DISCUSSION
The principal finding of our study was that during labour and the first
two hours postpartum, SI increased significantly in patients with NLA
compared to those without NLA. The difference between the groups
remained significant after adjusting for confounders. The increase in SI
was statistically and clinically significant, with a difference of 0.04
to 0.10 observed between groups (NLA and without NLA). According to
previous references, the expected variation in SI in the postpartum
period ranged from 0.7 to 0.9.13–16. Thus, a change
in SI above a specific level of 0.9 implies significant blood loss,
haemodynamic instability, and an increased risk of adverse outcomes.
Although small, a change of 0.05-0.1 in SI is of substantial relevance
in this setting.
Using a prospectively collected high-quality dataset from two hospitals,
we describe the most extensive set of SI values gathered longitudinally
in patients with and without NLA. A previous study by Nathan et al.,
which included 316 patients, noted that the SI was higher in those under
NLA (33% of their sample). The authors suggested that epidural
anaesthesia increased the mean SI by approximately
0.046.31. Other authors have explored the SI in
obstetric patients without reporting the NLA percentage used in their
population.9,10,12,28
Our data showed higher HR values during the postpartum period, with
similar SBP among patients with NLA compared to those without obstetric
analgesia. Extensive literature describes haemodynamic changes during
pregnancy and delivery, including an increase in HR and a decrease in
SBP at rest.29 These adaptations are more pronounced
during labour and the immediate postpartum period, probably due to pain,
medications, and maternal anxiety.30 During labour,
uterine contractions displace 300–500 mL of blood from the uterus into
the central circulation.31 Immediately postpartum,
there is an increase in cardiac output due to diminished lower extremity
venous pressure, sustained myometrial contraction, and loss of
low-resistance placental circulation.
Pregnancy increases the sympathetic system’s dependency on maintaining
haemodynamics, including the venous return and systemic vascular
resistance. This situation means that pregnant patients are at an
increased risk of hypotension and haemodynamic instability induced by
neuraxial analgesia and anaesthesia. Despite the advantages of epidural
analgesia over other techniques, this sympathetic block might explain
some of the increase in SI in our patients. Furthermore, a compensatory
mechanism needs to be activated in patients under NLA to maintain
haemodynamics after a decrease in systemic vascular resistance, which
generates a response based on a rise in HR.22 Another
potential explanation for the haemodynamic changes leading to a higher
SI in patients under NLA might be the addition of some medications, such
as uterotonics.32,33 Several studies suggest that
oxytocin induces a profound and transient decrease in both SBP and DBP
during caesarean delivery secondary to vasodilatation, with tachycardia
and an increase in cardiac output. This effect has been proposed as a
secondary to peripheral vasodilation.22,34,35
In a study by Munn et al.36, randomised women
undergoing intrapartum caesarean delivery received a prophylactic
infusion of oxytocin or bolus after delivery. A higher dose was
associated with clinically significant tachycardia and hypotension (SBP
of 100 mmHg or a decrease of ≥ 20% from baseline).
The increase in heart rate reported during the early first and second
stages of labour coincides with uterine contractions and bearing-down
efforts. This change in heart rate might be explained by the
displacement of blood from the choriodecidual space, increased venous
return to the heart, and increased catecholamine release due to pain and
other stimuli (anxiety). Additionally, during labour, uterine
contraction pain becomes more pronounced during the transition to the
second stage. This pain induces a neuroendocrine stress response,
increasing heart rate and cardiac output.37
Our results show that SI values between groups with and without NLA were
not modified by maternal age, parity, haemoglobin levels, gestational
age, or cervical dilation. Similarly, a previous study by our group
reported that labour, but not maternal anaemia, was associated with
lower SI values during the first and second stages of labour compared to
SI values in patients during the third trimester, possibly secondary to
maternal pain and anxiety.11
Our study has several limitations. The main weakness is the
nonrandomised and direct relationship between NLA exposure and SI
between centres, given that only one of the centres includes NLA during
labour. This relationship may be inseparable from the association
between the centre and SI. The unmatched analysis for oxytocin use
limited an interpretation of the SI differences among the studied
groups; consequently, we cannot explain whether NLA, oxytocin or both
were the reasons for the significant differences in SI.
Additionally, the study design was restricted to pain management between
the two clinical sites, implying differences in other interventions
during labour, such as fluid management and other medications with
potential influence on SI values. Despite this, we believe that the
adjustments for clinical variables and the repeated measures analysis
through labour and the postpartum period ameliorated biases associated
with these differences in clinical practice. Another limitation was that
almost all our patients were under the epidural technique; hence, the
variation in SI observed should be interpreted cautiously in patients
under NLA administered via different techniques. Other variables, such
as top-up interventions for inadequate analgesia, duration of neuraxial
analgesia, use of uterotonics other than oxytocin, and volume of blood
loss, were not collected; therefore, adjustments for these possible
confounders were not possible.
We did not consider the amount of blood loss in our analysis because our
study did not focus on patients with PPH. However, we categorised
patients according to the presence of PPH, without differences between
the groups.
The strengths of this study are its prospective collection of data in
different phases of the postpartum period for two groups (with and
without NLA). Future studies should include a larger sample of patients
with PPH and consider other potential confounders to establish reliable
cut-off values for SI values.