This document summarizes several physiological changes that occur during pregnancy. Key changes include increased blood volume, cardiac output, and respiratory rate. Hormonal changes lead to decreased sensitivity to local anesthetics and inhalational agents. The supine position can cause issues late in pregnancy due to compression of the inferior vena cava and aorta. Regional techniques require lower doses of local anesthetics during pregnancy. Overall, pregnancy results in significant cardiovascular and respiratory adaptations to meet increased metabolic demands of the mother and fetus.

1. Presenter:- Dr. SHALINI
Moderator:- Dr. PUNEET

2.  Pregnancy produces profound physiological
changes(adaptive to stress) that become more significant
as pregnancy progresses in duration.
 This changes can be due to:-
1) Hormonal alteration,
2) Mechanical effect of gravid uterus,
3) Increased oxygen & metabolic requirement,
4) Haemodynamical alteration.
 In addition unique challenges - two patients are cared for
simultaneously, failure to take care can be disastrous for
one or both of them.

3. Parameter Change
 Blood volume + 30%
 Plasma volume + 45%
 Cardiac output + 30-50%
 Stroke volume + 20-50%
 Heart rate + 15-25%
 Peripheral resistance - 15-20%
 CVP, PCWP Unchanged

4.  Fluid retention is the most fundamental systemic change of
normal pregnancy.
 The total plasma volume is increased during pregnancy
45%. The most marked expansion occurs in extra cellular
volume (ECV) with some increase in intra cellular water.
 The factors contributing –
 Increase sodium retention.(RAAS)
 Decrease in thirst threshold.
 Decrease in plasma oncotic pressure(↓ plasma
albumin levels)

5.  At term, maternal blood volume has increased by
1000—1500 mL in most women, allowing them to
easily tolerate the blood loss associated with
delivery.
Normal delivery = 400-500ml blood loss
Cesarean section = 800-1000ml blood loss
 Blood volume does not return to normal until 1—2
weeks after delivery

6.  Cardiac output(40%) increases to meet accelerated maternal and
fetal metabolic demands. This increase is mostly due to an
increase in stroke volume (30%) as heart rate increases only
slightly (about 15%).
 Heart rate elevation occurs in response to increased oxygen
demand.
 CO ↑ 40% by 12 weeks
50% for rest of pregnancy
60%-100% during labor & after delivery
 CO highest right after delivery (release of aorto-caval compression) due
to uterine contraction.

7.  Peripheral vascular resistance (VR) decreases due to
the vasodilatory effects of progesterone and the
proliferation of low resistance vascular beds in the
inter-villous spaces of the placenta.
 Because of the decrease in peripheral vascular
resistance(in spite of increased CO), arterial blood
pressure does not significantly change or may show a
slight fall in an uncomplicated pregnancy.
 Diastolic(20%) > Systolic(8%)
 The response to adrenergic agents and vasoconstrictors is
thus blunted.

8.  Despite the increase in blood volume, there is no
change in the central venous pressure(CVP) during
pregnancy. This is most likely due to dilated systemic
and pulmonary circulations.
 Cardiac chambers enlarge and myocardial hypertrophy is
often noted on echocardiography.(Eccentric due to
activation of RAAS).
 Also show variable ECG,
ECHO, CXR Changes.

9. 9
Effect of labor on maternal physiology
Stages of labor
1st stage 2nd stage 3rd stage
Starts with true labor
pains, ends by full
cervical dilation.
Starts with full cervical
dilation, fetal descent
occurs, ends with complete
delivery of fetus.
Extends from birth of the
baby to delivery of the
placenta.
Latent phase
Active phase
Progressive cervical effacement
& minor dilatation (2 – 4 cm).
Progressive cervical dilatation
up to 10 cm.
8 – 12 h in nulliparous
5 – 8 h in multiparous.
Contractions are 1.5- 2 min apart,
last 1 – 1.5 min
15 – 120 min.
15 – 30 min.

10. 10
Intense painful contractions
Maternal hyperventilation
MV ↑ up to 300%.
↑ O2 consumption 60%
above 3rd trimester values
Marked Hypocapnia
PaCo2 < 20 mmHg
Uterine Vasoconstriction
(fetal acidosis)
Periods of hypoventilation → transient
maternal & fetal hypoxemia in between
Contractions.

11. 11
Each contraction
Displaces 300 – 500ml blood from
uterus to central circulation.
CO ↑ 45% above 3rd trimesteric value.
Maximum strain on the heart occurs immediately
after delivery.
Uterine intense involution→ sudden relieve of IVC
→ ↑ COP 80% above pre-labor values.

12.  Effect of Pregnancy on Cardiovascular Investigations
Investigation Findings
Chest radiography Apparent cardiomegaly
Enlarged left atrium (lateral views)
Increased vascular markings
Straightening of left-sided heart border
Postpartum pleural effusion
ECG Right-axis deviation
Right bundle branch block
ST-segment depression on left precordial leads
Q waves in lead III
T-wave inversion in leads III, V2, and V3
Rotation of 15 degrees(QRS axis)
ECHO Trivial tricuspid regurgitation
Pulmonary regurgitation (up to 94% at term)
Increased left atrial size by 12%-14%
Increased left ventricle end-diastolic dimensions by 6%-10%
Inconsistent increase in left ventricle thickness
Mitral regurgitation (28% at term)
Pleural effusion (40% postpartum)

13. Occurs in 20% of women at term.
Aorto-caval compression
Compression of IVCCompression of lower aorta
↓ COP by 24% at term.↓ blood flow to kidneys,
utero-placental circulation &
lower extremities
Supine Hypotension syndrome
(hypotension associated with pallor, sweating,
or nausea and vomiting)
Decreases in cardiac output can occur in
the supine position after the 28th week of
pregnancy.
Fetal hypoxia

14. Compensatory mechanisms in
unanaesthetised Women
Venous Collaterals
↑ SV , ↑ HR & ↓ SVR
Para vertebral
Venous plexus
Abdominal
wall
Reduced during general
or regional anesthesia.
Severe Hypotension
Profound Fetal Hypoxia

15.  Women with a 28-week or longer gestation should
not be placed supine without left uterine
displacement.
 Can be done by
Left lateral decubitus
Tilting the table
Left side down
Rigid wedge (>15 degree)
under
The right hip
Fluid preloading before neuro-axial anesthesia
It does not completely avoid maternal hypotension but
It ↑ maternal CO → preserve utero-placental
blood flow.

16.  Physical examination of the term pregnant woman
may also be abnormal with auscultation commonly
revealing a wide, loud, split first heart sound, an S3
sound, and a soft systolic ejection murmur.
 Hence it is essential to differentiate the abnormal
cardiovascular changes from normal physiological
changes of pregnancy.

17. • Criteria to diagnose cardiac disease during pregnancy:
1) Presence of diastolic murmurs.
2) Systolic murmurs of severe intensity (grade 3).
3) Unequivocal enlargement of heart (X-ray).
4) Presence of severe arrhythmias, atrial fibrillation or
flutter

18.  Changes in the respiratory system during pregnancy
involve the upper airways, minute ventilation, lung
volumes, and oxygen consumption.
 Major physiological changes occur in the respiratory
system during pregnancy due to a combination of both
hormonal and mechanical factors.
 Dyspnoea is a common complaint in pregnancy
affecting over half of women at some stage.

19.  Respiratory Parameter Change
 Oxygen consumption + 20 to 50%
 Minute ventilation + 50%
 Tidal volume + 40 %
 Respiratory rate Unchanged/ Slight increase(+10-15%)
 PaO2 + 10%
 PaCO2 - 15%
 HCO3 - 15%
 FRC (functional residual capacity) - 20%
From Birnbach DJ, Gatt SP, Datta S (eds): Textbook of Obstetric Anaesthesia. New York, Churchill Livingstone, 2000, p 35.

20.  Due to increased metabolic demands, Oxygen
consumption (+ 20 - 50%) and minute ventilation
(+40 - 50%) progressively increase during pregnancy.
(Increased progesterone sensitizes the central
respiratory center to carbon dioxide – directly
stimulating ventilation)
 The pregnant woman thus takes larger Tidal
volumes(40-50%) to eliminate carbon dioxide.
 PaCO2 decreases to(28—32 mm Hg); significant
respiratory alkalosis is prevented by a compensatory
↓ in plasma HCO3 concentration.

21.  Hyperventilation may also increase PaO2.
 Elevated levels of 2,3-diphosphoglycerate offset
the effect of hyperventilation (↓PaCO2) on
hemoglobin affinity for oxygen.
 The combination of increased 2,3-DPG with
increase in cardiac output enhances oxygen
delivery to tissues.

23. The maternal respiratory pattern changes as the
uterus enlarges
Diaphragm rises up(4cm) compensatory increases in
Antero-posterior diameters
Diaphragm motion not restricted
Chest wall motion limitation
Thoracic breathing favored over Abdominal
20% decrease in FUNCTIONAL RESIDUAL CAPACITY(FRC).
* No change in CLOSING CAPACICITY (CC) & VITAL CAPACITY

24. ↓ FRC + ↑O2 Consumption + Unchanged CC
Rapid O2 de-saturation during
periods of apnea (diminished capacity to
tolerate apnea).
Supine Position & Regional Block
further diminishes FRC
Pre-oxygenation prior to induction of general
anesthesia should be given to avoid hypoxemia in
pregnant patients.
Rapid development of hypoxemia

25. Rapid gaseous induction
 The decrease in FRC coupled with the increase in minute
ventilation accelerates the uptake of all inhalational
anesthetics.
 ↓FRC → less dilution
 ↑MV → rapid deep depth

26. 26
Hormonal Changes Capillary engorgement of
respiratory tract mucosa
1) ↑ Incidence of difficult intubation.
2) Trauma and bleeding during
endotracheal intubation.
☼ Repeated attempts at laryngoscopy must be
minimized
☼ Use a small ETT (6 – 7 mm) during GA

27. 1) Progressive decrease in MAC .
40% at term
(Returns to normal by 3rd day postpartum).
Progesterone increases
20 times normal
level at term
β- endorphin surge during
labor & delivery

28.  LA requirements for subarachnoid or epidural anaesthesia
are reduced in pregnancy (30%)
 a) ↑ diffusion of LA to the receptor site.
b) ↑ sensitivity of nerve fibers to LA (Lower concentration
needed).
c) engorged epidural venous plexus.
 Spinal ligaments including ligament flavum SOFT hence
loss of resistance technique used for regional block may be
masked
CNS : its anaesthetic importance

29. IVC obstruction by enlarging
uterus
Engorged Epidural
Venous Plexus
1) ↓CSF Volume
2) ↓Volume of
Epidural Space
3) ↑Epidural space
Pressure
1,2: This enhances the cephalad spread of LA
during regional blocks.
3 : Predisposes to higher incidence of Dural puncture &
intravascular injection

30. The parturient should be considered a full stomach patient
during most of gestation
☼ Upward & ant. displacement of the stomach by the
uterus → Incompetence of gastro-esophageal
sphincter → Gastro-esophageal reflux & aspiration.
☼ ↑ Progesterone → ↓ tone of gastro-esophageal sphincter.
☼ Placental Gastrin → Hyper-secretion of gastric acid.
☼ Gastric emptying → Delayed with labor.

31.  Narcotics and anti-cholinergic reduce lower
oesophageal sphincter pressure (used with precaution)
For GA:
Pharmacological prophylaxis against aspiration.
Supine position with lateral tilt
No positive pressure ventilation before intubation
Rapid sequence induction.
Sellick’s maneuver

32.  Renal vasodilatation increases renal blood flow
early during pregnancy.
 ↑ Cardiac output(CO) ↑ GFR & ↑ RPF(renal
plasma flow) by 50%.
 ↑ Renin & Aldosterone level promotes Na+ retention
leading to volume overload.
 ↓ Renal tubular threshold for glucose & amino acids →
mild glycosuria & proteinuria (< 300mg/d).

33. ↑ GFR ↑ clearance of urea, uric acid and
creatinine
↓ plasma concentrations of
sr. Creatinine & BUN
BUN and Creatinine levels that would be considered
marginally elevated in pre-pregnant patients are usually
indicative of severe renal impairment in pregnancy.

34.  Hepatic function and blood flow are unchanged.
 A mild ↓ in serum albumin is due to an expanded
plasma volume. Thus, the free fraction of albumin-
bound medications is increased.
 A 25—30% decrease in serum pseudo cholinesterase
activity is also present at term, but it rarely produces
significant prolongation of NMB action.
 Increased cholesterol gall stone
formation(progesterone).

35. ↑ Blood Volume ( up to 90ml/Kg)
↑ by 1000 – 1500 ml at term.
↑ Plasma Volume(45%) > ↑ RBC mass(30%)
Dilutional anemia & ↓ blood viscosity
Facilitates maternal & fetal
exchange of respiratory gases,
nutrients & metabolites
↓ Impact of maternal blood
loss at delivery

36. • Pregnancy leads to a hypercoagulable state, due to,
a) factors VII, VIII, X, XII ,IX ( only factor XI  )
b) fibrinogen and FDP's
c) fibrinolytic activity - levels of plasminogen activators
d) antithrombin III
 Probably a protective adaptation to lessen the risks
associated with the acute haemorrhage that occurs at
delivery.
 Increased risk of thromboembolic disease (Post-Anaesthesia
ambulation )

37.  Leucocytosis up to 13,000/µL.
 ↑ ESR
 10-20% ↓ in platelet count.(Mild thrombocytopenia not a
contra-indication for neuraxial block).
 Marked ↓ cell mediated immunity→ ↑ susceptibility to
viral infection.

38.  Pregnancy is Diabetogenic
Human Placental lactogen(HPL) → relative insulin resistance.
• Biochemically Starvation like state
↓ Blood Glucose & Amino Acid levels.
↑ Free Fatty Acids, Ketones & triglycerides.
To promote fetal growth.
Maternal Insulin Levels Steadily Rise During Pregnancy
↓

39.  Secretion of HCG and elevated levels of estrogens promote
hypertrophy of the thyroid gland.
 Hyperplasia of Pancreatic ß Cells occurs in response to
increased demand for insulin secretions.
 ↑ TBG (↑ T3 & ↑ T4 ) → Free T3, T4 & TSH remain
normal.

40. • Increased level of relaxin - Softening Of Cervix
- Relax Symphysis Pubis
- Pelvic Joints
- Chest Wall Changes
 Increased risk of back pain(lax ligaments)

41. 41
Utero-placental Circulation
At term: uterine blood
flow is 10% of CO
≈ 600 – 700 ml/min.
80% to placenta
20% to myometrium

42. 42
Due to maximum dilatation of uterine vasculature its auto regulation is lost
Uterine Blood Flow
Directly proportional to difference between
uterine arterial and venous pressure.
Inversely proportional to uterine
vascular resistance.
Uterine vasculature has abundant α-adrenergic & some β-adrenergic receptors.
Previously , vasoconstrictor agents with predominant β-adrenergic activity
(e.g. Ephedrine) were of choice for hypotension during pregnancy.
Recent studies show that α-adrenergic drugs (e.g.Phenylephrine) have
similar effects causing less fetal acidosis.

43. 43
3 major factors ↓ uterine blood flow during pregnancy
Systemic
Hypotension
Uterine
Vasoconstriction
Uterine
Contractions
♦ Aortocaval compression.
♦ Hypovolemia.
♦ Sympathetic block
with regional anesthesia.
♦ stress-induced endogenous
Catecholamines during labor.
♦ α-adrenergic agonists.
♦ Hypertensive disorders
→ generalized vasoconstriction.
♦ Labor.
♦ Oxytocin infusions.
♦ Extreme hypocapnia
PaCO2 < 20 mmhg.
♦ Barbiturates &
Propofol.

44. 44
Placental transfer of anaesthetic agents
Placental transfer of drugs depends on:
1) Molecular weight : < 1000 Da cross easily.
2) Protein binding– inversely proportional
3) Lipid solubility: Highly ionized substances have poor lipid solubility.
4) Maternal & fetal pH : affect ionization of the drug.
5) Maternal drug concentration: affected by dose given
and route of administration.
6) Timing of administration.

45. 45
Limited effects if <
1MAC & delivery within
10 min. of induction
Cross placenta
freely
Inhalational Agents
Intravenous Agents:
Thiopental, ketamine
& propofol
Limited fetal effects in
usual induction doses
(drug distribution,
metabolism & placental
uptake)
Variable effects.Cross placenta freelyOpioids
Most significant respiratory depressant effectsMorphine
Significant respiratory depression peaking 1- 3
hr after administration.
Pethidine
Minimal effect if < 1µg/Kg.Fentanyl
Minimal effects on
fetus.
The highly ionized
property impedes
placental transfer.
Muscle Relaxants

46. 46
Local anesthetics → Placental transfer depends on:
1) pKa.
2) Maternal & fetal pH : Fetal acidosis → higher fetal to maternal
drug ratios . Binding of hydrogen ions to the nonionized form → trapping
of local anesthetic in fetal circulation
3) Degree of protein binding : highly protein bound agents
diffuse poorly across the placenta.
Chloroprocaine has the least placental transfer as it is rapidly
broken down by plasma cholinesterase in the maternal circulation.

47. Summary
To illustrate how all these changes may affect anaesthetic
management, lets imagine performing a general anaesthetic for
caesarean section and list some key points
1) Careful attention to the assessment of the airway and any
necessary preparation to deal with a potentially difficult airway
in the pre operative period.
2)When positioning the patient on the table, remember to use
either a left tilt of 15 – 30 degrees on the table or a wedge
under the right buttock to minimize aorto-caval compression.
3)Venous access often easier due to engorgement of the venous
system

48. 4) Pre oxygenation is essential and should be with a tight fitting
mask for at least 3 minutes.
5) Rapid sequence induction with the application of cricoid
pressure is mandatory. Intubation may be difficult and so
adjuncts for difficult intubation should be available.
6) Once the airway is secured, ventilation should be aimed to
keep the PCO2 in the normal range for pregnancy.
7) The MAC of volatile anaesthetic is slightly reduced.
8) There is decreased sensitivity to endogenous and exogenous
catecholamines and so if vasopressors are required to maintain
adequate blood pressure, the amounts needed may be greater.
10) Extubation should be done with the patient awake and on
their side to reduce the risk of aspiration of gastric contents.