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Physiological changes of pregnancy

Physiological changes of pregnancy

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Physiological changes of pregnancy

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  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 (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. Obesity Type II DM in 2008 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. 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.

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

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

  17. Pulmonary capillaries (edema) LV failure / ischemia Tricuspid Aortic Stenosis Pulmonic Mitral 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. Resistance arterioles– decreased SVR

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

  19. 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)

  20. Pressure overload eg AS Volume 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. from Google images

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

  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). 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. Obesity Two vicious cycles of type II DM in pregnancy: 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

  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: useleft 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