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

2. Outline Normal changes –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 (30%?) 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 Hyperglycemia Obesity Inflammation Insulin resistance Atherosclerosis Nephropathy Retinopathy Neuropathy Immune dysfunction Poor wound healing Pancreatic beta cell damage Decreased insulin output Genetic predisposition

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

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. 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.

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

16. Tricuspid Pulmonic Pulmonary capillaries Mitral Aortic stenosis Resistance arterioles Aortic stenosis at rest  Cardiac output not sufficient to cause critically high LV intracavitary pressure / LV failure. LV dilation / hypertrophy

17. Tricuspid Pulmonic Pulmonary capillaries (edema) Mitral Aortic Stenosis Resistance arterioles– decreased SVR Aortic stenosis with increased cardiac output / arteriolar vasodilation: Decreased SVR  Fall in systemic BP and / or increase in LV intracavitary pressure  ischemia or LV failure. LV failure / ischemia

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

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

20. www.pitt.edu/~super1/lecture/lec9691/018.htm Pressure overload eg ASVolume overload eg pregnancy or athletics

21. 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.

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

23. 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.

24. 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

25. Functional residual capacity (FRC) is our “air tank” for apnea. www.picture-newsletter.com/scuba-diving/scubawww.picture-newsletter.com/scuba-diving/scuba... from Google images

26. Pregnant Mom has a smaller “air tank”. Non-pregnant woman www.pyramydair.com /blog/images/scuba- web.jpg

27. 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!

28. At term, mother has respiratory alkalosis with metabolic compensation (less HCO3- buffer). ABGsNon- pregnant At term PaCO24030 PaO2100103 pH7.407.44 HCO3-2418 Chestnut

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

30. 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.

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

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

33. 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.

34. 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”.

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

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

37. 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!

38. Colman-Brochu S 2004

39. Chestnut chap. 2

40. The End