1. Physiological changes of pregnancy
Tom Archer, MD, MBA
UCSD Anesthesia

2. Outline Normal changes Implications for pathological conditions.CV
Respiratory
Hematologic
Endocrine
Urinary GI
Implications for pathological conditions.
Pregnancy as a “stress test for life”
Unveils problems that will appear later.

3. Outline Cardiovascular changes: To meet increased metabolic demand.
Increased blood volume / RBC mass
Decreased Hct and viscosity
Increased cardiac output deterioration in symptoms from stenotic heart lesions or pulmonary hypertension.

4. Outline Cardiovascular changes: Reversible cardiac hypertrophy (50%)
Valvular incompetency / conduction changes
All murmurs are not “flow murmurs”! But most are innocent.

5. Outline Hematologic changes: Increased clotting tendency
Increased fibrinogen
Decreased PT / PTT
Stasis in legs DVT
Increased platelet turnover.

6. Outline Respiratory changes: Increased O2 consumption / CO2 production
Decreased PaCO2 and venous HCO3-
Lots of normal saline will cause hyperchloremic metabolic acidosis.
Increased work of breathing
Decreased FRC (“airtank” reserve)
Decreased tolerance for apnea or hypoventilation.
Airway swelling.

7. Outline Endocrine (insulin) changes:
Pregnancy is diabetogenic due to placental hormones (Placental lactogen, HGH, cortisol, progesterone).
Insulin requirement increases during pregnancy.
Insulin requirement falls abruptly after delivery.
RAAS probably influences cardiac hypertrophy and increased RBC mass.

8. Type II DM in 2008 Obesity Hyperglycemia Inflammation Genetic
predisposition
Insulin resistance
Hyperglycemia
Atherosclerosis
Nephropathy
Retinopathy
Neuropathy
Immune dysfunction
Poor wound healing
Decreased insulin output
Pancreatic beta cell damage

9. Outline Urinary changes: GFR increases, normal creatinine falls.
“Normal” creatinine may show disease!
Ureteral obstruction with hydropnephrosis and pyelonephritis is common.
1/200 pregnancies will have urolithiasis

10. Outline GI changes: GERD is common
Gastric emptying is impaired during labor assume full stomach
Routine “triple Rx” before C/S? Bicitra, metoclopramide, famotidine.

11. Mom
4 ml O2 / kg / min
Feto-placental unit
12 ml O2 / kg / min
Mother is consuming and delivering
oxygen for two!

12. CV in pregnancy– Big Picture
Increase O2 demand Increased CO.
Stable BP with increased CO means decreased SVR.
Slight increase in HR, Increase in SV.

13. Cardiac output increases
35% by 12 weeks
50% for rest of pregnancy
60%-100% during labor
CO highest right after delivery (release of aorto-caval compression) and uterine contraction (autotransfusion).

14. Both delivery and oxytocin cause increase in cardiac output.
Delivery of baby
Oxytocin 5U IV push
Phenylephrine bolus for hypotension
C/S under epidural in pt with previous peripartum cardiomyopathy (May 30, 2007)

15. Increased CO in pregnancy increases symptoms from stenotic heart lesions or pulmonary hypertension
May need interventional procedure (balloon mitral valvuloplasty, AVR) or termination of pregnancy.
Case at UTHSCSA of AS, decompensation with balloon valvuloplasty, emergency AVR, fetal death, maternal improvement in AS.

16. For stenotic heart / lung lesions, highest stress ( highest CO) occurs immediately after delivery.

17. Eccentric cardiac hypertrophy in pregnancy
Due to increased activity of RAAS?

18. Non-pregnant vs late pregnant mouse hearts
Non-pregnant vs late pregnant mouse hearts. Note hypertrophy and conduction disturbance (QRS prolongation) in LP mouse heart.
Eghbali M (Trends Cardiovasc Med 2006;16:285–291)

19. Pressure overload eg AS
Volume overload eg pregnancy or athletics

20. Hematologic changes at term:
Blood volume increased by 45%.
RBC volume increased by 15%.
Hct falls blood viscosity falls
Pregnant woman may tolerate hemorrhage better than non-pregnant woman, before showing fall in BP.

21. Average blood loss at delivery:
600 ml with vaginal delivery.
1000ml with C/S.

22. Hematologic changes at term:
Fibrinogen increased.
PT, PTT shortened 20%.
Increased platelet turnover.
Increase in coagulation factors,
immobilization and aorto-caval compression all increase risk of DVT.

23. Physiological changes of pregnancy at term:
Maternal-fetal O2 consumption increases 40-50% over non-pregnant state.
Cardiac output increases by 50%.
Functional residual capacity (apneic reserve of O2) decreases by 20%
Pregnant patient has diminished capacity to tolerate apnea!
Chestnut chap. 53

24. Functional residual capacity (FRC) is our “air tank” for apnea.
from Google images

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

26. Pregnant woman: a respiratory disaster waiting to happen
Lung Volumes and implications:
FRC is reduced to 80% of non-pregnant value by term.
FRC of pregnant woman in supine position is 70% of that in sitting position.
Regional anesthesia further decreases the FRC!
HENCE: SUPINE, PREGNANT PATIENT WITH A REGIONAL BLOCK HAS A TRIPLY DIMINISHED FRC!!!
OBESITY IS A FOURTH FACTOR DECREASING FRC!
Anesthetic implication: VERY rapid desaturation in pregnant patients after apnea due to rapid sequence induction or seizure.
YOU MUST DO A GOOD PRE-OXYGENATION PRIOR TO INDUCTION OF GA!
YOU MUST HAVE ALL OF YOUR AIRWAY SUPPLIES IMMEDIATELY AVAILABLE!

27. At term, mother has respiratory alkalosis with metabolic compensation (less HCO3- buffer).
ABGs
Non-pregnant
At term
PaCO2 40 30
PaO2
100
103 pH
7.40
7.44
HCO3- 24 18
Chestnut

28. Compared to non-pregnant state, pregnant woman has less tolerance for:
Apnea
Acidosis

29. Vascular congestion
Swelling of respiratory mucosa (nose, rest of airway).
Don’t put anything through the nose if you can avoid it  prevent bad nose bleed.

30. Pregnancy is “diabetogenic”. Why?
Placental hormones plus obesity may overwhelm adaptive capacity of pancreatic insulin output.

31. Obesity Two vicious cycles of type II DM in pregnancy: #1
Inflammation
“Glucotoxicity”
Genetic
predisposition
Insulin resistance #1
Placental
hormones
Hyperglycemia
Placental vascular damage
Atherosclerosis
Nephropathy
Retinopathy
Neuropathy
Immune dysfunction
Poor wound healing
Decreased insulin output #2
Pancreatic beta cell damage

32. Gestational DM:
Appears in 4% of pregnancies. Possibly due to inability to make enough insulin to counteract the “counteregulatory hormones” which increase in pregnancy—placental lactogen, placental GH, cortisol and progesterone.
Gestational DM tends to recur in subsequent pregnancies. Gestational DM increases risk for type 2 DM later in life.

33. Pregestational DM:
Insulin requirements increase rapidly after the 26th week of gestation. Insulin requirement at term is about 50% more than pre-pregnant requirements.
Insulin requirements fall during first stage of labor, but rise during second stage of labor.
Insulin requirement falls up to 40% the day after delivery. Placental hormones are “diabetogenic”.

34. Urinary system Renal infections increase in incidence.
Progesterone relaxes ureters
Compression of ureters at pelvic brim obstruction infection

35. GI tract Decreased gastric emptying Increase GERD
Full stomach precautions

36. Avoid aorto-caval compression: use left uterine displacement (LUD)
LUD helps venous return. C/S as part of resuscitation?
LUD decreases chance of DVT
LUD increases O2 delivery to fetus:
Increases uterine artery pressure and decreases uterine venous pressure.
Why we don’t do it: It doesn’t look right!

37. Colman-Brochu S 2004

38. Chestnut chap. 2