TYPE OF HYPOXIA
- Hypoxaemic – low oxygen tension
- Stagnant – reduced tissue blood flow
- Anaemic – low Hb
- Histiotoxic/cytopathic – abnormal cellular oxygen utilisation
- cell dysfunction from high oxygen tension
OXYGEN DELIVERY MEASUREMENT
Inspired O2 (PiO2)
- PiO2 = FiO2 x (barometric pressure – saturated vapour pressure of H20)
- PiO2 = 0.21 x (760 – 47) – sea level
- PiO2 = 150mmHg
- gas supply pressures are continuously measured
- FiO2 is monitored within the inspiratory limb of ventilators
PiO2 to Alveoli
- PiO2 = PAO2 if:
- there is no upper airway obstruction
- expired tidal and minute volumes and airway pressures for the ventilated are within correctly set alarms
- there is an appropriate end-tidal CO2 waveform
Alveolar Gas (PAO2)
- marked variation in PO2 between lung units makes measurement of ETO2 pointless
- clinical assessment chest movement, air entry and CXR
- electrical impedance tomography: non-invasive tracking of lung volume changes
- assessment of V/Q mismatch: Multiple Inert Gas Technique (MIGET) -> impractical, FiO2 to SpO2 is more practical
- alveolar gas equation: PAO2 = PiO2 – PaCO2/0.8
Alveolar Gas to Arterial Blood (PAO2 -> PaO2)
- A-a gradient: see document in Ventilation
- PaO2/FiO2 ratio: see document
- venous admixture (Qs/Qt): use of the shunt equation, requires a PAC
- blood gas analysis and co-oximetry
- continuous intra-arterial blood gas monitoring: invasive, not validated yet, accurate
- transcutaneous PO2 and PCO2 monitoring: reliable CO2, not so accurate O2, heat skin -> burns, regular calibration required
- pulse oximetry
- haemoglobin-oxygen affinity: described by the oxy-Hb dissociation curve
OXYGEN CONSUMPTION MEASUREMENT
- oxygen delivery index (DO2I): CI x arterial oxygen content (CaO2) x 10, difficult to interpret because varies greatly in illness
- oxygen consumption index (VO2I): CI x (CaO2-CvO2) x 10 via the reverse Fick method or indirect calorimetry – many random error and inaccuracies
Mixed Venous Blood
- blood aspirated from an unwedged PA
- mixed venous PO2 (PvO2): low value -> intracellular hypoxia, high value -> doesn’t exclude histiotoxic hypoxia or tissue shunting.
- mixed venous oxygen saturation (SvO2): normal = 0.7-0.8, hypoxia + lactate acidosis = 0.3-0.5, > 0.8 = high flow states (sepsis, hyperthyroidism, severe liver disease)
- central venous saturation (SCVO2): normally 3% lower than SvO2, trends and response to management run in parallel.
- venoarterial PCO2 gradient (∆PCO2): normally about 6mmHg, markedly increases in low output states and cardiac arrest, lacks sensitivity and specificity as a global index of tissue hypoxia.
Plasma Lactate and Redox indices
- produced as a result of anaerobic metabolism in the context of inadequate tissue oxygenation.
- lactic acidosis: production exceeds metabolism or metabolism is decreased by organ dysfunction.
- normal = < 1mmol/L
Regional Oxygenation Indices
- regional PCO2: reflects the balance between PaCO2, tissue blood flow and tissue CO2 production, a rising gap between PaCO2 and tissue PCO2 signifies falling tissue blood flow (gastric tonometry and sublingual capnometry)
- cerebrovenous oxygen saturation monitoring: retrograde passing of catheter into jugular bulb to measure venous saturation (goal = 55-85%)
- direct tissue PO2 measurement: animal data, highly impractical
- othrogonal polarisation spectroscopy: microcirculation assessment
- in vivo MRI
- optical spectroscopy
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of LITFL.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of two amazing children.
On Twitter, he is @precordialthump.