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Maternal Physiology
Dr Kapila Hettiarachchi
Consultant Anaesthetist
SBSCH – Peradeniya
Sri Lanka
Hemodynamic
Changes
Systemic vascular resistance
Falls steadily over the first 20 weeks
primary cause
Erosion of maternal
resistance vessels
by the fetal
placenta
Progesterone
Dilate
cutaneous
and renal
vascular
Cardiac output
Cardiac output increase by 40-50%
Stroke Volume - 20-30%
Heart rate - 10-15%
Cardiac output
Stroke Volume
begins to rise very early (20–30%)
in pregnancy, mediated by an increase in
preload and contractility
Preload
Na+ and water retention
Placental hormones potentiate
Renin– angiotensin–aldosterone
system and thirst
Contractility
Sustained increases in cardiac output
Stimulate ventricular hypertrophy
• The heart is physiologically dilated and displaced in both cephalad and lateral directions.
• A normal pregnancy ECG may have 15 – 200
left axis deviation and T waves may be
inverted in lateral leads and lead III mimicking
left ventricular hypertrophy and other
structural disease.
Mean arterial pressure
Diastolic blood pressure falls
Pulse pressure widens
1. CO
2. Heart rate
3. Mean arterial pressure
4. Systemic vascular resistance
Increased diastolic runoff
Blood escapes the arterial system
more easily during diastole
Windkessel Effect
Evens out pressure and flow through the vasculature
over time
C. Physiologic anaemia
Plasma volume
increase by
40%–50%
Red blood cell
increase by
25%–35%
Physiologic benefit
Reduces blood viscosity
So, reduces
shear stress
Shear stress
high velocity to support
the sustained increases in cardiac out put
High-velocity flow increases shear stress on
the vascular lining, where it could become
damaging
Shear stress
When blood velocity and viscosity
increases Shear stress is increased
Reynolds equation
Haematocrit is the primary determinant of
blood viscosity
Anaemia reduces shear stress levels and lessens
the risk of vascular endothelial damage
Reynolds equation
The likelihood of turbulence can be predicted
NR is Reynolds number,
v is mean blood velocity,
d is vessel diameter,
ρ (rho) is blood density,
η is blood viscosity.
2. Murmurs
Functional murmurs
Venous hum
Cardiovascular Changes in Pregnancy
Variable
Heart rate
Stroke volume
Systolic blood pressure
Change
Increased
Increased
Increased
% change
20–30%
10–15% 2nd trimester
Diastolic blood pressure
Decreased
20–50%
Cardiac output
Systemic vascular resistance
Pulmonary vascular
resistance
PCWP
Central venous pressure
Increased
Decreased
Decreased
40–50% by 3rd trimest
20%
30%
Unchanged
Unchanged
Aortocaval Compression
Compensation occurs through
sympathetic stimulation and
collateral venous return via vertebral plexus
and azygous veins
Aortocaval Compression
• By 38–40 weeks gestational age, there is a 25
– 30% decrease in CO when turning from the
lateral to the supine position.
Blood flow to the
nasal mucosa is increased
Increase in blood flow to the skin, resulting in
warm, clammy hands and feet
Dissipate heat from the metabolically active
feto-placental unit
oEdema
Fetus, placenta, and amniotic fluid = ~8–10 kg
at term compresses inferior vena cava and other
smaller veins
oEdema
Compression causes venous pressures in the
lower extremities to rise
This causes
Increases mean capillary pressure and
Increases net fluid filtration from blood to the
interstitium
oEdema
Fall in colloid osmotic pressure
by 30%– 40% during
pregnancy
(from ~25 mm Hg prior to pregnancy to ~15
mm Hg postpartum)
Respiratory system
O2 demands
of the mother and growing fetus increase
rapidly during pregnancy
O2 consumption at term is
increased ~ 30%
Progesterone exerts a stimulant
action on the
respiratory centre and carotid
body receptors
Respiratory system
Progressive increase in minute ventilation
to ~50% over non-pregnant values during the
second trimester
Respiratory system
What is minute ventilation ?
Respiratory system
Minute ventilation increase is mainly by
An increase in tidal volume and
Small or no rise in respiratory rate
(2–3 breaths/min)
Respiratory system
Net effect is that
PaO2 rises by ~10 mm Hg,
and PaCO2 falls by ~8 mm Hg,
causing a slight respiratory alkalosis (<0.1 pH )
Respiratory system
20% decrease in
Functional residual capacity (FRC)
Expiratory reserve capacity (ERC)
Residual volume (RV)
caused by a rise in the diaphragm
Changes in Respiratory Function in Pregnancy
Variable
Non-Pregnant
Term
Pregnancy
Tidal volume ↑
450 mL
650 mL
Respiratory rate
16 min–1
16 min–1
Vital capacity
3200 mL
3200 mL
Inspiratory reserve volume
2050 mL
2050 mL
Expiratory reserve volume ↓
700 mL
500 mL
Functional residual capacity ↓
1600 mL
1300 mL
Residual volume ↓
1000 mL
800 mL
PaO2 slight ↑
11.3 kPa
12.3 kPa
PaCO2 ↓
4.7–5.3 kPa
4 kPa
pH slightly ↑
7.40
7.44
Renal blood flow is increased
Renal
Glomerular Filtration
Rate (GFR) rises
steadily to
~50% above normal
values at 16 weeks’
gestation
Renal Changes in Pregnancy
Parameter
NonPregnant
Pregnant
Urea (mmol L
2.5–6.7
2.3–4.3
70–150
50–75
200–350
150–350
22–26
18–26
−1)
Creatinine
(μmol L−1)
Urate (μmol L
−1)
Bicarbonate (mmol L
−1)
Aldosterone
• Action is enhanced to increase water
absorption causing increase in volume of
distribution.
Gastrointestinal Changes
Heart burn due to reduction in lower
oesophageal sphincter tone (but not upper
oesophageal sphincter) and cephalad passage
of acidic gastric content.
Increase in intragastric pressure and altered axis
due to upward movement of gravid uterus.
Gastrointestinal Changes
Gastrointestinal motility decreases but gastric
emptying is not delayed during pregnancy
However, it is delayed during labour but returns
to normal by 18 h after delivery
GI effects return to pre-pregnancy level in 24-48hrs
Liver Function Changes in Pregnancy
Parameter
Change in
Pregnancy
Albumin
Decreased
Alkaline phosphatase
Increased (from placenta)
ALT/AST
No change
Plasma cholinesterase
Decreased
NO increase in Liver blood
flow
Pregnancy induces a hypercoagulable state
Coagulation Changes in Late Pregnancy
Fibrinolysis – increased
Platelet function not changed
Haematological Changes Associated with Pregnancy
Variable
NonPregnant
Pregnant
Haemoglobin
14 g dL–1
12 g dL–1
Haematocrit
0.40–0.42
0.31–0.34
Red cell count
4.2 × 1012 L–1
3.8 × 1012 L–1
White cell count
6.0 × 109 L–1
9.0 × 109 L–1
ESR
10
58–68
Platelets
150–400 × 109 L–1
120–400 × 109 L–1
Haematological changes
Fibrinogen increased from 2.5 (non-pregnant
value) to 4.6–6.0 g L–1
Factor II slightly increased
Factor V slightly increased
Factor VII increased 10-fold
Factor VIII increased – twice non-pregnant
state
Factor IX increased
Factor X increased
Factor XII increased 30–40%
Plasminogen unchanged
Plasminogen activator reduced
Plasminogen inhibitor increased
Fibrinogen-stabilizing factor falls
gradually to 50% of non-pregnant
value
Factor XI decreased 60–70%
Factor XIII decreased 40–50%
Antithrombin IIIa decreased slightly
23. Features of Mendelson’s syndrome include:
a) Urticarial rash
b) Bronchospasm
c) Hypoxia
d) Hypotension
e) Aspiration of at least 100 ml of gastric
contents
• 23. FTTFF
2. Physiology of pregnancy: clinical anaesthetic implications
Compared with the non-gravid state, increased cardiac output in
pregnancy:
1. Occurs as a result of a high-flow, high-resistance
circulation.
2. Is likely to lead to non-pathological systolic and
diastolic murmurs.
3. Is associated with an electrocardiogram (ECG) that is
similar to that during pulmonary embolism.
4. Is likely to be reduced by aortocaval compression in
the first, second and third trimesters.
5. Combined with an altered haemoglobin
concentration, leads to an increase in oxygen delivery.
FTFTT
18. Appropriate statements regarding the respiratory system in
pregnant patients compared with non-pregnant patients
include:
1. There is a reduction in airway resistance.
2. Reduced functional residual capacity (FRC)
increases alveolar dead space.
3. Reduced FRC is expected to be associated with a
reduction in the rate of increase in
concentration of volatile anaesthetic agents.
4. Increased minute ventilation during labour can
cause acidaemia in the fetus.
5. During preoxygenation, denitrogenation is likely
to occur quickly.
• TFFTT
19. During pregnancy:
1. Urine glucose is helpful in assessing diabetic
control in pregnancy.
2. Thyroid function testing should include both
thyroid-stimulating hormone and free thyroxine.
3. Raised alkaline phosphatase is usually indicative
of liver disease.
4. Having normal renal functions is clinically
significant in pregnancy.
5. Proton pump inhibitors (PPIs) are
contraindicated.
19.
•
•
•
•
•
1. F
2. T
3. F
4. T
5. F
20. The following physiological
changes occur in normal pregnancy:
(a) Progesterone increases the sensitivity of the
respiratory center to carbondioxide.
(b) Systemic vascular resistance is increased in
trimesters I and II.
(c) Central venous pressure increases.
(d) Gastric emptying is delayed.
(e) FRC decreases to 80% of pre-pregnancy values.
20. The following physiological changes occur in normal pregnancy:
(a) True; (b) False; (c) False; (d) False; (e) True
(a) It also acts as a primary respiratory stimulant and the effects are
enhanced by oestrogen.
(b) Systemic vascular resistance decreases by 25--30%, the effect
mediated by progesterone, prostacyclin and oestrogen.
(c) Central venous pressure and pulmonary artery pressure are
unchanged during normal pregnancy. During labour each uterine
contraction expels 500 ml of blood into the circulation which produces
an increase in central venous pressure of 4--6 cm H2O.
21. Pregnancy-induced changes in lung volumes
cause:
• (a) Desaturation to occur more rapidly than in
non-pregnant patients.
• (b) Pre-oxygenation to be more effective.
• (c) A fall in minute ventilation due to
restricted diaphragmatic excursion.
• (d) Airway closure in the erect position in 50%
of parturients at term.
• (e) An increase in PaCO2.
21. Pregnancy-induced changes in lung volumes cause:
(a) True; (b) False; (c) False; (d) False; (e) False
• (a,b) The residual volume and the functional residual
capacity are reduced in pregnancy causing a decrease
in the O2 storage capacity. Thus, desaturation occurs
much faster and pre-oxygenation, although still
recommended, is less effective.
• (c) Although the diaphragm is displaced in later
pregnancy, an increase in the diameter of the chest
ensures increased minute volumes.
• (d) Airway closure occurs in the supine position. (e)
PaCO2 decreases as a result of an increased minute
ventilation.
22. In the third trimester of pregnancy:
• (a) A mild elevation of g-GT and ALT is abnormal.
• (b) Alkaline phosphatase plasma concentrations
return to normal.
• (c) A plasma creatinine concentration of 120
μmol l–1 is a normal finding.
• (d) A plasma urate concentration of 0.5 mmol l–1
is consistent with the diagnosis of pre-eclampsia.
• (e) The platelet count is frequently slightly
decreased.
22. In the third trimester of pregnancy:
(a) False; (b) False; (c) False; (d) True; (e) True
• (a) Mildly elevated liver enzymes are a normal
finding throughout pregnancy.
• (b) Alkaline phosphatase is produced in the
placenta and is often increased 2-fold compared
with non-pregnant women.
• (d) The upper normal limit for urate in pregnancy
is 0.35 mmol l–1 and urate is frequently elevated
in preeclampsia.
• (e) The platelet count tends to be slightly lower
than in non-pregnant women.
23. Aortocaval compression:
• (a) Does not occur before the end of the first
trimester.
• (b) Is symptomatic in about 10% of parturients in
the third trimester.
• (c) Can be unmasked by the institution of
effective epidural analgesia.
• (d) May occur on induction of general
anaesthesia despite a wedge under the
parturients right hip.
• (e) Can cause fetal hypoxaemia.
23. Aortocaval compression:
(a) False; (b) True; (c) True; (d) True; (e) True
• (a) Aortocaval compression usually occurs after
20 weeks’ gestation but may occur before. (b–e)
Aortocaval compression is only symptomatic in
about 10% of parturients but may be unmasked
by general, spinal anaesthesia, epidural
anaesthesia and sedation.A 15° left lateral tilt or
a wedge under the right hip have been described
to treat symptomatic aortocaval compression but
manual displacement of the uterus may
occasionally be necessary to treat its symptoms.
Untreated it will eventually lead to fetal
hypoxaemia.
24. The following changes occur in the gastro-intestinal
system during pregnancy:
• (a) Gastric emptying is delayed in the third
trimester.
• (b) Lower oesophageal sphincter pressure
decreases as a result of progesterone-mediated
smooth muscle relaxation.
• (c) Upper oesophageal sphincter pressure
decreases as a result of progesterone-mediated
smooth muscle relaxation.
• (d) Gastric volume increases in labour.
• (e) 80% of term parturients suffer from gastrooesophageal reflux.
24. The following changes occur in the gastro-intestinal system
during pregnancy:
(a) False; (b) True; (c) False; (d) True; (e) True
• (a) Although this has been claimed in the past, a
review of the literature reveals no evidence to
support this. (b–e) Gastro-oesophageal reflux is
due to the relaxation of the lower oesophageal
sphincter.The upper oesophageal sphincter is
made up from striated muscle which is not
affected by progesterone and therefore maintains
its tone. Only under sedation or general
anaesthesia and muscle relaxation is upper
oesophageal sphincter tone lost and aspiration of
gastric contents becomes a danger.
25. The following changes to the coagulation system are normal
in pregnancy:
• (a) The platelet count decreases to 50 000
mm–3.
• (b) Parturients are hypercoagulable.
• (c) There is decreased fibrinolysis.
• (d) Platelet function increases in pregnancy.
• (e) Clotting screens will usually be reported as
normal.
25. The following changes to the coagulation system are normal
in pregnancy:
(a) False; (b) True; (c) False; (d) False; (e) True
• (a) Although the platelet count decreases in
pregnancy it is only <100 000 mm–3 in 2% of
parturients.
• (b–e) There is an increase in most coagulation
factors and the coagulation system is activated.
As a result of increased coagulation, there has to
be increased fibrinolysis. Platelet function
remains normal throughout pregnancy. It is
activity and consumption that are increased. In
routine clotting tests, the changes to the
coagulation system are not detected.