physiology of pregnancy

1. Physiological
changes
in
pregnancy
Presenter- Dr Abna
Moderator- Dr Sekar

2. Introduction
• Marked changes occur during pregnancy to adapt to
developing fetus and its metabolic demands
• Changes occurs due to
1) Changes in hormone activity
2) Increased maternal metabolic demands and
biochemical alterations
3) Mechanical effects by enlarged uterus
4) Hemodynamic alterations

3. Cardiovascular system
• Changes include
a. Increase in intravascular volumes and
hematology
b. Increase in cardiac output
c. Decrease in vascular resistance
d. Presence of supine hypotension

4. Hematological changes
• Intravascular volume increases (45%)
• Due to rising progesterone
changes in RAAS
Increased sodium and water retention
plasma protein concentration reduced
colloid osmotic pressure decreases
increased intravascular volume

5. • Red cell volume increases by only 30% leads to
physiologic anemia of pregnancy
• Leukocytosis( upto 13000/mm3)
• Platelet count <1.5 lakhs/mm3
• increase in factors 1,7,8,9,10,12 & von Willibrand Factor
• Decrease in factor 11,13,antithrombin 3, tPA
• factors II and V remain unchanged

6. Cardiac output
• First trimester-increases 35%
• 2nd and 3rd trimester -45-50%
• 1st stage of labor-10-25% prelabor values
• 2nd stage-50%
• Highest –immediately afer postpartum 80%-100%
Due to autotransfusion from final uterine
contraction,reduced vascular capacitance,
decreased lower extremity pressure from release
of aortocaval compression

7. Systemic vascular resistance
• Peripheral vascular resistance (VR) decreases due
to the vasodilatory effects of progesterone
• proliferation of low resistance vascular beds in the
inter-villous spaces of the placenta.
sistvascular beds in the inter-villous spaces of the
placenta.

8. Parameter Change Amount(%)
Heart rate Increased 15-25%
Stroke volume Increased 25-30%
Cardiac output Increased 40-50%
Systemic vascular
resistance
decreased 20%
Pulmonary vascular
resistance
decreased 35%
Central venous
pressure
No change
Pulmonary capillary
wedge pressure
No change

9. Aortocaval compression
• Supine hypotension –decrease in mean arterial
pressure >15 mm Hg and increase in heart rate> 20
beats /mt
• Symptoms-diaphoresis,nausea,vomiting,changes in
mentation

10. Aortocaval compression
compression of compression of IVC
Lower aorta
SV AND CO
blood to uteroplacental
Circulation
Supine hypotension syndrome
fetal hypoxia venous stasis in legs
DVT

11. • Compensatory mechanisms
1. Reflex increase in sympathetic system-
increased systemic vascular resistance
2. Increased venous pressure over IVC – diverts
blood to paravertebral plexus to azygous vein
to SVC

13. • BP – decrease slightly
• Auscultation-wide ,loud,split in first heart sound,
S3, soft systolic ejection murmur
• Chest X ray- apparent cardiomegaly
- increased vascular markings
-enlarged LA
- Straightening of left sided heart border
-postpartum pleural effusion

14. ECG
• right axis deviation
• RBBB
• ST depression of 1mm on left precordial leads
• Q waves in lead 3
• T wave inversion in lead 111,V2,V3

15. Echo
- trivial TR
- PR,MR
-Increased left atrial size
-increased left ventricular thickness
-Pericardial effusion

16. Anaesthetic implications
• Avoid aortocaval compression by placing wedge in
right hip
• Maternal hypotension due to anaesthetic drugs
causes reduced uteroplacental blood flow
• Maximum increase in cardiac output occurs
immediately after delivery
• Venodilatation increase risk of intravascular
migration of epidural catheter

17. Respiratory system
Changes in
1. Upper airway
2. Lung volumes and minute ventilation
3. Oxygen consumption and metabolic rate

18. Upper airway
• Capillary engorgement occurs with tissue friability
and edema of mucosal lining
• Leads to bleeding during intubation
• Suctioning may cause bleeding
• Increased risk for airway obstruction
• After extubation,airway may be compromised as a
result of edema

19. Lung volumes & minute ventilation
• MV increased 45-50% due to larger tidal
volume(50%) and increased respiratory rate
• Hormonal changes and increased rate of CO2
production results in increased ventilation
• Progesterone sensitises respiratory centre to
CO2 results in PaCO2 to fall
• significant respiratory alkalosis is prevented by a
compensatory ↓ in plasma HCO3 concentration.

20. • Expanding uterus forces diaphragm cephalad and creates
20% decrease in FRC
• Thoracic breathing favoured
• Closing capacity remains unchanged
• FRC/CC reduced- more rapid small airway closure with
reduced lung volumes
• Desaturation and hypoxia occur more rapidly

21. Parameter change Amount(%)
Tidal volume increased 40-45
Respiratory rate increased 0-15
Minute ventilation increased 45-50
Vital capacity No change
Total lung capacity decreased 0-5
Inspiratory capacity increased 5-15
Functional residual
capacity
decreased 20
FEV1,CC No change
FEV1/FVC No change

22. Oxygen consumption
• At term,increased by 20%
• 1st stage of labor-increased by 40% than prelabor values
• 2nd stage- increased by 75%

23. Anaesthetic implications
• Increased risk of hypoxemia( oxygen
consumption, less oxygen reserve, rapid airway
collapse)
• Airway management –challenging
a) weight gain and breast engorgement hinders
laryngoscopy
b) Mucosa bleeds easily
c) Use smaller size endotracheal tube
d) Full stomach considerations

24. • Response to anaesthetics
1. MAC is reduced
2. Reduced FRC –Faster induction with insoluble
agents
3. Increased minute ventilation-speeds induction
with soluble agents
4. Reduced requirement of LA

25. Gastrointestinal changes
• Stomach and pylorus displaced
cephalad by gravid uterus
• Displaces intraabdominal portion of esophagus
intrathoracic and decrease competence of LES
• High estrogen and progesterone decrease LES tone
• Gastrin from placenta increase gastric secretion
• Increased gastric pressure from uterus
• Gastric emptying is delayed during labor,pain,anxiety

26. Anaesthetic implications
• Pharmacological prophylaxis against aspiration
• Supine position against lateral tilt
• No positive pressure ventilation before intubation
• Rapid sequence intubation

27. Neurologic changes
• Increased sensitivity to both local and inhaled
anaesthetics
• At term,epidural veins engorged-decreases epidural
space and volume of CSF
• CSF pressure increases during labor in pulsatile
manner during contractions and pushing

28. Anaesthetic implications
• LA requirement is less
• Enhanced cephalad spread of LA
• Higher chance of dural puncture and intravascular
injection

29. Hepatobiliary systems
• Serum bilirubin,ALT,AST and LDH increase to upper limit
of normal range
• Plasma protein concentration reduced
• Elevated free blood levels of highly protein bound drugs
• Plasma cholinesterase activity decreased
• Prolong duration of succinylcholine but rarely of clinical
significance
• Risk of gall stone formation is high

30. Renal changes
• Renal blood flow and GFR increases 50-60%
• Blood urea nitrogen and creatinine levels are
reduced
• Levels of urine protein and glucose are increased
due to decreased renal tubular resorption capacity
• Dilation and atony of ureters due to progesterone
and ureteric compression results in urinary stasis
and UTI

31. Musculoskeletal changes
• Lumbar lordosis enhanced
• Anterior flexion of neck and slumping of neck
results in brachial plexus neuropathy
• Relaxin causes mobility of ligaments and skeleton
leading to backpain and pelvic discomfort
• Also may be cause for carpal tunnel syndrome in
pregnancy

32. References
• Millers 8 th edition
• Stoeltings physiology and pharmacology
• Schnider and levinson’s anaesthesia for obstetrics