The document provides information on the anatomical and physiological changes that occur during pregnancy. It discusses changes in various body systems like cardiovascular, respiratory, gastrointestinal and renal systems due to hormonal changes and increasing size of the uterus and fetus. It also summarizes the fetal circulation pattern and how it differs from adult circulation. The key points are: 1. Hormonal changes and increasing size of uterus causes anatomical and physiological changes in mother's body to support the growing fetus. 2. Cardiovascular changes include increased blood volume, cardiac output and sensitivity to medications. Respiratory changes are increased minute ventilation and oxygen demand. 3. Fetal circulation has parallel arterial systems with ductus venosus, foramen oval

1. MODERATOR:DR.SURESH.L
PRESENTER:DR.KEERTHY
UNNIKRISHNAN

2. Changes occur in pregnancy to
1. Support the fetus.
2. Prepare mother for delivery.
Changes are due to
1. Hormonal changes.
2. Increasing size of uterus and fetus.
3. Anatomical changes.

3. Uterus increases in size progressively.
Chest circumference increases and diaphragm is
elevated.
Postural changes with forward head,rounded
shoulder,lordotic spine shift in centre of gravity.
Skin pigmentation.
Breast size increases and milk ducts grow.

4. Weight gain 17% of pre pregnancy weight or 12kg.
Begin as early as 5 weeks and increase
progressively.
Changes are due to progesterone and estrogen.
TRIMESTER FIRST SECOND THIRD
BODY WEIGHT 1-2 kg 5-6kg 5-6kg

5. Fluid retention,Increased plasma volume.
Half of weight gain is due to increased plasma volume.
Increased size of uterus,fetus,amniotic fluid,body fat and
protein.

6. Increase in cerebral blood flow.
Increased sensitivity to general anaesthetics:
Reduced MAC of volatile anaesthetics by up to 30% from
non-pregnant state.
More rapid uptake of volatile anaesthetics.
Altered pain threshold.
Increased susceptibility to sedatives as progesterone has
sedative effects.
Increased sensitivity to benzodiazepines and propofol.

7. Increased sensitivity to local anaesthetics:
 Epidural venous engorgement resulting in:
-Raised peak local anaesthetic concentration.
-Increased incidence of bloody tap.
 Reduced volume of CSF due to:
-swelling of epidural veins.
-increased epidural and CSF pressure:
This occurs due to raised intra-abdominal pressure.
 Epidural pressure is positive in term pregnant women.
 It is usually negative in 90% of non-pregnant women.
 Epidural pressure returns to non-pregnant level by 6-12 hours
post-partum.

8. Increased lumbar lordosis causing more cephalad
spread of local anaesthetic.
30% reduction in LA dose at term due to neuronal
sensitivity to LA.

9. Cardiac muscle hypertrophy.
Eccentric hypertrophy.
Reversible.
No compromise on the size of chambers.
Coronary blood flow is preserved.

10. Blood volume increases by 45-50% at term.
Heart rate increases by 15-20%,elevated by 10-20
bpm at term.
Increased cardiac output by 40-50% by term:
-Cardiac output increases from 5th week of gestation.
-Most of the increase occurs by 20 weeks of gestation.
-Cardiac output reaches maximum by 32 weeks.

11. -Approximately 1L of blood is contained in uterus and
placenta.
-Initial increase in cardiac output is due to increase in
heart rate.
-Thereafter,increased stroke volume causes increase
in cardiac output.

12. Contractility(variable)+10%.
Systemic vascular resistance reduced by 20% causing a
fall in DBP.
Systolic BP decreases in mid-trimester by 10-20 mm Hg.
DBP reduces in mid trimester by 10-20 mm Hg.
Central venous pressure and PCWP remains unchanged.
Pulmonary arterial pressure and pulmonary vascular
resistance slightly decreased by 30%.
Wide,loud and split S1,S3 and soft ejection systolic
murmer.

13. Left axis deviation,due to upward displacement of
heart by uterus on ECG.
 Increased incidence of arrhythmias:
-Sinus tachycardia
-Ventricular ectopics
-Paroxysmal supraventricular tachycardia.
-Paroxysmal atrial complexes
-Ventricular arrhythmias

14. Left ventricular wall thickness and left ventricular wall
mass increases by 28% and 52%.
Increase in right ventricular mass.
Dilatation of 4 chambers.
Annular widening-regurgitant lesions of tricuspid and
pulmonary valves.

15. Grade Ⅲ systolic murmurs.
Diastolic murmer.
Dyspnoea at rest.
Unexplained fatigability.
Syncope,palpitations.

16. Greater blood flow to skin,kidney and uterus.
Uterine blood flow increase to 1000ml/min.
Low resistance circuit
Nil auto regulation
Perfusion is dependent on arterio venous pressure
difference

18. Hypotension (reduction of SBP by at least 15-30mm
Hg)occurring when a parturient adopts supine
position.
This occurs due to compression of abdominal aorta
and IVC by the enlarging uteroplacental mass.
Occurs in up to 15% of pregnant patients near term.
Also called Supine hypotension syndrome.

19. Obesity
Multiple pregnancy
Polyhydraminos
Pregnancy induced hypertension
Dehydration,bleeding,hypovolemia.

20. Syndrome has been clinically demonstrated from
middle of 2nd trimester onwards.
IVC compression:
-Occurs as early as 13-16 weeks gestation.
-Causes 50% rise in femoral venous pressure in
supine position at 16 weeks.
-At term,femoral venous pressure increases to 2.5
times the normal value.

21. Aortic compression:
-Aortic compression by gravid uterus occurs later by
28-30 weeks gestation.
-This results in lower femoral arterial pressures in
supine position.
This causes a profound drop in venous return to the
heart.
Cardiovascular system may not be able to
compensate for the drop in venous return.

22. Concealed caval compression:
-Occurs when compensatory mechanisms act to
restore venous return to heart.
-No clinical symptoms.

23. Revealed caval compression:
-When compensatory mechanisms are insufficient to
maintain preload to heart.
-Occurs in 10% of patients causing serious reduction in
venous return to heart.
-Clinical symptoms manifest.

24. Usually occur within 3-10 minutes of assuming supine
position.
Symptoms:
-Faintness,giddiness,visual
disturbances,numbness,paresthesias.
-Dyspnoea,restlessness.
-Nausea,vomiting.
-Pallor,sweating,cold and clammy skin.

25. On long standing;
-Pooling of venous blood.
-Edema,varicose veins,thrombophlebitis.
SIGNS:
Hypotension.
Tachycardia and narrow pulse pressure(earliest sign).
Reduced femoral artery pressures:poseiro sign.
Placental abruption may occur due to transmission of
raised venous pressures.

26. Aggravated by:
-Spinal anaesthesia.
-Epidural anaesthesia.
-Thiopentone
-Halothane.
Fetal effects:
-Fetal hypoxia
-Slow irregular fetal heart rate.

27. Lateral position.
Manual left uterine displacement.
Tilting the OR table to 30 degree left.
Wedge under the right buttock 10-15 cms.

28. Venodilatation increases incidence of accidental
epidural vein puncture.
Healthy parturients tolerate upto 1500 mL blood loss.
High hematocrit(›42%) indicates low volume states
and dehydration.
Cardiac output remains high for first few hours
postpartum.

29. ANATOMICAL CHANGES:
Friable mucosa of nasopharynx due to estrogen-
epistaxis.
Capillary engorgement of mucosa ,edema of
oropharynx,larynx and trachea.
Reduced airway resistance due to bronchiolar dilatation
by progesterone.
Vocal cord fatigue with decrease in maximum time of
phonation.

30. GAS EXCHANGE:
Increase in minute ventilation by 45-50%.
Increased oxygen demand and consumption by up to
35% due to:
-Increased metabolic needs of fetus,uterus and
placenta.
- Increased respiratory work.
-Increased cardiac work.

31. Increased requirement for CO2 elimination.
Increased work of breathing.
Rightward shift of ODC facilitating oxygen delivery to
foetus.
PaO2 increases to 100-106 mm Hg due to increased
minute ventilation.
PaCO2 falls to 30 mm Hg by 12 weeks and remains
at this level.

32. Mostly diaphragmatic pattern of breathing due to:
Limited thoracic cage movement.
Pressure of gravid uterus.

33. Changes in pulmonary function tests:
Increased tidal volume by 45%,unchanged respiratory
rate.
Increased minute volume by 45%.
Reduced FRC by 20% due to:
-Increased intra-abdominal pressure.
-Upward displacement of diaphragm.

34. Closing capacity unchanged.
Reduced total lung capacity by 5%.
Reduced expiratory reserve volume by 25%.
Reduced residual volume by 15%.

35. Airway management is more challenging:
Breast engorgement may hinder laryngoscopy.
Swollen,edematous mucosa which bleeds easily.
Smaller size endotracheal tube preferred.

36. Greater risk of hypoxemia due to:
Decreased oxygen reserve due to reduced FRC.
Increased oxygen consumption.
Rapid airway obstruction.

37. Blood volume:
Plasma volume increases by 45-50% by 34 weeks
gestation.
RBC volume increases by only 30% at term.
The increase in plasma volume exceeds the increase in
RBC volume.
This results in physiological anemia of pregnancy.
Hemoglobin ranges from 9.5 to 15g% and HCT from 28-
40% in 3rd trimester.
Platelet count remains unchanged and may be increased
in 3rd trimester.

38. Increased oxygen transport:
Oxygen transport is increased inorder to deliver more
oxygen to fetus.
This occurs due to:
-Increased PaO2 due to increased minute
ventilation.
-Rightward shift of ODC facilitating easy delivery of
oxygen.
-Increased cardiac output increasing uterine blood
flow.

39. Plasma proteins:
Increased total protein levels.
Reduced albumin levels and albumin:globulin ratio.
Reduced plasma colloid oncotic pressure by up to
14%.
Raised levels of clotting factors:
-Factors Ⅶ ,Ⅷ,Ⅸ,Ⅹ,Ⅻ.
-Fibrinogen.
-Plasminogen,prothrombin fragment.

40. Reduced anticoagulant activity:
-Reduced protein C and S,antithrombin Ⅲ.
-Impaired fibrinolysis.
Relative reduction in protein levels due to increased
plasma volume:raised free drug fraction.

41. Changes in tests of coagulation:
Prothrombin time shortened by 20%.
Partial thromboplastin time shortened by 20%.
No change or decreased platelet count.
Increased plasminogen and fibrin degradation
products.

42. Anemia of pregnancy occurs due to disproportionate
raise in plasma volume.
Increase in blood volume prepares the parturient for
blood loss during delivery.
Hemodynamic changes due to blood loss are not
seen till it exceeds 1500 mL.
Due to alterations in coagulation system,risk of
thromboembolism is increased.

43. Impaired oesophageal and intestinal motility due to
relaxant effect of progesterone.
Increased risk of aspiration and GERD due to:
Raised intragastric pressures(up to 40 cm H2O at
term).
Relaxation of lower oesophageal sphincter:Reduced
LES tone.
Delayed gastric emptying.

44. Shift in stomach position:
Enlarging uterus changes angle of GE junction and
rotates the stomach.
This increases the risk of aspiration.

45. Gastric and placental secretions:
Placental gastrin secretion increases volume and
acidity of gastric secretions.
Increased secretion of human placental lactogen:
-This causes reduced glucose tolerance.
-This causes hyperglycemia and ketosis.

46. Rapid sequence induction with cricoid pressure for
more than 12 weeks gestation.
Consumption of clear fluids promotes gastric
emptying.
Therefore,current ASA recommendations encourages
clear liquid consumption by labouring patients.

47. Increased renal blood flow by 50-80%.
Kidneys enlarge by upto 30%.
GFR increases by 40-65%(from 100ml/min to 150 ml/min)
causing:
-Raised creatinine clearance(from 120ml/min to 150-
200ml/min).
-Lower BUN and creatinine values(9mg/dl and 0.5mg/dl during
pregnancy).
-Glycosuria up to 1-10g/day.
-Proteinuria up to 200-300 mg/day.
Dilatation of calyces,pelvis and ureters:urinary stasis causing
frequent UTIs.

48. Gravid uterus may compress ureters and cause
hydronephrosis.
Urinary stasis results in increased risk of urinary
infections.
BUN and creatinine values which are normal for non-
parturients indicate upnormal renal function during
pregnancy.
Glucosuria and mild proteinuria is normal during
pregnancy.

49. Technical considerations:
 Increased lumbar lordosis:
-Causes a reduction in vertebral interspinous gap.
-Results in difficulty in administering neuraxial anaesthesia.
 Apex of thoracic kyphosis at higher level.
 Lateral position:
-Head down tilt occurs when pregnant women lies in lateral
position.
-This is due to a wider pelvis resulting in a downward tilt.
-This may result in rostral spread of local anaesthetic when
administered in lateral position.

51. Treatment of hypotension:relative resistance to
vasopressors.
Local anaesthetic dose requirements:
Subarachnoid dose reduced by 25%.
Epidural dose is unaltered or slightly reduced.

52. Drugs:
Thiopentone:
-Reduced induction dose.
-Prolonged elimination half life
Propofol:
-Reduced induction dose.
-Unaltered elimination halflife.
Volatile anaesthetic agents:
-Minimum alveolar concentration decreased.
-Increased speed of induction.

53. succinylcholine:unaltered duration of blockade.
Rocuronium:increased sensitivity.
Chronotropic agents and vasopressors:reduced
sensitivity.
Tracheal intubation:
Accelerated desaturation during apnea.
Smaller endotracheal tube required.
Increased risk of bleeding with nasal intubation.

54. Fetal lungs are functionally inactive and fetus derives
oxygen and nutrients from placenta.
Fetus receives blood from placenta through umbilical
vein which is only 80% saturated as placenta has
extracted some oxygen.

55. 1 UMBILICAL VEIN: brings oxygenated blood and
nutrients to the fetus.
2 UMBILICAL ARTERIES:return deoxygenated
blood,fecal waste,carbon dioxide to placenta.

56. Parallel arrangement of two main arterial systems and
their respective ventricles.
High resistance and low flow of pulmonary circulation.
Low resistance and high flow of placental circulation.
Presence of shunts.

57. DUCTUS VENOSUS(between umbilical vein and fetal
IVC).
FORAMEN OVALE(between RA and LA).
DUCTUS ARTERIOSUS(between pulmonary artery
and aorta).

58. From umbilical vein blood enters liver of fetus and
some amount bypasses liver and enters IVC through
ductus venosus.
IVC drains into RA.
50% of blood from RA enters LA through Foramen
ovale.
Another 50% enters RV from there into pulmonary
artery.
But fetal lungs are collapsed.

59. So only small amount of blood reaches LA through
pulmonary veins.
The main bulk of blood from RV enters aorta through
ductus arteriosus.
Blood from aorta is then distributed to the whole body.
2 umbilical arteries which arise from fetal aorta
transport blood to placenta for oxygenation.

61. Closure of umbilical veins.
Closure of ductus venosus.
Expansion of lungs.
As lungs fill with air pulmonary vascular resistance
decreases.
Closure of foramen ovale cause change in pressure
gradient between atria.

62. Responsible for circulation of maternal blood through
the intervillous space.
Blood supply to the intervillous space is derived from
120-200 spiral arteries.
These arteries funnel out as they pierce the
intervillous space.
This results in the formation of utero-placental
arteries.

63. Uteroplacental arteries supply blood to the intervillous
space at low pressure(10-15 mm Hg).
Mature placenta has approximately 500ml of blood:
-150 ml is present in the intervillous space.
-350 ml is present in the system of villi.
Blood in the intervillous space is completely replaced
3-5 times/minute.

64. The uterine blood flow is dependent on:
-Uterine perfusion pressure.
-Uterine venous pressure.
Uterine perfusion pressure is determined by:
-Uterine arterial pressure.
-Uterine venous pressure.

65. UBF=(Uterine arterial pressure)-(Uterine venous
pressure)/Uterine vascular resistance.

66. Decreased perfusion pressure:
Decreased uterine arterial pressure:
Supine position
Hemorrhage
Hypovolemia
Drug-induced hypotension
Sympathetic blockade.

67. Increased uterine venous pressure:
-Vena caval compression.
-Uterine contractions.
-Valsalva maneuver.

68. Increased uterine vascular resistance:
Endogenous vasoconstrictors:
-Catecholamines
-Vasopressin
Exogenous catecholamines:
-Epinephrine
-Phenylephrine>ephedrine

69. Using Ficks principle:
-Substances used include nitrous oxide and 4-amino-
antipyrine.
-Not commonly used as it is error prone.

70. Radioactive tracers:
Tracers used include:
-Xenon-133
-Radiolabelled albumin
Uteroplacental perfusion is indicated by:
-Decrease in radioactivity.
-Directly using scintigraphy.

71. Doppler ultrasonography:
-Most commonly used technique.
-Uterine artery is identified using color Doppler.
-Blood flow is quantified using continuous wave
Doppler derived variables:
Mean blood flow velocity
Vessel cross sectional area

72. Effect of neuraxial block on UPP depends on
interactions between many factors:
ANALGESIA:Pain relief due to NA blockade
increases uterine perfusion due to:
-Reduced circulating catecholamines
-Preventing hyperventilation
-Reducing uterine vascular resistance

73. HYPOTENSION:
Sympathetic blockade due to NA anaesthesia may
cause hypotension.
This decreases UPP by several mechanisms:
-Reduction in perfusion pressure.
-Reflex release of vasoconstrictors.
-Reducing uterine vascular resistance.

74. USE OF VASOPRESSORS:
Commonly used vasopressors are:
-Phenylephrine
-Ephedrine
Both these drugs cause transient reduction in UPP.
However,clinical effects on the fetus are minimal as
suggested by:
-Fetal blood pH
-Base excess

75. LOCAL ANAESTHETIC AGENTS:
Local anaesthetics do not produce clinically relevant
reductions in UPP.
However,UPP may be reduced due to inadvertent
systemic injection.

76. OPIOIDS:
Intrathecal opioids may result in increased uterine
tone and reduced UPP.
This causes fetal bradycardia commonly seen with
intrathecal opioids.

77. Causes of increased uterine blood flow under
neuraxial blockade:
Pain relief
Decreased sympathetic activity
Decreased maternal hyperventilation

78. Causes of decreased uterine blood flow under
neuraxial blockade:
Hypotension
Local anaesthetic systemic toxicity.

79. Induction agents:
Commonly used induction agents have no direct
effects on UPP.
Indirect mechanisms altering UPP at induction
include;
-Systemic vasodilatation
-Intubation response

80. Inhalational agents:
Effects of inhalational agents on UPP depens upon the
dose of administration.
At MAC values 0.5-1.5,no clinically relevant change in
UPP is produced.
At MAC values >2,changes in UPP may be determined
by:
-Reduction in systemic BP causing reduced perfusion.
-Uterine relaxation improving UPP.
Anaesthetic drug which donot produce clinically relevant
changes include:
Opioids
Neuromuscular blocking agents

81. Medications administered to pregnant women may
cross the placenta.
This may have harmful effects on the fetus.
Placental permeability and pharmacokinetics
determines fetal exposure to maternal drugs.

82. SIMPLE DIFFUSION
 Most drugs cross the placenta by simple diffusion.
 Transfer of drugs occurs along concentration gradient.
 Simple diffusion requires no carrier molecule/energy.
 Transfer occurs through synctitiotrophoblast layer or through
water channels.
 Examples of drugs transferred by simple diffusion:
-Midazolam.
-Paracetamol.

83. Formula for rate of diffusion:
Rate of diffusionQ/t=KA(Cm-Cf)/D
Q/t=rate of diffusion
K=diffusion coefficient
A=surface area for membrane available for exchange
Cm-Cf=Concentration gradient between maternal&
fetal circulation
D=thickness of membrane

84. FACILITATED DIFFUSION
It is a form of passive transport dependent on
transmembrane proteins.
It occurs along concentration gradient and requires a
carrier molecule.
Examples:
-Cephalosporins
-Glucocorticoids

85. ACTIVE TRANSPORT
Transport occurs against concentration gradient.
Requires carrier molecules and energy for transport
across the membrane.
Examples:
-Norepinephrine
-Dopamine

86. PINOCYTOSIS:
Molecules are engulfed by invagination of placental
membrane.
These molecules are then transferred across the
membrane to the opposite side.
Molecules are therefore transferred to fetal
circulation.
These processes are very slow to have a significant
impact on fetal drug concentration.

87. DRUG FACTORS
Molecular weight:
Low molecular weight molecules(<1000 Da) cross the
placenta.
Most drugs have molecular weight less than 500 Da.
These molecules are easily transferred across the
placenta.
Drugs with molecular weight >500 Da show incomplete
transfer.

88. Lipid solubility:
Lipid soluble drugs cross placenta.
Examples of lipid soluble drugs:
-Thiopentone
-Local anaesthetics
-benzodiazepines

89. Protein binding:
Protein binding determines the amount of free drug
available to cross placenta.
Drugs may be bound to albumin or α-1-acid
glycoprotein(AAG).
Highly protein bound drugs do not cross placenta.

90. Degree of ionization:
Ionized drugs donot cross placenta.
Examples of ionized drugs:
-Glycopyrrolate
-Heparin
-Succinylcholine
-Non-depolarizing neuromuscular blocking agents.

91. pKa:
If pKa of drugs is close to physiological pH,more drug
will be ionized and won’t cross placenta.

92. MATERNAL FACTORS
Total dose and maternal drug concentration.
Addition of adjuvants like adrenaline reduces peak LA
level.
Route of administration:injection into high vascular
epidural space increases peak concentration of drug.
Maternal metabolism and excretion:hepatic/renal
dysfunction increases toxicity.
Maternal protein binding:increased protein binding
reduces transfer.
Maternal pH alters extent of ionization and transfer.

93. PLACENTAL FACTORS
Placental blood flow:
Reduction in placental blood flow reduces the drug
delivery to the membrane.
This reduces the drug available for transfer.
Factors reducing placental blood flow include:
-Hypotension
-Low cardiac output states
-Aortocaval compression
-Uterine contraction
-Umbilical cord compression

94. Placental ageing.
Placental area available for shunting:
The area available ranges from 3.4m2 at 28 weeks to
12.6 m2 at term.
Shunting of blood flow occurs in pre-eclampsia.
This may present an increased barrier to transfer of
molecules.
Thus placental blood flow has to be adequate to
ensure adequate transfer.

95. FETAL FACTORS
Solubility of drug in fetal blood.
Concentration of drug in fetal blood returning to
placenta.
Uptake by fetal tissues.
Fetal hepatic metabolism and renal excretion.
Non placental routes of fetal drug excretion.
Fetal protein binding.
Fetal pH and adequacy of fetal circulation.

96.  Anticholinergic agents:
-Atropine
-Scopolamine
 Benzodiazepines:
-Diazepam
-Midazolam.
 Induction agents:
-Propofol
-Ketamine
-Etomidate
-Thiopentone

97. Volatile anaesthetics:
-Halothane
-Isoflurane
-Sevoflurane
-Desflurane
-Nitrous oxide
Opioids.
Local anaesthetics
Vasopressors:ephedrine.

98. Anticholinergic agents:glycopyrrolate.
Anticoagulants:heparin.
Muscle relaxants:
-Depolarizing agents:succinylcholine.
-Nondepolarizing agents.
Vasopressor:phenylephrine.

99. Miller’s anaesthesia.
Stoelting’s pharmacology&physiology in anaesthetic
practice.
morgan&Mikhail’s clinical anaesthesiology.