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Maternal Physiology
Dr K S 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
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 Pregnancy
Variable Change % change
Heart rate Increased 20–30%
Stroke volume Increased 10–15% 2nd trimester
Systolic 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 Unchanged
Central 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 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
Progesteroneexerts 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
Parameter
Non-
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 gastrinincreases 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
Parameter
Change 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
Variable
Non-
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 reduced
Plasminogen inhibitor increased
Fibrinogen-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 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%
Factor XI decreased 60–70%
Factor XIII decreased 40–50%
Antithrombin IIIa decreased slightly

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Maternal physio

  • 1. Maternal Physiology Dr K S Hettiarachchi Consultant Anaesthetist SBSCH – Peradeniya Sri Lanka
  • 3. Systemic vascular resistance Falls steadily over the first 20 weeks
  • 4. primary cause Erosion of maternal resistance vessels by the fetal placenta
  • 8. Stroke Volume begins to rise very early (20–30%) in pregnancy, mediated by an increase in preload and contractility Cardiac output
  • 9. Preload Na+ and water retention Placental hormones potentiate Renin– angiotensin–aldosterone system and thirst
  • 10. Contractility Sustained increases in cardiac output also Stimulate ventricular hypertrophy
  • 11. Mean arterial pressure Diastolic blood pressure falls Pulse pressure widens
  • 12.
  • 13. Increased diastolic runoff Blood escapes the arterial system more easily during diastole
  • 14.
  • 15. Evens out pressure and flow through the vasculature over time Windkessel Effect
  • 16. C. Physiologic anaemia Plasma volume increase by 40%–50% Red blood cell production increase by 25%–35%
  • 17. Physiologic benefit Reduces blood viscosity So, reduces shear stress
  • 18. 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
  • 20. Reynolds equation Haematocrit is the primary determinant of blood viscosity Anaemia reduces stress levels and lessens the risk of vascular endothelial damage
  • 21. 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.
  • 22.
  • 23.
  • 24.
  • 26. Cardiovascular Changes in Pregnancy Variable Change % change Heart rate Increased 20–30% Stroke volume Increased 10–15% 2nd trimester Systolic 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 Unchanged Central venous pressure Unchanged
  • 27. Aortocaval Compression Compensation occurs through sympathetic stimulation and collateral venous return via the vertebral plexus and azygous veins
  • 28. Liver blood flow is not increased
  • 29. Blood flow to the nasal mucosa is increased
  • 30. Increase in blood flow to the skin, resulting in warm, clammy hands and feet Dissipate heat from the metabolically active feto-placental unit
  • 31. Edema Fetus, placenta, and amniotic fluid = ~8–10 kg at term compresses inferior vena cava and other smaller veins
  • 32. 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
  • 33. Fall in colloid osmotic pressure by 30%– 40% during pregnancy (from ~25 mm Hg prior to pregnancy to ~15 mm Hg postpartum) Edema
  • 34. Respiratory system O2 demands of the mother and growing fetus increase rapidly during pregnancy
  • 35. O2 consumption at term is increased ~ 30% Respiratory system
  • 36. Progressive increase in minute ventilation to ~50% over non-pregnant values during the second trimester Respiratory system
  • 37. Minute ventilation increase is effected largely by An increase in tidal volume and Small rise in respiratory rate (2–3 breaths/min) Respiratory system
  • 38. 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
  • 39. 20% decrease in Functional reserve capacity, Expiratory reserve capacity, Residual volume caused by a rise in the diaphragm Respiratory system
  • 40. 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
  • 41. Progesteroneexerts a stimulant action on the respiratory centre and carotid body receptors
  • 42. 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
  • 43. Renal blood flow is increased
  • 44. Renal Glomerular Filtration Rate rises steadily to ~50% above normal values at 16 weeks’ gestation
  • 45. Renal Changes in Pregnancy Parameter Non- 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
  • 46. Gastrointestinal Changes Reduction in lower oesophageal sphincter pressure Increase in intragastric pressure and a decrease in the gastro-oesophageal angle
  • 47. Placental gastrinincreases 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
  • 48. Liver Function Changes in Pregnancy Parameter Change in Pregnancy Albumin Decreased Alkaline phosphatase Increased (from placenta) ALT/AST No change Plasma cholinesterase Decreased
  • 49. Pregnancy induces a hypercoagulable state Coagulation Changes in Late Pregnancy
  • 50. Haematological Changes Associated with Pregnancy Variable Non- 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
  • 51. Haematological changes Plasminogen unchanged Plasminogen activator reduced Plasminogen inhibitor increased Fibrinogen-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 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% Factor XI decreased 60–70% Factor XIII decreased 40–50% Antithrombin IIIa decreased slightly