This document discusses the physiological changes that occur in the cardiovascular, respiratory, and urinary systems during pregnancy. Some key points: - Cardiac output increases 30-50% by term due to rises in heart rate, stroke volume, and plasma volume. This supports the metabolic demands of the enlarged uterus and growing fetus. - Respiratory alkalosis occurs due to progesterone-induced hyperventilation and a drop in carbon dioxide levels. This helps facilitate oxygen transfer from the mother to the fetus. - Glomerular filtration rate increases up to 50% by the second trimester to support the higher circulating blood volume. This causes increases in urinary frequency. - The diaphragm is elevated

1. CARDIOVASCULAR ,
RESPIRATORY AND
URINARY SYSTEM
PHYSIOLOGICAL CHANGES IN
PREGNANCY
Presenter:
Maj Anuradha Sawant
Moderator:
Lt Col Bikram Bhardwaj

2. ANATOMICAL CHANGES
• Diaphragm is progressively elevated up to 4 cm
• Heart is displaced upwards and outwards
• Left heart border is straightened
• Apex beat moves laterally to 4th intercostal space
• Some gravida may have benign pericardial effusion
• SIGNIFICANCE: Large cardiac silhouette in chest x-ray
• ? Pathological cardiomegaly!

3. CARDIOMEGALY IN A 36 WEEK PREGNANT LADY

4. PLASMA VOLUME
• Increase in plasma volume begins at 6-8 weeks
• Max volume (4700-5200ml) @ 32 weeks –(
increase of 45% )
• MECHANISM- unclear/ related to NO mediated
vasodilation-HYPOTENSION – induces RAAS-
increases Na & H2O retention
SIGNIFICANCE-(i) meets the metabolic demands of
enlarged uterus and the hypertrophied vascular
system
(ii)Provides nutrients to support growing placenta
and fetus
(iii)protects the women and fetus from
deleterious effects of impaired venous return in
supine
(iv)Safeguards the mother against parturition
related blood loss

5. RBC VOLUME
Increases by 250 ml to 450 ml (20-30%) by term
Production of RBC increases /not the life
Increased Erythropoiesis stimulated by-
(i) chorionic somatotropins
(ii) progesterone
(iii) prolactin
SIGNIFICANCE : It causes increase in maternal demand of iron by 500 mg
NOTE: (i) 300 mg of iron is transferred from the mother to the foetus
(ii) 200 mg of iron is taken for daily loss compensation
(iii) 200mg of iron is saved due to amenorrhea
(iv)200 mg of iron lost during parturition
(v) Therefore a total of 1 gm of iron is required In pregnancy
ref: Creasy and Resnik’s maternal fetal medicine

6. REASON FOR
HEMODILUTION?
Disproportionate increase in plasma volume to RBC
mass which causes – fall in HCT (max in 3rd trimester)
& physiological anemia
• SIGNIFICANCE –
• protective
• Reduces blood viscosity & counters for
thromboembolic events in pregnancy
• Beneficial for intervillous perfusion

7. CARDIAC REMODELLING IN
PREGNANCY
• Increasing plasma
•
• enlarging cardiac end diastolic and end systolic dimensions
• increased cardiac compliance i.e physiologically dilated
heart
• Compensatory ventricular remodelling(mass increases by
30-35% at term)- efficiency of cardiac work increases by
25%
• (No fall in ejection fraction)
• VENTRICULAR FUNCTION IS NORMAL IN PREGNANCY –i.e
for a given filling pressure the CO is appropriate
• cardiac remodelling returns back to normal after 3 months
of delivery
• LA dimensions normalise in 10 days postpartum
• LV dimensions take 4-6 months to stabilise

8. SYSTEMIC VASCULAR
RESISTENCE
Decreases as early as 5th week
Reasons:
(i) Vasodilatory effects of progesterone / prostacyclin PGI2
(ii) AV fistula like function of uteroplacental circulation
(iii) NO secreted by endothelium
Reduced systemic vascular resistance is the primary
trigger for (i) increase in HR/STROKE VOLUME/CO
(ii) & mid trimester fall in blood pressure!

9. HEART RATE

10. CARDIAC
OUTPUT
• CO= HR X SV (functional capacity
of heart)
• When measured in lateral
recumbent position , Cardiac
output increases by 30-50%
throughout pregnancy
• End of 1st trimester (#)– 40% rise
• Peaks @ 30-32 weeks -30-50%
rise(#)
• In multifetal cardiac output
increases by 20% higher than
singleton

11. INTRAPARTUM
CHANGES:
• 1st stage- 12-31%rise in
CO because of 22% rise in
stroke volume
• 2nd stage -increases
vigorously-49% rise (#)
• Immediate postpartum-
(autotransfusion)
• 80% rise in CO within 10-
15 mins (vaginal delivery)
(#)
• 60% in caesarean with
anaesthesia C
Cardiac output returns to
normal 1 hr after delivery

12. CHANGES IN CARDIAC
OUTPUT WITH POSITION
SUPINE POSITION:
uterus compresses over the gravid uterus –reduced venous
return-reduces cardiac filling = reduced cardiac output
From roll of supine to lateral cardiac output
• Increases by 20% @26- 30 wks
• Increases by 10% @32 to 34 wks
SIGNIFICANCE : If Labouring woman lies in lateral recumbent
position -foetal oxygen saturation will improve by 10%(simpson’s
and jame’s 2005)
STANDING POSITION:
cardiac output reduces to non pregnant state

13. SUPINE HYPOTENSIVE
SYNDROME
10% women
(Reason: collateral paravertebral and azygous are not
developed –causes reduced preload)
Rx?
SIGNIFICANCE-(i) lscs-wedge under rt back elevate rt hip(10-
15cm)
(ii) Compensatory sympathetic overactivity- but under SA/GA
this is blocked –so risk of sudden hypotension+ in lscs

14. CARDIAC OUTPUT: SELECTIVE
REGIONAL DISTRIBUTION
(i) Uterine blood flow – 10 times rise(500-800ml/hr) – i.e. from 2% of total CO in non
pregnant state to 17% in pregnant
(ii)Renal/Breast/Skin- rise by 50% in pregnancy( reason for flushing /sweating)
(iii) Brain and liver- no alteration in blood flow

15. BLOOD PRESSURE
• ABP falls early by 7th week
• max fall # mid trimester
• Reason?
• No mid trimester fall-#preeclampsia risk
• In left lateral recumbent :
both SBP /DBP decrease by 5-10 mmHg @24 weeks
and 10 -15 mmHg @32 weeks
MAP=(2 DBP + SBP)/3 - falls by 15 mmHg in
pregnancy
In sitting/standing :
SBP remains relatively stable but DBP falls by 10
mmHg and increases towardsterm

16. VENOUS PRESSURE
• Antecubital venous pressure remains unchanged in
pregnancy
• In supine femoral venous pressure increases-(improves on
lateral recumbent)
@early pregnancy-8 mmHg
@ term-24 mmHg
@ pregnant standing – 100 mmHg
• CLINICS: Stagnation –peripheral pooling- Vulval
oedema/pedal oedema/DVT/varicose veins/haemorrhoids
CENTRAL HEMODYNAMICS- no significant change in
CVP/MAP/PCWP

17. HEART SOUNDS
S1- CLOSURE OF MITRAL AND TRICUSPID VALVES
Heard loud in- tachycardia,MVP,hyperdynamic states,exercise,thyrotoxicosis
Split – mitral component closes earlier than tricuspid- early LV contraction/ delay in
right ventricular contraction(RBBB)/ASD/PVC
S2- CLOSURE OF PULMONARY AND AORTIC VALVES
Heard loud in- systemic hypertension/ coarctation of aorta /PAH
Split- Aortic valve closes slightly prior to pulmonary valve(pronounced in
inspiration)- RBBB/PAH/SUBVALVULAR STENOSISMR/VSD

18. HEART SOUNDS
S3- EARLY DIASTOLIC SOUND DUE TO RAPID FILLING OF VENTRICLES
best audible at apex
occurs in hyperdynamic states /volume overload state/AR/MR/TR/PHTN
S4- LATE DIASTOLIC
During late ventricular filling in active atrial contraction-
best heard at apex
Heard in - LVH/RVH/PULMONARY STENOSIS/PH /ACUTE MI

19. CARDIAC
SOUNDS
• Exaggerated loudness and
splitting of s1(as in RBBB)
• NO changes in s2
• Loud and easily heard s3
(rapid diastolic filling)
• 90% gravida have a systolic
murmur-(torsion of vessels
and decrease in blood
viscosity)
• 10%have a continuous hissing
murmur(mammary )

20. SOUFFLÉ IN PREGNANCY

21. ECG:
• left axis deviation because of
altered heart position &
concentric remodelling
• Q wave in lead ii ,iii, aVF
• (?old MI)
• Flat or inverted T in III,V1,V3
• (MI,RBBB,VENTRICULAR
HYPERTROPHY)

22. AGENTS MODIFYING THE
CARDIOVASCULAR PHYSIOLOGY IN
PREGNANCY

23. 1. RENIN ,ANGIOTENSIN II AND
PLASMA VOLUME
• Controls BP via Na+ and water balance
• All components of RAAS axis increase in pregnancy
• Renin secreted by maternal kidney & placenta
• Angiotensin secreted by maternal liver and foetal liver-its rise is due to high
oestrogen – maintains BP in first trimester

24. 2. CARDIAC NATRIURETIC PEPTIDES
ANP/BNP
Secreted by cardiomyocytes in response to wall
stretching
These regulate
blood volume
by natriuresis/
diuresis/
vascular smooth
muscle
relaxation
Level remain < 20 pg/ml in
normal pregnancy
Increase in severe
preeclampsia because of
severe cardiac strain and
afterload
Levels can be used to
screen left ventricular
systolic function or
chronic heart failure

25. 3. PROSTAGLANDINS
Controls vascular tone /BP/Na
balance
PGI2(prostacyclin)
Secreted by endothelium
/regulates BP & platelet
function
Maintains vasodilation in
pregnancy-deficiency causes
pathological vasoconstriction
PGE2
Renal medulla-rises late in
pregnancy (natriuretic)
PGI2 to
thromboxane ratio
in maternal urine
and blood is marker
for precclampsia

26. 4. ENDOTHELINS
Endothelin I
(potent
vasoconstrictor)
1. Production
stimulated by
angiotensin II
,thrombin and
vasopressin
2. Secreted by smooth
muscles and endothelium
–regulates the vasomotor
tone
3. In turn stimulates
ANP, aldosterone
,catecholamine
secretion
4.Pathologically raised
level is indicator of
pre-eclampsia

28. CARDIOVASCULAR SYSTEM
•PREGNANY IS A HYPERDYNAMIC
CIRCULATORY STATE!!!!

29. RESPIRATORY SYSTEM

30. ANATOMICAL
CHANGES
Diaphragm rises 4 cm in pregnancy
Subcostal angle widens from 68.5
degree to 103.5
Transverse chest diameter increases
by 2 cm
Overall thoracic circumference
increase by 6 cm
(not enough to compensate the fall
in lung volume because of raised
diaphragm)

31. PULMONARY
FUNCTION
TESTS
• Oxygen consumption is
increased by-
• - 20% in pregnancy
• --10% higher in multi
gestation
• - 40-60% higher in
labour
Unchanged- TLC/ RR/ LUNG
COMPLIANCE/VC

32. ACID BASE BALANCE
• Greater awareness of desire to breath is present during
pregnancy
• Which is wrongly interpreted as dyspnea
• Caused by increase in tidal volume and reduced PCO2 –
• Reason- progesterone reduces the threshold and
increases the sensitivity of chemoreflex response to CO2
which in turn causes hyperventilation-CO2 washout –
respiratory alkalosis-compensated by NaHCO3 renal
excretion

33. • Shift to left- (increased affinity of
maternal Hb to O2)-BOHR EFFECT-
reduced O2 releasing capacity of
maternal blood )
• But this is offset because Ph rise in
maternal blood stimulates rise of 2,3
BPG in maternal erythrocytes which
shifts the curve back to right
• i.e it lowers the affinity of maternal Hb
for O2- facilitates dissociation of O2
from Hb hence enhancing O2 transfer
to foetus
• Also , reduced Pco2 because of
washout helps co2 transfer from the
foetus to the mother and release of o2
to the foetus

34. RESPIRATORY SYSTEM
•PREGNANCY IS A STATE OF
CHRONIC RESPIRATORY
ALKALOSIS!

35. URINARY SYSTEM

36. URINARY
SYSTEM
• Kidney size increases by 1 cm
• GFR &PFR increases in pregnancy
• GFR increases by 25% by 2 week / 50 % by 2 trimester –
persists till day1 postpartum –
Reason:
Hypervolemia induced haemodilution lowers protein
concentration and oncotic pressure of plasma entering the
glomerular microcirculation
• Clinics: Because of Raised GFR – 60% nulliparous women
experience urinary frequency and nocturia

37. RELAXIN
• Produced by decidua
• Causes rise in GFR and RPF by
• (i) increase in renal NO –renal vasodilation –reduces
resistance in efferent and afferent renal vessels
• (ii) increased vascular gelatinase activity in pregnancy –
renal vasodilation- raised GFR

38. RFT
• Increased GFR causes reduction in maternal plasma creatinine , BUN &uric acid
• Serum creatinine-
• Mean value reduces from 0.7 to 0.5mg/dl
• >0.9 mg/dl means underlying renal disease and prompts further evaluation
Creatinine clearance in pregnancy is 30% more than (100-115ml/min) in non pregnant
state
BUN- 12mg/dl to 11mg/dl in 1st trimester ; 09mg/dl in 2nd trimester; 10mg/dl in 3rd
trimester
• Nocturia- because @day time -pooling in feet- oedema - On lying down – fluid
mobilises and hence leads to nocturia

39. URINE ANALYSIS
• Glycosuria in 1/6th women- because of raised GFR and impaired tubular
reabsorption of glucose from renal tubules
• If persistent glycosuria - mother needs to be tested for DM
• Haematuria - frequent because of (i)contamination during sample collection
• (ii)urinary tract infection
• (iii)common after a difficult labour
• Proteinuria- non pregnant- <150 mg/dl protein is excreted
• - In pregnant - >300 mg/dl(albumin minimal 5-30mg/dl)
• -is directly proportional to GFR

40. HOW TO MEASURE URINE PROTEIN
URINARY
PROTEIN
MEASUREMENT
QUALITATIVE
(DIPSTICK)
24 HRS
URINARY
PROTEIN
SPOT
PCR
Pitfall- fails to
account for renal
conc or dilution
of urine
Promising
approach-quick
collection and
reporting- but
doesn’t account for
diurinal variation
6 am- first hydrate the patient well –position in left lateral
for 45-60 mins – void the first 6 am morning sample
then start collecting for next 24 hrs- at final hour(6 am
next morning) – patient is again put in left lateral
recumbent position for an hour and at the end of this hour
final sample is collected.

41. URETERS
• Ureters become atonic due to high
progesterone levels
• Gravid uterus presses on the ureters
due to compression at the pelvic
brim- the intra-ureteral tonus
increases- leads to dilatation
• more on rt side in 60% women –
• Reasons:
• (i)left side the sigmoid colon provides
cushioning
• (ii)uterus is dextro-rotated
• (i)right ovarian vein complex is
oblique to right ureter and
contributes to dilatation
• ? DEXTROROTATED UTERUS
!URETER!AND LSCS!

42. BLADDER
• Hyperaemia and hyperplasia of bladder muscle and
connective tissue.
• Bladder mucosa is unchanged – only increase in size &
tortuosity of the blood vessels
• Bladder pressure in primigravida increases from 8 cm
H2O to 20 cm H2O at term
• Therefore to compensate for reduced bladder capacity
the length of urethra is increased( absolute =6.7 mm &
functional (4.8 mm)
• Max intraurethral pressure increases to only 70-93cm
H2O ,therefore continence is maintained

43. URINARY SYSTEM
•PREGNANCY IS A STATE OF COMPENSATORY RENAL
HYPERTROPHY AND HYPERFUNCTION!

44. THANKYOU