Maternal Physiology Dr K S Hettiarachchi Consultant Anaesthetist SBSCH – Peradeniya Sri Lanka
Maternal Physiology
Dr K S HettiarachchiConsultant AnaesthetistSBSCH – PeradeniyaSri Lanka
Hemodynamic Changes
Systemic vascular resistance
Falls steadily over the first 20 weeks
primary cause
Erosion of maternal resistance vessels by the fetal placenta
Dilate cutaneous and renal vascular beds
Progesterone
Cardiac output
Cardiac output
Heart rate (10-15%)
Stroke Volume begins to rise very early (20–30%)in pregnancy, mediated by an increase in
preload and contractility
Cardiac output
Preload
Na+ and water retention
Placental hormones potentiate
Renin– angiotensin–aldosterone system and thirst
Contractility
Sustained increases in cardiac output also Stimulate
ventricular hypertrophy
Mean arterial pressure
Diastolic blood pressure falls Pulse pressure widens
Increased diastolic runoff
Blood escapes the arterial system
more easily during diastole
Evens out pressure and flow through the vasculature over time
Windkessel Effect
C. Physiologic anaemia
Plasma volume
increase by
40%–50%
Red blood cell production 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
blood velocity Shear stress
and viscosity
Reynolds equation
Haematocrit is the primary determinant of
blood viscosity
Anaemia reduces 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 PregnancyVariable Change % changeHeart rate Increased 20–30%Stroke volume Increased 10–15% 2nd trimesterSystolic blood pressure Increased
Diastolic blood pressure Decreased 20–50%
Cardiac output Increased 40–50% by 3rd trimester
Systemic vascular resistance Decreased 20%Pulmonary vascular resistance
Decreased 30%
PCWP UnchangedCentral venous pressure Unchanged
Aortocaval Compression
Compensation occurs through
sympathetic stimulation and collateral venous return via the vertebral plexus and azygous veins
Liver blood flow is not increased
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
Edema
Fetus, placenta, and amniotic fluid = ~8–10 kg at term compresses inferior vena cava and other smaller veins
Compression causes venous pressures in the lower extremities to rise
Increases mean capillary pressure and Increases net fluid filtration from blood to the interstitium
Edema
Fall in colloid osmotic pressure
by 30%– 40% during pregnancy
(from ~25 mm Hg prior to pregnancy to ~15 mm Hg postpartum)
Edema
Respiratory system
O2 demands of the mother and growing fetus increase rapidly during pregnancy
O2 consumption at term is
increased ~ 30%
Respiratory system
Progressive increase in minute ventilation
to ~50% over non-pregnant values during the second trimester
Respiratory system
Minute ventilation increase is effected largely by
An increase in tidal volume and
Small 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 reserve capacity, Expiratory reserve capacity,Residual volume
caused by a rise in the diaphragm
Respiratory system
Changes in Respiratory Function in PregnancyVariable Non-Pregnant Term
PregnancyTidal 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
Progesterone exerts a stimulant action on the
respiratory centre and carotid
body receptors
Physiological Changes of Pregnancy Which Increase the Risk of Hypoxaemia
Interstitial oedema of the upper airway, especially in pre-eclampsia
Enlarged tongue and epiglottis
Enlarged, heavy breasts which may impede laryngoscope introduction
Increased oxygen consumption
Restricted diaphragmatic movement, reducing FRC
Renal blood flow is increased
Renal
Glomerular Filtration Rate rises steadily to ~50% above normal values at 16 weeks’ gestation
Renal Changes in Pregnancy
ParameterNon-Pregnant
Pregnant
Urea (mmol L−1) 2.5–6.7 2.3–4.3
Creatinine (μmol L−1)
70–150 50–75
Urate (μmol L−1) 200–350 150–350
Bicarbonate (mmol L−1)
22–26 18–26
24 h creatinine clearance
Increased
Gastrointestinal Changes
Reduction in lower oesophageal sphincter pressure
Increase in intragastric pressure and a decrease in the gastro-oesophageal angle
Placental gastrin increases gastric acidity
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
Gastrointestinal Changes
Liver Function Changes in Pregnancy
ParameterChange in Pregnancy
Albumin Decreased
Alkaline phosphatase Increased (from placenta)
ALT/AST No change
Plasma cholinesterase Decreased
Pregnancy induces a hypercoagulable state
Coagulation Changes in Late Pregnancy
Haematological Changes Associated with Pregnancy
VariableNon-Pregnant
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
Plasminogen unchanged Plasminogen activator reducedPlasminogen inhibitor increasedFibrinogen-stabilizing factor falls
gradually to 50% of non-pregnant value
Fibrinogen increased from 2.5 (non-pregnant value) to 4.6–6.0 g L–1
Factor II slightly increasedFactor V slightly increasedFactor VII increased 10-foldFactor VIII increased – twice non-pregnant stateFactor IX increasedFactor X increased Factor XII increased 30–40%
Factor XI decreased 60–70%Factor XIII decreased 40–50%
Antithrombin IIIa decreased slightly