Basic respiratory physiology including oxygen therapy Dr Felix Woodhead Consultant Respiratory Physician

Aerobic respiration Occurs in mitochondria Chemiosmotic synthesis of ATP Final sink for electrons O2 consumed, CO2 generated RQ = [CO2]/[O2] C6H12O6 + 6 O2 → 6 CO2 + 6 H2O (RQ=1) C16H32O2 + 23 O2 → 16 CO2 + 16 H2O (RQ = 16/23 = 0.7)

CO2 Soluble Stored as HCO3- (catalysed by CA) Carboxyhaemoglobin Linear relationship CaCO2 and pCO2

O2 Much less soluble in water Most stored as oxyhaemoglobin Non-linear relationship (sigmoid) Flat top → loading still occurs if PAO2 ↓ Maintains good pressure gradient along alveolus Steep portion assists off loading in tissues Shifted to right by temp, acid and pCO2

Acid-base: CO2 H2CO3 → H+ + HCO3- K`A = ([H+] x [HCO3-])/[H2CO3] KA = [H+] x [HCO3-] /[CO2] log KA = log [H+] + log ([HCO3-])/[CO2]) - log [H+] = - log KA + log ([HCO3-])/[CO2]) pH = pKA + log ([HCO3-])/[CO2])

Control of ventilation Acidity of brain stem Blood-brain barrier imperm to ions, perm to CO2 ↑pCO2 → ↓pH CSF few proteins → pH changes quickly pCO2 kept very steady ↑pCO2 implies ventilatory failure Gradual ↑ HCO3- by kidney to compensate Low pO2 only relevant in chronic vent insufficiency

Partial pressures Total pressure = sum of partial pressures of constituent gases Atmosphere predom N2 (80%) and O2 (20%) patm = pN2 + pO2 FiO2 = fraction inspired O2 = 0.20 1 atm = 100 kPa pO2 (at sea level) = 20 kPa

A-a gradient Idealised lung arterial pO2 same as alveolar Alveolar pO2 = inhaled pO2 – used up O2 Used up O2 related to generated CO2 by RQ pAO2 = pIO2 – (pCO2/R) A-a gradient = pAO2 - paO2 Fudge factor for pACO2 + pAH20 ≈ 5 Greater A-a gradient implies problem with lungs (V/Q mismatch)

V/Q ratio V/Q = 0 V/Q = ∞ V/Q mismatching Shunt PaO2 → mixed venous pO2 V/Q = ∞ No flow Gases approximate PAO2 but ventilation wasted V/Q mismatching always → ↓pO2 (A-a gradient ↑) pCO2 may be normal as total vent ↑

Partial pressure vs concentration In a perfect gas pp prop conc In a liquid, depends on solubility and chemical binding Pp like voltage determines diffusion Concentration like thermal energy depends on material

Oxygen carriage Depends on cardiac output, [Hb] and SaO2 Once Hb saturated O2 stored dissolved ↑ FiO2 →↑ pO2 ++ but only ↑ CaO2 a little Possible to ↑ pO2 without ↑ CaO2 pO2 affects rate of diffusion and control of breathing Cannot increase pO2 of individual alveolar units by ↑ ventilation

Respiratory Failure pO2 < 8 kPa Type I Type II Normal/low pCO2 V/Q mismatch/diffusion limitation Ventilation able to compensate Type II ↑ pCO2 ↓pH if acute Ventilatory failure Needs controlled O2 ± ventilation

O2 or ventilation Is there impaired ventilation? If there is impaired ventilation is it the only problem or is it part of multi-organ failure? Is invasive ventilation appropriate?

O2 delivery systems High flow vs low flow systems Does flow rate exceed minute ventilation? Low flow rates, FiO2 ↑ with ↓ minute vent Nasal specs comfortable and cheap, not for acutely unwell High flow FiO2 independent of vent rate (Venturi) Non-rebreathing (reservoir bag) Higher pO2 requires complete seal

Basic respiratory anatomy including radiology Dr Felix Woodhead Consultant Respiratory Physician

Lobes Heart on left 3 lung lobes on Right 2 lobes on left Left main bronchus deviates horizontally to miss heart RMB straighter (inhaled foreign body) Lingula (tongue) is analogous to RML, arises LUL Upper and lower lobes pyramidal Lower lobes one apical and four basal segs Oblique (major) fissure bilat (seen on lat), horizontal only on R (PA)

Radiological patterns 1 Pleural effusions/mass Dense white with no air bronchograms Meniscus Beware the supine effusion Tumours Spiculated & single (primary) vs round & multiple (mets) May present as collapse Collapse Volume loss (shift of fissure/hilum) Obliteration of adjacent silhouette

Alveolar space filling (≡ consolidation) Fairly dense, with air bronchograms (patent airways) Neutrophils ± microrganisms (pneumonia/organising pneumonia) Eosinophils (eosinophilic pneumonia) Blood (pulm haemmorhage) Fluid (severe pulm oedema) Surfactant (alveolar proteinosis) Tumour (bronchoalveolar carcinoma – BAC)

Interstitial shadowing Less dense than consolidation, dots and lines on CXR (reticulonodular) Interstitial fluid (pulm odema) Trapped lymph (lymphangitis carcinomatosis) Inflammation/fibrosis Interstitial lung disease Diffuse parenchymal lung disease Fibrosing alveolitis “pulmonary fibrosis”

An approach to chest radiographs Normal or abnormal? If abnormal, how long? If consolidation ?pneumononia treat with antibiotics and repeat film 6-8/52 If interstitial ?pulm oedema Treat with diuretics and repeat film in a few days Remember Not all LRTIs are pneumonia (bronchitis/bronchiectasis) Pulm oedema also seen with fluid resus and renal pts Long-standing shadowing ?diffuse parenchymal lung disease

CT radiology terminology Fleischner Society: Glossary of Terms for Thoracic Imaging Consolidation Dense, white opacity, obliterating vessels Ground glass Less dense, grey. Alveolar filling or fibrosis Reticulation Thickened septal lines, usually indicates fibrosis Honeycombing Cysts, usually basal and peripheral. Typical in IPF Traction bronchiectasis Airways in abnormal lung pulled apart. Indicates fibrosis Secondary pulm lobule Smallest part of lung surrounded by connective tissue. Central arteriole/bronchiole, periph venule/lymphatics/septal thickening Mosaicism Patchy ground glass often of sec pulm lobules. Airways, vessels or interstitium

CXRs vs CTs CXR CT Cheap Quick Good screen Serial change Low radiation dose CT Better spatial resolution Staging Patterns of disease ?too sensitive