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Editor's Notes

• #6: Samson and Young Anaesthesia 1987; 42: 487-90 looked at 1980 obstetric patients and found the incidence of failed intubation to be 1: 280 vs 1:2230 for non-obstetric patients. No obvious anatomical abnormalities but in 6:7 MPIV. Rocke showed impossible intubation in 1:750 and very difficult in 2%.
• #7: 4 cm rise of diaphragm due to gravid uterus Causes FRC to fall (to a value of 500ml) FRC falls by 5th month to 20% sitting and 30% supine Increase in transverse and AP diameters of chest wall may compensate for elevation of diaphragm, so there's no change in TLC. Diaphragm not splinted but moves freely Therefore increased diaphragmatic excursion and reduced chest wall movement
• #8: Data on respiratory rate variable Data on dead space variable - likely that it is increased due to dilatation of smaller bronchioles ?? lung compliance changes
• #9: Progesterone virtually undetectable in CSF Oestrogen has weak hyperventilation effect Progesterone and oestrogen act synergistically Increasing carbonic anhydrase facilitates CO2 transfer which tends to decrease PCO2 independendly of any change to ventilation
• #10: Same as 14,000 feet
• #12: AVO2 difference reduces impact of venous admixture on PaO2
• #14: The decrease in AVO2 difference in early pregnancy is due to increase in cardiac output that is proportionately greater than the increase in O2 consumption As pregnancy progresses, O2 consumption continues to increase while cardiac output increases to a lesser degree resulting in decreased mixed venous oxygen content with a rising AVO2 difference AVO2 difference == 33 ml / l in 3rd month vs 45 ml / l in 9th month (non-pregnant value) This results in the small but progressive fall in PaO2 in the 2nd and 3rd trimesters Although arterial pH is essentially normal venous pH is higher than the normal value of 7.35 at 7.38
• #17: Following 5 minutes of pre-oxygenation, the PaO2 in parturients was 63 kPa VS 67.6 kPa in non-pregnant women During apnoea, PaO2 falls by 18 kPa / min vs 7.7 kPa in non-pregnant women The decreased cardiac output due to aortocaval compression contributes to hypoxaemia because it causes a reduction in mixed venous oxygen content and increased AVO2 difference Ventilate obstetric patients to a PCO2 of 4kPa or an acute respiratory acidosis ensues. Therefore use a MV of 121L/kg/min. Since PCO2 reaches 4kPa in T1 this also follows for anaesthesia at this stage. Avoid hyperventilation as can cause fetal hypoxaemia due to decreased cardiac output (  venous return 2° IPPV +  umbilical blood flow 2°  PCO2) Epidurals prevent hyperventilation (due to painful contractions) and increase VO2.
• #21: N.B: Normal pregnancy with fixed cardiac pacemaker
• #23: Normally, with a sphygmomanometer, SBP is 3-4 mmHg too low and DBP is 8 mmHg too high. The error in any single measurement is  8 mmHg. In pregnancy, both are overestimated, SBP by 7 mmHg and DBP by 12 mmHg. SBP does not increase due to increases aortic compliance / size.
• #24: CO increases due to vasodilatation secondary to oestrogen, PGs, and calcitonin-GRP. The effect of these mediators is to increase blood flow to the uterus, skin and kidneys. Since CO is increased and BP remains virtually the same, TPR must decrease. Normal value for TPR = 1700 The increases in TPR from T2 to T4 may be due to aortic compression.
• #25: Hydrodynamic obstruction is due to outflow of blood at a relatively high pressure from the uterus (probably only important during uterine contractions). N.B: Remember aortic compression too !
• #26: In many women with SHS, evidence of lack of any collateral circulation through the vertebral and azygous venous systems. Renal veins may also be affected.