The features of supine hypotensive syndrome were then elucidated. It occurs in:
1. late pregnancy,
2. the supine, and to a lesser extent, the sitting position, and
3. more frequently in those with varicose veins.
It is caused by compression of the inferior vena cava (IVC) by the gravid uterus with a consequent reduction in venous return. Three to seven minutes are generally required for significant hypotension to become manifest (2). Supine hypotension is most severe in the latent stage of labour and is more severe in non-labouring patients undergoing caesarean section than those who are labouring (6, 7). The magnitude of IVC compression is reduced during contractions because the uterus rides away from the IVC (2). Supine hypotension is cured by delivery.
Two compensatory mechanisms are available for attenuating the degree of hypotension which occurs as a result of impairment of venous return. Firstly, there may be a generalised increase in sympathetic tone and, secondly, the internal vertebral venous plexus and the azygos vein can act as a collateral conduit for blood returning from the lower part of the body (Figure 28.1).
It was subsequently recognised that aortic compression could be as important as caval compression in the generation of decreased utero-placetal perfusion and fetal distress.
During labour, aortic compression occurs almost exclusively during uterine contractions. It occurs in up to 86% of parturients. It is less dependent upon posture and less responsive to lateral tilt than IVC compression (4, 5). Compression of the aorta occurs at the level of maximal lumbar lordosis (L4 - L5).
'Aortocaval compression' is a blanket term which describes compression of the inferior vena cava and the aorta by the gravid uterus in women at term (1, 2, 3, 4). On assuming the supine position, 46% of women at term develop brachial and femoral hypotension; a further 31% develop femoral hypotension in the absence of brachial hypotension (10). This has implications for both mother and fetus. Maternal hypotension as measured by a reduction in brachial artery blood pressure, occurs as a result of a diminution in venous return. It is most pronounced in hypovolaemic states, either actual, as occurs with haemorrhage, or relative, as occurs following sympathetic blockade. Acute fetal distress can be caused by: 1. hypoperfusion of the uteroplacental unit secondary to maternal hypotension, or 2. occult aortic compression (in the presence of a normal maternal brachial arterial blood pressure) causing a reduction in iliac arterial flow (8) (Chapter 76).
The efficacy of left lateral displacement was demonstrated in 1972 (9). The full left or right lateral position completely relieves aortocaval compression (Figure 28.2). Elevating the mother's right hip 10-15cm completely relieves aortocaval compression in 58% of term parturients (1, 5, 8).
Lateral displacement remains an important technique in the prevention of supine hypotension and in the management of hypotension in all women during late pregnancy.
References:
1. Leighton BL: Anaesthetic Complications:Intraoperative. in: Obstetric Anesthesia Norris MC (ed), JB Lippincott Co. Philadelphia, 1993; p.616-618.
2. Howard BK, Goodson JH, Mengert WF. Supine hypotensive syndrome in late pregnancy. Obstet Gynecol 1953; 1: 371.
3. Wright L. Postural hypotension in late pregnancy Br. Med. J. 1962; 1: 760.
4. Goodlin RC. Importance of the lateral position during labor. Obstet Gynecol 1971 37:698.
6. Clark RB, Thompson DS, Thompson CH. Prevention of spinal hypotension associated with cesarean section. Anesthesiology 1976 45: 670.
7. Brizgys RV, Dailey PA, Schnider SM, Kotelko DM, Levinson G. The incidence and neonatal effects of maternal hypotension during epidural anesthesia for cesarean section Anesthesiology 1987 67:782.
Footnote:
Recent papers on this subject include those by: