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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 2, March/April 2016
90
AFRICA
An increase in stroke volume is possible due to the early
increase in ventricular wall muscle mass and end-diastolic
volume (but not end-diastolic pressure) seen in pregnancy. The
heart is physiologically dilated and myocardial contractility
is increased. Although stroke volume declines towards term,
the increase in maternal heart rate (10–20 bpm) is maintained,
thus preserving the increased cardiac output. Blood pressure
decreases in the first and second trimesters but increases to
non-pregnant levels in the third trimester.
There is a profound effect of maternal position towards
term upon the haemodynamic profile of both the mother and
foetus. In the supine position, pressure of the gravid uterus on
the inferior vena cava (IVC) causes a reduction in venous return
to the heart and a consequent fall in stroke volume and cardiac
output. Turning from the lateral to the supine position may
result in a 25% reduction in cardiac output. Pregnant women
should therefore be nursed in the left or right lateral position
wherever possible. If the woman has to be kept on her back,
the pelvis should be rotated so that the uterus drops to the side
and off the IVC, and cardiac output and uteroplacental blood
flow are optimised. Reduced cardiac output is associated with
a reduction in uterine blood flow and therefore in placental
perfusion, which could compromise the foetus.
Although both blood volume and stroke volume increase
in pregnancy, pulmonary capillary wedge pressure and central
venous pressure do not increase significantly. Pulmonary vascular
resistance (PVR), like systemic vascular resistance (SVR),
decreases significantly in normal pregnancy. Although there is no
increase in pulmonary capillary wedge pressure (PCWP), serum
colloid osmotic pressure is reduced by 10–15%. The colloid
osmotic pressure/pulmonary capillary wedge pressure gradient
is reduced by about 30%, making pregnant women particularly
susceptible to pulmonary oedema. Pulmonary oedema will be
precipitated if there is either an increase in cardiac pre-load
(such as infusion of fluids) or increased pulmonary capillary
permeability (such as in pre-eclampsia) or both.
Labour is associated with further increases in cardiac output
(15% in the first stage and 50% in the second stage) Uterine
contractions lead to an auto-transfusion of 300–500 ml of blood
back into the circulation and the sympathetic response to pain
and anxiety further elevate the heart rate and blood pressure.
Cardiac output is increased between contractions but more so
during contractions.
Following delivery there is an immediate rise in cardiac
output due to relief of the inferior vena cava obstruction and
contraction of the uterus, which empties blood into the systemic
circulation. Cardiac output increases by 60–80%, followed by
a rapid decline to pre-labour values within about one hour of
delivery. Transfer of fluid from the extravascular space increases
venous return and stroke volume further.
Those women with cardiovascular compromise are therefore
most at risk of pulmorary oedema during the second stage of
labour and the immediate postpartum period. Cardiac output
has nearly returned to normal (pre-pregnancy values) two
weeks after delivery, although some pathological changes (e.g.
hypertension in pre-eclampsia) may take much longer.
The above physiological changes lead to changes on
cardiovascular examination that may be misinterpreted as
pathological by those unfamiliar with pregnancy. Changes may
include a bounding or collapsing pulse and an ejection systolic
murmur, present in over 90% of pregnant women. The murmur
may be loud and audible all over the precordium, with the first
heart sound loud and possibly sometimes a third heart sound.
There may be ectopic beats and peripheral oedema.
Normal findings on ECG in pregnancy that may partly relate
to changes in the position of the heart include:
•
atrial and ventricular ectopics
•
Q wave (small) and inverted T wave in lead III
•
ST-segment depression and T-wave inversion in the inferior
and lateral leads
•
left-axis shift of QRS.
Adaptive changes in renal vasculature
The primary adaptive mechanism in pregnancy is a marked fall
in systemic vascular resistance (SVR) occurring by week six of
gestation. The 40% fall in SVR also affects the renal vasculature.
4
Despite a major increase in plasma volume during pregnancy, the
massive decrease in SVR creates a state of arterial under-filling
because 85% of the volume resides in the venous circulation.
5
This arterial under-filling state is unique to pregnancy. The fall
in SVR is combined with increased renal blood flow and this is in
contrast to other states of arterial under-filling, such as cirrhosis,
sepsis or arterio-venous fistulas.
3,6
Relaxin, a peptide hormone produced by the corpus luteum,
decidua and placenta, plays an important role in the regulation
of haemodynamic and water metabolism during pregnancy.
Serum concentrations of relaxin, already elevated in the luteal
phase of the menstrual cycle, rise after conception to a peak at
the end of the first trimester and fall to an intermediate value
throughout the second and third trimester. Relaxin stimulates
the formation of endothelin, which in turn mediates vasodilation
of renal arteries via nitric oxide (NO) synthesis.
7
Despite activation of the renin–angiotensin–aldosterone
(RAA) system in early pregnancy, a simultaneous relative
resistance to angiotensin II develops, counterbalancing the
vasoconstrictive effect and allowing profound vasodilatation.
8
This insensitivity to angiotensin II may be explained by the
effects of progesterone and vascular endothelial growth factor-
mediated prostacyclin production, as well as modifications in
the angiotensin I receptors during pregnancy.
9
The vascular
refractoriness to angiotensin II may also be shared by other
vasoconstrictors such as adrenergic agonists and arginine
vasopressin (AVP).
10
It is possible that in the second half of
pregnancy, the placental vasodilatators are more important in
the maintenance of the vasodilatatory state.
6
Changes in renal anatomy and function
As a consequence of renal vasodilatation, renal plasma flow
and glomerular filtration rate (GFR) both increase, compared
to non-pregnant levels, by 40–65 and 50–85%, respectively. In
addition, the increase in plasma volume causes decreased oncotic
pressure in the glomeruli, with a subsequent rise in GFR.
11
Vascular resistance decreases in both the renal afferent and
efferent arterioles and therefore, despite the massive increase in
renal plasma flow, glomerular hydrostatic pressure remains stable,
avoiding the development of glomerular hypertension. As the
GFR rises, both serum creatinine and urea concentrations decrease
to mean values of about 44.2 μmol/l and 3.2 mmol/l, respectively.