Physiology

Question 1

Obstetric Airway Considerations

Answer 1

Oedematous/vascular airway - higher risk of bleeding,
Greater risk of obstruction
Reduced Lower Oesophageal Sphincter tone
Volume effect on the stomach from gravity uterus
Reduced gastric motility in labour - assume a full stomach from 16 weeks

Question 2

Obstetric Respiratory Physiology

Answer 2

Gravity uterus causes diaphragmatic displacement
Reduced FRC, moderate when sitting up, severe when lies down
Increased O2 consumption, decreased CO2 production
Hyperventilation to allow foetal normocarbia

Reduced respiratory reserve and so rapid deterioration if compromised

Question 3

Obstetric effect on oxygen dissociation curve

Answer 3

Question 4

Obstetric circulation

Answer 4

Blood volume increases by 40% (plasma volume&raquo_space; RBC volume —> anaemia of pregnancy)
Increased cardiac output (both HR and stroke volume)
Reduced SVR
Reduced diastolic and systolic BP (low point 26 weeks, normal at term) (NB if low likely to be pathological: don’t dismiss as being normal offhand)
Unchanged CVP
Reduced baroreceptor reflex

Aortocaval compression —> left lateral position.

Question 5

Foetal blood supply

Answer 5

not autoregulated: foetal distress if lie patient on their back due to reduced blood flow to placental arteries

Question 6

ECG changes in pregnancy

Answer 6

LAD, TWI in lateral leads

This happens because of physical cardiac shift up and to the left due to the gravity uterus

Question 7

Uterine physiology postpartum

Answer 7

300-500ml auto transfused blood, assisted by uterotonics
Blood loss well tolerated
Phenylephrine/norad first line agents

Question 8

Obstetric neurology

Answer 8

Increased sensitivity to anaesthetic drugs
Increased sensitivity to LA (? Progesterone effect)
Engorged epidural veins
Lumbar cistern stretched/squashed

Question 9

Obstetric renal effects

Answer 9

Renal vasodilation 
Increased renal size and blood flow
Leads to reduced urea and creatinine
Can lead to false reassurance when developing an AKI leading to underestimation
Activation of RAAS

Question 10

Obstetric Endocrine physiology

Answer 10

Placental hormones: relaxin (ligamentous relaxation, NO pathway so vascular relaxation too),
Oxytocin and vasopressin: oxytocin (uterine contractions, but vasodilatation leading to hypotension), vasopressin (similar structurally so can also cause uterine contractions)
Insulin resistance from the second trimester (cortisol and human placental growth hormone) leads to insulin levels rising 2-3x. Leads to greater placental transfer to baby. This sometimes leads to gestational diabetes.
Thyroid hormone production increases due to molecular mimicry. Tend to be euthyroid as TBG also increases.

Question 11

Obstetric clotting

Answer 11

Pro-thrombotic state
Separation of the placenta leads to exposure of the intima and therefore increased hypercoagulability
Most clotting factors increased, protein C/S reduced too.
Stasis, trauma, hypercoagulability. - virchow’s triad

Give LMWH if in hospital, stop before labour/Caesarian section