Respiratory

Crash revision

Omar K.
MRCP Ireland
ABG
• Normal pH is 7.35–7.45. A pH <7.35 indicates acidosis and a pH >7.45 indicates
alkalosis.

• Normal PaO2 is 10.5–13.5kPa. Hypoxia is caused by one or more of the following

reasons: ventilation/perfusion (V/Q) mismatch, hypoventilation, abnormal diff
usion, right to left cardiac shunts. Of these, V/Q mismatch is the commonest cause.
Severe hypoxia is defined as a PaO2 <8kPa (see p180).

• Normal PaCO2 is 4.5–6.0kPa.

PaCO2 <4.5kPa indicates hyperventilation and a PaCO2 >6.0kPa indicates

hypoventilation.

Type 1 respiratory failure is defi ned as PaO2 <8kPa and PaCO2 <6.0kPa.
Type 2 respiratory failure is defi ned as PaO2 <8kPa and PaCO2 >6.0kPa
Spirometery
Spirometry measures functional lung volumes.
Forced expiratory volume in 1s (FEV1) and forced vital capacity (FVC) are measured
from a full forced expiration into a spirometer (VitalographR); exhalation continues
until no more breath can be exhaled. FEV1 is less eff ort-dependent than PEF.

The FEV1/FVC ratio gives a good

estimate of the severity of airfl ow obstruction; normal ratio is 75–80%.

Obstructive defect (eg asthma, COPD) FEV1 is reduced more than the FVC, and the
FEV1/FVC ratio is <75%.

Restrictive defect (eg lung fi brosis) FVC is  and the FEV1/FVC ratio is  or . Other
causes: sarcoidosis; pneumoconiosis, interstitial pneumonias; connective tis sue
diseases; pleural eff usion; obesity; kyphoscoliosis; neuromuscular problems.xt
Click to add text
Pneumonia
Classification and causes
 1_Community-acquired pneumonia (CAP) . Streptococcus pneumoniae is the commonest cause,
followed by Haemophilus influenzae and Mycoplasma pneumoniae. Staphylococcus aureus,

 Legionella species, Moraxella catarrhalis, and Chlamydia account for most of the
remainder. Gram negative bacilli, Coxiella burnetii and anaerobes are rarer.

Viruses account for up to 15%. Flu may be complicated by community-acquired MRSA pneumonia
(CA-MRSA).

 2_Hospital-acquired (nosocomial; >48h after hospital admission). Most commonly

Gram negative enterobacteria or Staph. aureus. Also Pseudomonas, Klebsiella,
Bacteroides, and Clostridia. Aspiration Those with stroke, myasthenia, bulbar palsies,
consciousness (eg postictal or drunk), oesophageal disease (achalasia, reflux), or with poor dental
hygiene
risk aspirating oropharyngeal anaerobes.

 3_Immunocompromised patient: Strep. pneumoniae, H. infl uenzae, Staph. aureus, M.

catarrhalis, M. pneumoniae, Gram –ve bacilli and Pneumocystis jiroveci (formerly named P.
carinii, p410–p411). Other fungi, viruses (CMV, HSV), and mycobacteria.
Severity & TX
Click to add text
SARS
Severe acute respiratory syndrome (SARS) is caused by SARS-COV virus—a
coronavirus.
Major features are persistent fever (>38°C), chills, rigors, myalgia, dry cough,
headache, diarrhoea, and dyspnoea—with an abnormal CXR and WCC.
Respiratory failure is the big complication; >50% need supplemental O2; ~20%
progress to acute respiratory distress syndrome requiring invasive ventilation.

Mortality is 1–50%, depending on age. Close contact with an index case, or travel to
an area with known cases should raise suspicion.
The mechanism of transmission of SARS-CoV is only by close contact with other
patients.
Management is supportive. No drugs have convincing efficacy (experts may advise
on antivirals). Rapid diagnosis, early isolation, and good infection control
measures are vital. Communicate with your consultant in infectious diseasesdd
text
Bronchiectasis
Causes
Congenital: cystic fi brosis (CF); Young’s syndrome;
primary ciliary dyskinesia; Kartagener’s syndrome .
Post-infection: measles; pertussis; bronchiolitis;
pneumonia; TB; HIV.
Postobstructive: bronchial obstruction (tumour,
foreign body);
Allergic bronchopulmonary aspergillosis (ABPA,;
hypogammaglobulinaemia; rheumatoid arthritis;
ulcerative colitis; idiopathic
MX
PABS
P
A
B
S
--------------------
Cystic fibrosis (CF)
Cystic fibrosis
Diagnosis Sweat test: sweat sodium and chloride
>60mmol/L; chloride usually > sodium.
Genetics: screening for known common CF mutations
should be considered.
Faecal elastase is a simple and useful screening test for
exocrine pancreatic dysfunction.
Management of cystic fibrosis
MDM (multi disciplinary teams mx)
Chest+ GI + PT+ rehab + genetics
Fungi ( 5 letters = 5 effects)
1_asthma (Hyper type 1)
2_Allergic bronchopulmonary aspergillosis (ABPA): Results from type I and III
hypersensitivity reactions to Aspergillus fumigatus

Investigations:
positive Aspergillus skin test and/or Aspergillus-specifi c IgE RAST
(radioallergosorbent test);
positive serum precipitins; eosinophilia; raised serum IgE.

Treatment: prednisolone 30–40mg/24h PO for acute attacks; maintenance

dose 5–10mg/d. Sometimes itraconazole is used in combination with
corticosteroids.
Bronchodilators for asthma. Sometimes bronchoscopic aspiration of
mucous plugs is needed
3_Aspergilloma (mycetoma): A fungus ball within a
pre-existing cavity (TB or sarcoidosis). HALO sign
Tx only if symp +ve (itraconazole or surgery)
4_Invasive aspergillosis (immune compromised)
Tx voriconazone & amphotericine

5_Extrinsic allergic alveolitis (EAA) may be caused by

sensitivity to Aspergillus clavatus (‘malt worker’s lung’)

Tx symptomatic
Lung ca
Squamous (35%); adenocarcinoma (27%); small (oat)
cell (20%); large cell (10%); alveolar cell carcinoma
(rare, <1%).
Clinically the most important division is
between small cell (SCLC) and non-small cell
(NSCLC).
Complications:

Local: recurrent laryngeal nerve palsy; phrenic nerve palsy; SVC obstruction;
Horner’s syndrome (Pancoast’s tumour); rib erosion; pericarditis; AF.

Metastatic:
brain; bone (bone pain, anaemia, Ca2+); liver; adrenals (Addison’s).

Endocrine: (paraneoplastic syndrome )

ectopic hormone secretion, eg SIADH (Na+ and ADH, p678) and ACTH (Cushing’s) by
small cell tumours;
PTH (Ca2+) by squamous cell tumours.

 neurological:
confusion; fits; cerebellar syndrome (anti Hu antibodies) ; proximal myopathy; neuropathy; polymyositis;
Lambert–Eaton syndrome . Other: clubbing, HPOA, dermatomyositis;
acanthosis nigricans ; thrombophlebitis migrans (p564).
tx
Non-small cell tumours: Excision is the treatment of
choice for peripheral tumours, with no metastatic
spread: stage I/II (~25%).
Curative radiotherapy is an alternative if respiratory
reserve is poor.
Chemotherapy & RT & monoclonal antibodies for
advanced disease
Small cell (oat`s)
Small cell tumours are nearly always disseminated at presentation. They may
respond to chemotherapy but invariably relapse

Palliation: Radiotherapy is used for bronchial obstruction, SVC

obstruction, haemoptysis, bone pain, and cerebral metastases.
SVC stent + radio therapy and dexamethasone for SVC obstruction.

Endo bronchial therapy: tracheal stenting, cryotherapy,

laser, brachytherapy (a radioactive source is placed close to the tumour).

Pleural drainage/pleurodesis for symptomatic pleural effusions. Drugs: analgesia;

steroids; antiemetics; cough linctus (codeine); bronchodilators; antidepressants
Solitary nodule
Click to add text
B.Asthma Management
Non pharmacological :
Pharmacological (BTS)

Step 1 Occasional short-acting inhaled 2-agonist as required for symptom relief. If

used more than once daily, or night-time symptoms, go to Step 2.

Step 2 Add standard-dose inhaled steroid, eg beclometasone 200–800μg/day, or

start at the dose appropriate for disease severity, and titrate as required.

Step 3 Add long-acting b2-agonist (eg salmeterol 50μg/12h by inhaler). If benefit—

but still inadequate control—continue and dose of beclometasone to 800μg/day. . Leukotriene receptor
antagonist or oral theophylline may be tried.

Step 4 Consider trials of: beclometasone up to 2000μg/day; modified-release oral

theophylline; oral leukotriene receptor antagonist

Step 5 Add regular oral prednisolone (1 dose daily, at the lowest possible dose).
Continue with high-dose inhaled steroids. Refer to asthma clinic.
COPD
Causes :
COPD mx
Click to add text
Acute respiratory distress syndrome (ARDS)
ARDS, or acute lung injury, may be caused by direct lung injury or
occur secondary to severe systemic illness. Lung damage and release
of inflammatory mediators cause increased capillary permeability
and non-cardiogenic pulmonary oedema, often accompanied by
multiorgan failure.

Causes
Pulmonary: Pneumonia; gastric aspiration; inhalation; injury;
vasculitis; contusion. Other: Shock; septicaemia; haemorrhage;
multiple transfusions; DIC; pancreatitis; acute liver failure; trauma;
head injury; malaria; fat embolism; burns; obstetric events
(eclampsia; amniotic fl uid embolus); drugs/toxins (aspirin, heroin,
paraquat).
Dx & mx
Diagnostic criteria
1 Acute onset.
2 CXR: bilateral infi ltrates.
3 Pulmonary capillary wedge pressure (PCWP) 19mmHg
or a lack of clinical congestive heart failure.
4 Refractory hypoxaemia with PaO2 : FiO2 <200 for
ARDS.
mx
Respiratory support In early ARDS, continuous
positive airway pressure (CPAP) with 40–60% oxygen
may be adequate to maintain oxygenation

Circulatory (blood & fluids)

Tx infection & cx (renal failure etc)

Px Overall mortality is 50–75%.

Resp failure
gas exchange is inadequate
Pulmonary embolism (PE)
Virchow`s triads (HIS)
Recent surgery, especially abdominal/pelvic or
hip/knee replacement
• Thrombophilia, eg antiphospholipid syndrome (p368)
• Leg fracture
• Prolonged bed rest/reduced mobility
• Malignancy
• Pregnancy/postpartum; Pill/HRT
• Previous PE
ECG may be normal, or show tachycardia, right bundle
branch block, right ventricular strain (inverted T in V1 to
V4). The classical SI QIII TIII pattern (p92) is rare

1_Anticoagulate with LMW heparin .

2_Start warfarin. Stop heparin when INR is >2 and continue
warfarin for a minimum of 3 months aim for an INR of 2–3.
3_Thrombolysis for massive PE (alteplase).
4_Consider placement of a vena caval filter in patients who
develop emboli despite adequate anticoagulation
D dimers
D-dimers: only perform in those patients without a
high probability of a PE.
A negative D-dimer test effectively excludes a PE in
those with a low or intermediate clinical probability,
and imaging is NOT required.
However, a positive test does not prove a diagnosis of a
PE, and imaging is required.

V/q SCAN IS OUTDATEEEEEEEEEDDDDD 

Pleural effusion
BBC ( Omar K abbreviation )

Mx

Dxtic
Theraputic
Sarcoidosis
A multisystem granulomatous disorder of unknown cause
Pulmonary disease 90% have abnormal CXRs with bilateral hilar
lymphadenopathy.
Non-pulmonary signs
1_lymphadenopathy; hepatomegaly; splenomegaly;
2_uveitis; conjunctivitis; keratoconjunctivitis sicca; glaucoma;
3_terminal phalangeal bone cysts; enlargement of lacrimal & parotid
glands;
4_Bell’s palsy; neuropathy; meningitis; brainstem and spinal syndromes;
space-occupying lesion;
5_Erythema nodosum; lupus pernio; subcutaneous nodules; cardio
myopathy;
5_arrhythmias; hypercalcaemia; hypercalciuria; renal stones; pituitary
dysfunction
 invx
 Blood: ESR, lymphopenia, serum ACE increas ~60% (non-specifi c), increase Ca2+,
 Increase immunoglobulins. 24h urine: Ca2+. Tuberculin skin test is –ve in two-thirds;

 CXR is abnormal in 90%: Stage 0: normal. Stage 1: BHL. Stage 2: BHL + peripheral pulmonary infi
ltrates. Stage 3: peripheral pulmonary infiltrates alone. Stage 4: progressive pulmonary fi brosis;

 ECG may show arrhythmias or bundle branch block.

 Lung function tests may be normal or show reduced lung volumes, impaired gas transfer, and a
restrictive ventilator defect.

 Tissue biopsy (lung, liver, lymph nodes, skin nodules, or lacrimal glands) is diagnostic and shows
non-caseating granulomata. Kveim tests are now obsolete.

 Bronchoalveolar lavage (BAL) shows lymphocytes in active disease; neutrophils with

pulmonary fi brosis.

 Ultrasound may show nephrocalcinosis or hepatosplenomegaly.

 Bone X-rays show ‘punched out’ lesions in terminal phalanges.

 CT/MRI may be useful in assessing severity of pulmonary disease or diagnosing neurosarcoidosis.
Ophthalmology assessment (slit lamp examination, fluorescein angiography) is indicated in ocular
disease.
tx
Indications for corticosteroids:
• Parenchymal lung disease (symptomatic, static, or
progressive)
• Uveitis
• Hypercalcaemia
• Neurological or cardiac involvement.

Prednisolone (40mg/24h) PO for 4–6 wks, then dose

over 1yr according to clinical status.
Click to add text
Interstitial lung disease (ILD
 Any condition causes lung fibrosis

Classification The ILDS can be broadly grouped into three categories:

1_Those with known cause, eg
 •Occupational/environmental, eg asbestosis, berylliosis, silicosis, cotton worker’s lung (byssinosis)
 • Drugs, eg nitrofurantoin, bleomycin, amiodarone, sulfasalazine, busulfan
 • Hypersensitivity reactions, eg extrinsic allergic alveolitis
 • Infections, eg TB, fungi, viral
 • Gastro-oesophageal refl ux

2_Those associated with systemic disorders, eg

 • Sarcoidosis
 • Rheumatoid arthritis
 • SLE, systemic sclerosis, mixed connective tissue disease, Sjogren’s syndrome
 • Ulcerative colitis, renal tubular acidosis, autoimmune thyroid disease

3_Idiopathic, eg
 • Idiopathic pulmonary fi brosis (IPF, p190)
 • Cryptogenic organizing pneumonia
 • Lymphocytic interstitial pneumonia
 Extrinsic allergic
Extrinsic allergic alveolitis (EAA)
In sensitized individuals, inhalation of allergens
(fungal spores or avian proteins) provokes a
hypersensitivity reaction.

In the acute phase, the alveoli are infiltrated with

acute inflammatory cells.

With chronic exposure, granuloma formation and

obliterative bronchiolitis occur.
SX
Causes
• Bird-fancier’s and pigeon-fancier’s lung (proteins in bird
droppings).
• Farmer’s and mushroom worker’s lung (Micropolyspora faeni,
Thermoactinomyces vulgaris).
• Malt worker’s lung (Aspergillus clavatus).
• Bagassosis or sugar worker’s lung (Thermoactinomyces sacchari).

Clinical features 4–6h post-exposure: Fever, rigors, myalgia, dry

cough, dyspnoea, crackles (no wheeze).
Chronic: Increasing dyspnoea, weight LOSS, exertional dyspnoea,
type I respiratory failure, cor pulmonale.
DX
Tests Acute: Blood: FBC (neutrophilia); ESR; ABGS; positive serum
precipitins (indicate exposure only).

CXR: upper-zone mottling/consolidation; hilar lymph adenopathy

(rare).

Lung function tests: reversible restrictive defect; reduced gas transfer

during acute attacks.

Chronic: Blood tests: positive serum precipitins. CXR: upper-zone fi

brosis; honeycomb lung. Lung function tests: persistent changes (see
above).
Bronchoalveolar lavage (BAL) fluid shows lymphocytes and mast cells.
MX
Management Acute: Remove allergen and give O2 (35–
60%), then: Oral prednisolone (40mg/24h PO),
followed by reducing dose.

Chronic: Avoid exposure to allergens + STEROIDS

Click to add text
Industrial dust diseases
1_Coal worker’s pneumoconiosis (CWP)
CXR: many round opacities (1–10mm), especially in
upper zone. MX Avoid exposure & can acclaim $ .
2_Progressive massive fi brosis (PMF)
Cxr upper lobe fibrosis .

3_Caplan’s syndrome is the association between

rheumatoid arthritis, pneumoconiosis, and pulmonary
rheumatoid nodules.
4_Silicosis
Clinical features: Progressive dyspnoea, increases incidence
of TB, CXR shows diffuse military or nodular pattern in
upper and mid-zones and egg-shell calcification of hilar
nodes. Spirometry: restrictive ventilatory defect
5_Asbestosis
Also causes pleural plaques, increases risk of bronchial
adenocarcinoma and mesothelioma
6_Malignant mesothelioma
CXR/CT: pleural thickening/eff usion. Bloody pleural fluid
Pemetrexed + cisplatin chemotherapy can improve survival.
Surgery is hard to evaluate (few randomized trials).
Radiotherapy is controversial.
Pleurodesis and indwelling intra-pleural drain may help.
Obstructive sleep apnoea syndrome
intermittent closure/collapse of the pharyngeal airway
causing apnoeic episodes during sleep. These are terminated by partial arousal

Complications Pulmonary hypertension; type II respiratory failure .increases

risk factor for hypertension
Dx sleep study

Tx Management
1_ Weight reduction
2_Avoidance of tobacco and alcohol
•3_CPAP via a nasal mask during sleep is effective and recommended for those
with moderate to severe disease
4_• Surgery to relieve pharyngeal obstruction (tonsillectomy, uvulopalatop
haryngoplasty, or tracheostomy) is occasionally needed, but only after seeing a
chest physician.
Cor pulmonale
Cor pulmonale is right heart failure caused by chronic
pulmonary arterial hypertension
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add text
Click to add title
Click to add text