- fetus considered viable at 24-25 weeks with a weight of > 750g
- progesterone mediated hyperaemia and oedema of mucosal surfaces -> down size tubes
- difficult -> higher incidence of failure to intubate
- higher O2 consumption
- desaturate quickly
- increased aspiration risk
- increased risk of pulmonary oedema (increased blood volume and lower oncotic pressure)
- mechanical ventilation can be problematic
- difficult to implement protective ventilation -> hypercapnia produces fetal acidosis
- cephalad movement of diaphragm @ 37 weeks -> place chest drain higher than normal
- spirometry, flow volume loops and peak flow rates -> unchanged
- TLC decreases 5% c/o cephalad movement of diaphragm
- FRC decreases by 20% -> decreased ERV and RV
- MV increases by 50% from increase in TV -> chronic respiratory alkalosis (pH 7.4 to 7.47, PaCO2 30-32mmHg, slightly elevated PaO2, kidneys excrete HCO3- to compensate to keep HCO3- 18-21mmol/L, BE 3-4)
- O2 consumption increased 20%
- tachycardia, low BP, increased Q and warm peripheries -> normal in pregnancy
- aortocaval compression
- PAC’s can be helpful in severe pre-eclampsia, APO and cardiac disease (non-invasive Q monitors are useless)
- uterine bed is sensitive to vasoconstrictors
- phenylephrine better than ephedrine -> less fetal acidosis
- no evidence favouring any particular inotrope
- diaphragm pushed upward and heart rotated to left -> changes Q waves inferiorly and gives TWI
- maternal blood volume increases 40%, red cell mass increases 25% -> relative anaemia of pregnancy
- normal ejection systolic murmur and third heart sound
- normal echo: increase in all cardiac chamber dimensions, increased LV thickness, small pericardial effusions, mild TR, mild MR
- x 5 increased in VTE -> prophylaxis is important
- GORD -> aspiration
- hypoalbuminaemia from haemodilution
- increase in ALP
- appendicitis and cholecystitis happen
- at 12/40 bladder becomes an abdominal structure -> susceptible to blunt trauma
- at 20/40 fundus at umbilicus -> susceptible to blunt or penetrating trauma
- GFR increases by 50% -> lower Cr, urea, uric acid
- uterine blood flow @ term = 10% (600-700mL/min)
- under stress maternal blood flow will be maintained at the expense of the fetus
- oxygen consumption = 20mL/min -> can survive 10 min by shunting blood flow to vital organs and decreasing O2 consumption.
(TIME) -> its like the liver, kidney & the lungs all in one!
- gas exchange (O2 & CO2) – fetal Hb (higher concentration, greater affinity for O2)
- delivery of nutrients (glucose, aa, lipids)
- removal of wastes (urea, bilirubin)
- transport of other substances (drugs)
- heat transfer
- protection of foetus from infection
- protection of foetus from rejection by mother (immunological barrier function)
- trophoblast cells do display Class I or II MHC (major histocompatibility complex) proteins thus they cannot present antigen to lymphocytes and cannot be recognised by activated cytotoxic T lymphocytes.
- synthesis of glycogen, cholesterol, FFA’s and enzymes
- synthesis of 4 main hormones: hCG, oestriol, progesterone, human placental lactogen
- synthesis of various other hormones & growth factors
Mother and Baby
- monitor for preterm labour
- think about placental transfer of drugs
- maintenance of placental perfusion and oxygenation
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.