Cardiovascular Journal of Africa: Vol 27 No 2 (March/April 2016)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 2, March/April 2016 AFRICA 89
Physiological changes in pregnancy
Priya Soma-Pillay, Catherine Nelson-Piercy, Heli Tolppanen, Alexandre Mebazaa
Abstract
Physiological changes occur in pregnancy to nurture the
developing foetus and prepare the mother for labour and
delivery. Some of these changes influence normal biochemical
values while others may mimic symptoms of medical disease.
It is important to differentiate between normal physiological
changes and disease pathology. This review highlights the
important changes that take place during normal pregnancy.
Keywords: hypercoagulable state, diabetogenic, uterine contrac-
tions
Submitted 31/8/15, accepted 4/3/16
Cardiovasc J Afr 2016; 27: 89–94
DOI: 10.5830/CVJA-2016-021
During pregnancy, the pregnant mother undergoes significant
anatomical and physiological changes in order to nurture and
accommodate the developing foetus. These changes begin after
conception and affect every organ system in the body.1 For
most women experiencing an uncomplicated pregnancy, these
changes resolve after pregnancy with minimal residual effects.
It is important to understand the normal physiological changes
occurring in pregnancy as this will help differentiate from
adaptations that are abnormal.
Haematological changes
Plasma volume increases progressively throughout normal
pregnancy.2 Most of this 50% increase occurs by 34 weeks’
gestation and is proportional to the birthweight of the baby.
Because the expansion in plasma volume is greater than the
increase in red blood cell mass, there is a fall in haemoglobin
concentration, haematocrit and red blood cell count. Despite this
haemodilution, there is usually no change in mean corpuscular
volume (MCV) or mean corpuscular haemoglobin concentration
(MCHC).
The platelet count tends to fall progressively during normal
pregnancy, although it usually remains within normal limits.
In a proportion of women (5–10%), the count will reach levels
of 100–150 × 109 cells/l by term and this occurs in the absence
of any pathological process. In practice, therefore, a woman is
not considered to be thrombocytopenic in pregnancy until the
platelet count is less than 100 × 109 cells/l.
Pregnancy causes a two- to three-fold increase in the
requirement for iron, not only for haemoglobin synthesis but
also for for the foetus and the production of certain enzymes.
There is a 10- to 20-fold increase in folate requirements and a
two-fold increase in the requirement for vitamin B12.
Changes in the coagulation system during pregnancy
produce a physiological hypercoagulable state (in preparation
for haemostasis following delivery).3 The concentrations
of certain clotting factors, particularly VIII, IX and X, are
increased. Fibrinogen levels rise significantly by up to 50% and
fibrinolytic activity is decreased. Concentrations of endogenous
anticoagulants such as antithrombin and protein S decrease.
Thus pregnancy alters the balance within the coagulation system
in favour of clotting, predisposing the pregnant and postpartum
woman to venous thrombosis. This increased risk is present from
the first trimester and for at least 12 weeks following delivery. In
vitro tests of coagulation [activated partial thromboplastin time
(APTT), prothrombin time (PT) and thrombin time (TT)] remain
normal in the absence of anticoagulants or a coagulopathy.
Venous stasis in the lower limbs is associated with venodilation
and decreased flow, which is more marked on the left. This is due
to compression of the left iliac vein by the left iliac artery and
the ovarian artery. On the right, the iliac artery does not cross
the vein.
Cardiac changes
Changes in the cardiovascular system in pregnancy are profound
and begin early in pregnancy, such that by eight weeks’ gestation,
the cardiac output has already increased by 20%. The primary
event is probably peripheral vasodilatation. This is mediated
by endothelium-dependent factors, including nitric oxide
synthesis, upregulated by oestradiol and possibly vasodilatory
prostaglandins (PGI2). Peripheral vasodilation leads to a 25–30%
fall in systemic vascular resistance, and to compensate for this,
cardiac output increases by around 40% during pregnancy. This
is achieved predominantly via an increase in stroke volume, but
also to a lesser extent, an increase in heart rate. The maximum
cardiac output is found at about 20–28 weeks’ gestation. There is
a minimal fall at term.
Department of Obstetrics and Gynaecology, University of
Pretoria and Steve Biko Academic Hospital, Pretoria, South
Africa
Priya Soma-Pillay, MB ChB, MMed (O et G) Pret, FCOG, Cert
(Maternal and Foetal Med) SA,
Department of Obstetric Medicine, Women’s Health Academic
Centre, King’s Health Partners; Guy’s and St Thomas’
Foundation Trust, and Queen Charlotte’s and Chelsea
Hospital, Imperial College Healthcare Trust, London, UK
Catherine Nelson-Piercy, MA, FRCP, FRCOG
INSERM UMRS 942, Paris, France
Heli Tolppanen, MD
Alexandre Mebazaa, MD
Heart and Lung Centre, Helsinki University Central
Hospital, Finland
Heli Tolppanen, MD
University Paris Diderot, Sorbonne Paris Cité, Paris;
Department of Anesthesia and Critical Care, Hôpital
Lariboisière, APHP, France
Alexandre Mebazaa, MD