (malignant) pleural effusion, you should order what?
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.
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.
Y
Binucleated lymphocytes (Reed-Sternberg cells) are diagnostic of what?
Hodgkin’s lymphoma
Differentiate asthma and COPD
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.
What are the different classes of drugs used to treat asthma and/or COPD
- 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) - 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
- 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) - Oxygen
Can also give oral drugs - e.g. oral steroids, xanthine derivatives, leukotriene antagonists, biologics, phosphodiesterase inhibitors
Differentiate bronchitis and pneumonia
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)
Why do we get SOB at altitude?
- Less PaO2 in high altitude
- Hence decreased conc gradient between oxygen in alveoli and oxygen in blood
- Hence less gas exchange —> hypoxia
- Hypoxia causes breathlessness and compensatory hyperventilation (hyperventilation can cause respiratory alkalosis)
Hypoxia makes people feel breathless
Respiratory alkalosis due to hyperventilation causes light-headedness
How does the altitude sickness drug Acetazolamide work?
Acetazolamide inhibits carbonic anhydrase
- Causes buildup of CO2 –> increased ventilatory drive
- 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.
Differentiate T1RF and T2RF
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)
What is cor pulmonale
RHF secondary to lung problems
What is Eisenmengers syndrome and how can it cause heart failure
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
If you hear bibasal crepitations, what are the 4 ddx and what signs would confirm them?
- Pulmonary oedema - displaced apex, raised JVP, ankle oedema, orthopnoea, IHD
- ILD - reduced expansion, clubbing, crepitations that don’t vary with cough
- Bronchiectasis - chronic productive cough, wheeze, crepitations that vary with cough, clubbing
- Pneumonia - acute productive cough, fever, chest pain, bronchial breathing, dull percussion
How do you manage a PE?
LMWH, start warfarin, anti-embolism stockings
