1. Dr. Swadheen kumar Rout
1st year P.G
Dept. of Anaesthesiology
M.K.C.G College & hospital

2.  INDIA -204 / 1,00,000 live births.
 USA - 7 / 1,00,000 live births.
 Although no studies in india, studies in usa have
shown that, 4-5% of total deaths are due to over
zealous anaesthetic practices & its complications.
 So one must be familiar not only with the effect of
various drugs and techniques on the pregnant women
and foetus but also the physiological changes in
pregnancy which alter response to anaesthesia.

3.  Pregnancy produces profound physiological
changes(adaptive to stress) that become more significant
as pregnancy progresses.
 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.

4. 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, PAWP Unchanged
From Birnbach DJ, Gatt SP, Datta S (eds): Textbook of Obstetric Anesthesia. NewYork, Churchill Livingstone, 2000, p 34.

5.  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(↓ albumin)

6.  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

7.  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.

8.  Peripheral vascular resistance (VR) decreases due to
the vaso-dilatory 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(inspite of increased CO), arterial blood
pressure does not significantly change or may show a
slight fall in a uncomplicated pregnancy.
 Diastolic(20%) > Systolic(8%)
 The response to adrenergic agents and vasoconstrictors is
thus blunted.

9.  Despite the increase in blood volume, there is no
change in the central venous pressure(CVP) during
pregnancy. This is 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.

10.  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)
From Gei AF, Hankins GDV: Cardiac disease and pregnancy.

11. 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 extremeties
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

12. Compensatory mechanisms in
unanaesthetised Women
Venous Collaterals ↑ SVR & HR
Paravertebral
Venous plexus
Abdominal
wall
Reduced during general
or regional anesthesia.
Severe Hypotension
Profound Fetal Hypoxia

13.  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 COP → preserve utero-placental
blood flow.

14.  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 essential to differentiate abnormal
cardiovascular changes from normal physiological
changes of pregnancy.

15. • 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 arrythmias, atrial fibrillation or
flutter

16.  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.

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

18.  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 pasma HCO3 concentration.

19.  Hyperventilation may also increase Pa02.
 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.

20. 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 limitation
Thoracic breathing favoured over Abdominal
20% decrease in FUNCTIONAL RESIDUAL CAPACITY(FRC).
* No change in CLOSING CAPACICITY (CC) & VITAL CAPACITY

21. Pregnant woman has a smaller “air tank”.
Non-pregnant
woman

22. ↓ FRC/CC + ↑O2 Consumption
=
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 devlopment of hypoxemia

23. 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

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

25. 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

26.  LA requirements for subarachnoid or epidural anaesthesia
are reduced in pregnancy (30%)
 a) ↑ diffusion of LA to the receptor site.
b) ↑ sensitivity of nerve fibres to LA (Lower CONCN.
needed).
c) engorged epidural venous plexus.
d) ? raised CSF progesterone levels.
 Spinal ligaments including ligament flavum SOFT hence
loss of resistance technique used for regional block may be
masked
CNS : its anaesthetic importance

27. 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

28. 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.

29.  Narcotics and anti-cholinergic reduce lower
esophageal 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

30.  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).

31. ↑ 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.

32.  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 pseudocholinesterase
activity is also present at term,but it rarely produces
significant prolongation of SCh action.
 Increased cholesterol gall stone
formation(progesterone).

33. ↑ 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

34. • 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 )

35.  Leucocytosis up to 21,ooo/µL.
 ↑ ESR
 10-20% ↓ in platelet count.(Mild thrombocytopenia not a
contra-indication for neuraxial block).
 Marked ↓ cell mediated immunity→ ↑ susceptibility to
viral infection.

36.  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.
Insulin levels steadily rise during pregnancy

37.  Secretion of HCG and elevated levels of estrogens
promote hypertrophy of the thyroid gland.
 ↑ TBG (↑ T3 & ↑ T4) → Free T3, T4 & TSH remain
normal.

38. • Increased level of relaxin - softening cervix
- relax symphysis pubis
- & pelvic joints
 Increased risk of back pain(lax ligaments)

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

40. Maximally dilates uterine vasculature so autoregulation is absent.
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-adrenengic drugs (e.g.Phenylephrine) have
similar effects causing less fetal acidosis.

41. 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.

42. Placental transfer of anaesthetic agents
Placental transfer of drugs depends on:
1) Molecular weight : < 500 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.

43. Limited effects if < 1MAC
& delivery within 10 min.
of induction
Cross placenta
freely
Inhalational Agents
Intravenous Agents:
Thipental, 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.
Meperidine
Minimal effect if < 1µg/Kg.Fentanyl
Minimal effects on
fetus.
The highly ionized
property impedes
placental transfer.
Muscle Relaxants

44. 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 cholinestrase in the maternal circulation.

45. 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 dilataton (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.

46. 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.

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

48. Summary
To illustrate how all these changes may affect anaesthetic
management, lets imagine performing a general anaesthetic for
caesarean setion 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 between 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

49. 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.