Preventing and treating hypotension during spinal anaesthesia for caesarean section

Spinal anaesthesia is often used for Caesarean section because of speed, reliability, low placental drug transfer, and the benefits of the mother being awake during surgery. However, in comparison with epidural anaesthesia, spinal anaesthesia causes more severe and more frequent hypotension that may led to adverse outcomes for both the mother and fetus if not treated or prevented.¹

Cardiovascular responses to spinal anaesthesia

Spinal anaesthesia results in sympathetic vasomotor blockade leading to decreased systemic vascular resistance, primarily from arterial dilation but with some venodilation. In healthy individuals compensation is mediated via baroreceptors, resulting in increased HR and stroke volume, and vasoconstriction in the unblocked segments.²

In the term pregnant woman, baseline HR, stroke volume, and cardiac output are already increased to meet the metabolic demands of the fetus, impairing the ability of the cardiovascular system to compensate. The supine position causes the gravid uterus to compress the inferior vena cava, reducing venous return and cardiac output.

Definition and incidence of hypotension

Definitions of hypotension in research studies use a decrease in the absolute value of systolic arterial pressure (SAP; usual threshold between <80 and <100 mmHg), a decrease compared with a baseline value, or a combination.

In clinical practice a baseline SAP taken in the operating theatre may be artificially increased; in a recent study median baseline SAP values at elective Caesarean section were 15 mmHg higher than that measured on the morning of surgery, and 20 mmHg higher than that measured at the last antenatal clinic visit.³

Hypotension after spinal anaesthesia has been found to occur in the majority of elective cases when a robust strategy for prevention and management was not followed. The incidence of extreme hypotension, defined as SAP <75% of baseline, has been reported as 38%.⁴

Adverse effects of hypotension

Hypotension may lead to poor placental perfusion. In the early days of spinal anaesthesia for Caesarean section, severe or prolonged hypotension was associated with fetal acidosis, lower Apgar scores, and even neonatal neurobehavioural changes at 4–7 days old. However, with modern management as described below, the differences in neonatal blood gases and pH between alternative drugs or regimens are not significant clinically, and are often not statistically significant.⁵

Therefore, an important reason nowadays for effective systemic arterial BP control before delivery of the neonate is to reduce nausea and vomiting, thought to occur because of reduced brainstem perfusion and ischaemia in the vomiting centre. The focus of management should be on prevention of hypotension, rather than reactive treatment once it has developed. This was well demonstrated in a study where a phenylephrine infusion was used in an attempt to maintain SAP at ≥100%, ≥90%, or ≥80% of baseline. Nausea and vomiting occurred in 40% of the ≥80% group vs 4% of the ≥100% group (p=0.006), a 10-fold difference.⁵

The incidences of nausea and vomiting after delivery are considerably lower than before delivery, and tight arterial pressure control is no longer required at this stage.

Prevention and treatment of hypotension

The mainstay of management is effective use of a vasopressor drug. Adjunctive prophylactic measures consist of left lateral displacement of the uterus using table tilting or a wedge, aiming for at least 15° of pelvic tilt, and i.v. fluids. Preloading with i.v. crystalloid fluids before spinal anaesthesia has been found to be largely ineffective in reducing hypotension. Preloading with i.v. colloids is more effective, but this is rarely used in the UK. The recommendation is therefore to use a free-flowing infusion of 1 L crystalloid during the onset of spinal anaesthesia, using a pressure bag if required, immediately after the spinal injection.

Choice of vasopressor drug

There is good evidence that ephedrine, which is predominantly a $\mathrm{\beta }-$adrenergic agonist, causes fetal acidosis when used to prevent or treat hypotension. It crosses the placenta and has direct sympathomimetic effects in the fetus.⁶ This leads to a degree of acidaemia, although the incidence of defined fetal acidosis (umbilical artery pH<7.2) is not changed.

Alpha-adrenergic agonists are therefore preferred. These have a variable amount of accompanying $\mathrm{\beta }-$activity. Phenylephrine, a pure $\mathrm{\alpha }-$agonist, is the standard choice because of the amount of supporting data available, including studies to assess optimal dosage regimens. However, it carries a higher risk of maternal bradycardia than mixed agonists, because baroreceptor activation is unopposed when systemic arterial pressure is increased.

Other α-agonists that have some $\mathrm{\beta }-$activity include metaraminol and noradrenaline (norepinephrine). These agents may have a preferable profile for preserving cardiac output by promoting cardiac positive inotropy and maintaining HR. A recent network meta-analysis has suggested that they are less likely to adversely affect the fetal acid–base status than phenylephrine, although further direct comparison studies are warranted.⁷ Metaraminol is associated with a higher incidence of reactive hypertension than phenylephrine.⁸ There are concerns around tissue necrosis after extravasation of noradrenaline when administered peripherally, and many organisations only permit infusions via a central venous catheter.

Strategy for using vasopressors

• •It is important to use an accurate baseline SAP; this should be a reading taken before coming to the operating theatre. We recommend documenting this, as well as calculated values for 90% and 80% baseline SAP, and displaying prominently.
• •An infusion of an α-agonist should be started immediately after injection of the spinal anaesthetic, with the goal of maintaining SAP at ≥90% baseline. We suggest a starting rate of phenylephrine 15–30 ml h⁻¹ at 100 μg ml⁻¹ concentration (25–50 μg min⁻¹), which can be altered in 5–10 ml h⁻¹ increments in response to SAP<90% or hypertension. If SAP<80%, then 100 μg rescue boluses should be given.
• •Hypotension combined with a low HR should be treated with ephedrine 3–6 mg if SAP<90%; or an anticholinergic (glycopyrrolate or atropine) if SAP<80% baseline and HR<60 beats min⁻¹.
• •After delivery, the phenylephrine may be weaned rapidly over approximately 5 min, accepting some hypotension if the patient is asymptomatic; but note that oxytocin and carbetocin may precipitate further hypotension. Ongoing hypotension at the end of the case may be associated with hidden blood loss, dehydration, or cardiovascular problems and a full assessment is advised.
• •In resource-limited environments, boluses of phenylephrine (50–100 μg), ephedrine (10 mg), metaraminol (0.5 mg), or adrenaline (10 μg) are recommended to keep SAP ≥90% baseline and HR≤120% baseline.

Special situations

Hypotension is less frequent and severe during Caesarean section in labouring women; spinal anaesthesia should not be delayed to set up a vasopressor infusion in Category 1 cases.

Phenylephrine has the same advantages over ephedrine in women with pre-eclampsia. The dose requirement is lower, and therefore the starting infusion rate should be reduced. The aim should be to avoid a rapid decrease in arterial pressure that may reduce uteroplacental blood flow to an already-compromised fetus.

Conclusions

Intraoperative hypotension is common after spinal anaesthesia for Caesarean section. Inadequate treatment may lead to significant maternal, fetal, or both adverse outcomes.

Consensus guidelines for management of hypotension during Caesarean section have recommended a standard approach and include detailed guidance on how to introduce phenylephrine infusions into practice. Other agents with a preferable adrenergic profile may be the focus of further study.

Declaration of interests

The authors declare that they have no conflicts of interest.

Biographies

Jonathan Bower MRCP FRCA is a clinical fellow in anaesthesia at University Hospitals Bristol and Weston NHS Trust.

Stephen Michael Kinsella FCAI is a consultant obstetric anaesthetist at St Michael's Hospital Bristol.

Matrix codes: 1A01, 2B03, 3B00