Obstetric Physiology

Question 1

What physiological changes are seen in pregnancy?

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Answer 1

3 categories:
Improving uterine oxygen delivery
Protecting against blood loss during parturition
As a result of a gravid uterus

Most change happens in the first trimester, stimulated by progesterone & oestrogen - highest risk of teratogenicity.
In the second trimester, the mechanical impact of the enlarged uterus increases.

Cardiovascular
CO increases by 50% (30% by end of first trimester), peaking at end of second trimester. Can further increase by 40-50% during labour.
This can unmask undiagnosed cardiac disease
Caval compression reduces cardiac output anytime after 20 weeks.
Stroke volume increases by 35% (peaking at end of second trimester), HR increases by 25%
SVR drops
Heart is displaced cranially and to the left, with LV hypetrophy - causing left axis deviation, ST depression, flattened T waves.

Respiratory
Anatomical changes (mucosal oedema & engorgement) - may need smaller ETT, higher bleeding risk
Fluid overload PIH & pre-eclampsia
Thoracic changes - breast enlargement, diaphragmatic splinting (4cm elevation), but take deeper breaths and hyperventilate.
Compensatory increase in transverse & antero-posterior chest diameters.

VC, Total capacity & FEV1 remain equal.
From 20 weeks until term, the following decrease progressively by 20%
Expiratory reserve volume, residual volume, FRC, Closing capacity.

Inspiratory reserve volume increases

Physiological
Increased O2 consumption & CO2 production (60%), reduced FRC & higher closing capacity make pre-oxygenation less effective.
pCO2 Hyperventilation to 4.1kPa by end of first trimester, TV increasing by 40% and RR by 15%.
PaO2 increases in third trimester, until CO becomes limiting factor, with increased A:a gradient.
Increased 2,3-DPG

Neurological
Reduced epidural space volume (venous engorgement)
Increased sensitivity to hypnotics

Haematological
Anaemia of pregnancy, reduction in platelets
Blood volume - increases from 6 weeks, peaks at 34 weeks, returns to normal 10-14 days post-partum. Progesterone and oestrogen activate RAAS, increasing total body water retention.
Breast tissue, uterus, mucosa and skin all engorge.
Uterine contraction at delivery delivers approx 500ml auto-transfusion, which can delay signs/symptoms of MOH

Renal EPO increases, RBC mass increases by up to 30%, but less than plasma, so haemodilution to approx 120g/L

White cells rise during pregnancy until after delivery, which may mask sepsis

Increased fibrinogen & all clotting factors bar 11 and 13 - normal clotting but reduced fibrinolysis

Renal
Increased perfusion & GFR (50-60%)
Lower urea/creatinine
Small amount of proteinuria/glycosuria
Reduced plasma osmolarity (water retention via RAAS)
Increasd bicarbonate excretion, buffering respiratory alkalosis
Increased risk of UTI (smooth muscle relaxation via progesterone)
Uterus can compress ureters in later pregnancy

Endocrine
Enlarged pituitary, increased T4/T3
Increased insulin production & resistance (via human placental lactogen) - allows glucose across placenta into foetal circulation
Maternal hyperglycaemia causes foetal hyperinsulinaemia & risks post-natal hypoglycaemia
Diabetic mothers have macrosomic babies - insulin is anabolic.

GI
Increased intragastric pressure
Reduced lower oesophageal sphincter tone (upper is striated so not affected by progesterone)
Increased reflux, especially supine (hence the use of PPI & prokinetic, plus sodium citrate for emergency LSCS)
Gastric stasis in labour (worsened by opioids)
Increased ALP (3x normal - produced by placenta)
Gallstones more frequent

Question 2

What pharmacokinetic & pharmacodynamic changes occur in pregnancy?

Answer 2

Increased volume of distribution (prolonged elimination half-life)
Redcued plasma cholinesterase (clinically insignificant increase in suxamethonium duration)
Reduced MAC requirement

Question 3

What is aortocaval compression, and how should it be managed?

Answer 3

From week 20, the uterus compresses the IVC & Aorta in supine position
This reduces venous return, increasing afterload, with a fall in CO
Compression of aorta may reduce renal & uterine blood flow, compromising foetal blood supply.

Women should lie on a tilt, usually left side down, displacing the uterus.

GA and neuraxial both suppress the sympathetic autonomic response (which usually compensates for supine hypotension), increasing the importance of adequate tilt)

Question 4

How does pregnancy affect administration of anaesthesia?

Answer 4

GA:
Risk of foetal depression
Increased MV and reduced FRC causes faster onset of inhaled agents
Reduced MAC requirement of up to 30%

Neuraxial:
Increased lumbar lordosis and intra-abdominal pressure, with epidural venous engorgement means smaller volume of local anaesthetic required