Physiological changes of pregnancy

Tom Archer, MD, MBA

UCSD Anesthesia

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.

OutlineCardiovascular 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.

OutlineCardiovascular changes:

Reversible cardiac hypertrophy (50%)

Valvular incompetency / conduction changes

All murmurs are not “flow murmurs”! But most are innocent.

OutlineHematologic changes:

Increased clotting tendency

Increased fibrinogen

Decreased PT / PTT

Stasis in legs DVT

Increased platelet turnover.

OutlineRespiratory changes:

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

OutlineEndocrine (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.

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

OutlineUrinary 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

OutlineGI changes:

GERD is common

Gastric emptying is impaired during labor assume full stomach

Routine “triple Rx” before C/S? Bicitra, metoclopramide, famotidine.

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

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.

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).

Phenylephrine bolus for hypotension

Delivery of baby

Oxytocin 5U IV push

C/S under epidural in pt with previous peripartum cardiomyopathy (May 30, 2007)

Both delivery and oxytocin cause increase in cardiac output.

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.

For stenotic heart / lung lesions,highest stress ( highest CO) occurs

immediately after delivery.

Eccentric cardiac hypertrophy in pregnancy

• Due to increased activity of RAAS?

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.

www.pitt.edu/~super1/lecture/lec9691/018.htm

Pressure overload eg AS Volume overload eg pregnancy or athletics

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.

Average blood loss at delivery:

• 600 ml with vaginal delivery.

• 1000ml with C/S.

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.

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

Functional residual capacity (FRC) is our “air tank” for apnea.

www.picture-newsletter.com/scuba-diving/scuba... from Google images

Pregnant Mom has a smaller “air tank”.

Non-pregnant woman

www.pyramydair.com/blog/images/scuba-web.jpg

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!

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

Compared to non-pregnant state, pregnant woman has less tolerance for:

• Apnea

• Acidosis

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.

Pregnancy is “diabetogenic”. Why?

• Placental hormones plus obesity may overwhelm adaptive capacity of pancreatic insulin output.

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

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.

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”.

Urinary system

• Renal infections increase in incidence.

• Progesterone relaxes ureters

• Compression of ureters at pelvic brim obstruction infection

GI tract

• Decreased gastric emptying

• Increase GERD

• Full stomach precautions

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!

Colman-Brochu S 2004

Chestnut chap. 2

http://www.manbit.com/OA/f28-1.htm