Maternal Cardiovascular Changes During Pregnancy

Maternal Changes During Pregnancy

• All specialities must understand the effects pregnancy has on a patient.
• Pregnancy is more than just a female with an enlarged uterus.
• The pregnant woman undergoes several profound anatomic and physiologic changes, beginning almost immediately after conception, evolving through delivery, and mostly reverts back following delivery.
• These adaptations are to accommodate new demands to support and protect the fetus and mother; volume, nutrition, oxygen, starvation, toxins, drugs, labor and fetal waste.

Cardiovascular Changes

• Cardiac output is the stroke volume multiplied by the heart rate
• CO rises by 30-50% overall during pregnancy, half of this by week 8
• The increase in CO is caused initially by increased stroke volume
• Heart Rate becomes the major contributor in late pregnancy.
• Posture affects blood flow, the left lateral recumbent position will have the highest CO
• Lying in the supine position lowers CO by 30% due to IVC compression
• Ejection fraction remains unchanged
• Elevated cardiac performance results from changes in preload, afterload, and maternal rate:
• Preload is ventricular filling and Afterload is the load the heart must eject blood against

Cardiac Output

• Preload is increased with an increase in volume
• Afterload is reduced because of decreased Systemic Vascular Resistance (SVR)
• Maternal heart rate increases by 20bpm
• Blood pressure falls early in gestation to a mean of 105/60 in the second trimester
• Diastolic pressures decreases more than systolic
• Reduced SVR is a result of high flow, low resistance, and vasodilation
• Related possibly to increased Nitric Oxide, and increased endothelial prostacyclin

Regional Blood Flow

• The majority of an increased CO is distributed to the placenta, kidneys, and skin, providing nutrients to the fetus, excretion of waste, and temperature control
• Uterine blood flow increases from 25ml/min to 1200ml/min with a blood flow of 750ml/min at term
• It's important in event of hemorrhage, trauma during labor and delivery
• Each contraction forces about 500ml of blood from the uterus into systemic circulation
• CO increases 15% in early labor, 25% in active phase, and 50% in second stage
• CO Peaks 80% above prelabor immediately postpartum due to autotransfusion from uterine compression

Hematologic Changes

• Plasma volume increases by 40-50% above nonpregnant levels, rising at week 4 and peaking between weeks 28-34
• There's is a gain of 1100 to 1600ml on average
• An increase in sodium retention of 900-1000mEq, reset of osmostat, and further increases in Na does not increase volume
• Red blood cell mass increases beginning at weeks 8-10 then rising steadily.
• There is a 20-30% increase in women taking iron and 15-20% increase if no iron

Physiologic Anemia

• Increased plasma erythropoietin causes an increase in the red blood cell mass.
• Intravascular volume increases ore than red blood cell mass.
• Dilutional/Physiologic Anemia causes a drop in Hematocrit despite increased red blood cells.
• A decrease in viscosity promotes placental perfusion and decreases cardiac work.
• There is a reserve against blood loss at parturition and postpartum hemorrhage

Systemic Coagulation

• Pregnancy is in a hypercoagulable state
• There is a resistance to activated Protein C
• Protein S decreases
• Increased Factors I, II, V, VII, VIII, X, XII occur
• Venous Thromnosis occurs in 0.7/1000 pregnancies
• Thrombosis is associated with risks of pulmonary embolus, spontaneous abortion, and intrauterine fetal demise.

Pulmonary changes

• Mucosal edema and vascularity increase and rhinitis and epistaxis may occur.
• There is an 8% increase in thoracic circumference
• The diaphram elevates 5cm due to increase of uterus
• An increased of dyspnea of 15% by 10 weeks, 50% by 19 weeks, 76% by 31 weeks
• As pregnancy progresses, the uterus elevates the resting position of the diaphragm causing normal diaphragmatic contractility

Pulmonary Adaptations

• FEV1 remains unchanged
• Functional Residual Capacity(FRC) decreases 10-25%
• Total Lung Capacity (TLC) minimally decreases
• Minute Vent increases 20-40%
• Alveolar Vent increases 50-75%
• Total body oxygen consumption increases 15-20% with half accounted for by the uterus and the other half attributed to maternal renal and cardiac work.
• Pregnancy results in compensated respiratory alkalosis because carbon dioxide diffuses faster than oxygen.
• Expect a decreased PaCO2 (27-34), increased bicarb (18-21), pH between 7.40 and 7.45, increased PaO2 (101-104), and increased A-a gradient (14.3).
• Despite unchanged or decreased airway resistance during pregnancy, up to 70% of women complain of dyspnea
• Marked decrease in PCO2 may be the cause, as may be increased tidal volume

Renal Changes

• The urinary collecting system undergoes dilation including calyces, renal pelvises, ureters due to the effects of progesterone and mechanical obstruction.
• Progesterone also decreases ureteral tone, peristalsis, and intraureteral pressure.
• The enlarged uterus obstructs the ureter at the pelvic brim along with the enlargement of ovarian vessels.
• Hydronephrosis can develop from these ureter obstructions.
• Dextrorotation of the uterus makes the right side more common to develop Kidney problems.
• The dilated collecting system can hold 200-300ml of urine creating a reservoir for bacteria, increasing risks for UTIs, stones, and pyelonephritis

Renal Blood Flow

• Renal blood flow and GFR both rise markedly in pregnancy, beginning within the first month.
• Both will plateau at 40-50% above nonpregnant levels by end of first trimester.
• Kidneys enlarge by 1.5 cm due to 80% increase in renal blood flow.
• Elevated GFR is reflected in lower serum creatinine and urea nitrogen blood tests.
• Higher rates of filtration may result in small amounts of glucosuria or ketonuria.
• Persistent hyperventilation leads to renal losses of bicarb and a compensated respiratory alkalosis.
• Reduced renal buffering ability due to loss of bicarb can predispose pregnant women to metabolic acidosis.

Endocrine Changes

• Gland may enlarge in many pregnancies particularly in regions with iodine deficiencies
• Reduced TSH is produced by anterior pituitary in first trimester in response to human chorionic gonadotropin(hCG)
• T3 and T4 thyroid levels are significantly increased, active thyroid hormone remains at normal nonpregnant levels
• Only 85% of T3 and T4 are bound to TBG, TBG increases twofold due to estrogen, and as TBG increases, the thyroid increases as well
• Maternal T4 crosses placenta throughout pregnancy
• Fetal thyroid function begins around 20 weeks

Adrenal Activity

• Glucocorticoid production increases along with Coricosteroid Bonding Globulin (CBG)
• The placenta produces Corticotropin Releasing Hormone(CRH), stimulate the production of maternal ACTH and cortisol is three times higher in the third trimester compared to pregnancy
• Placental hormones affect maternal glucose, lipid metabolism in order to ensure an adequate supply of fuel and other nutrients
• CHO metabolism supplies glucose, amino acids, free fatty acids, ketones, and glycerol for maternal fuel sources .

Metabolic Adaptations and Carbohydrates

• Pancreatic Beta cells increase in size along with progressively increasing amounts of insulin secretion.
• Insulin resistance normally occurs primarily due to Human Placental Lactogen(HPL)/Human Chorionic Somammotropin(hCS).
• Insulin resistance markedly increases at the middle of the second trimester
• The diagnosis of Gestational diabetes is diagnosed when maternal pancreatic function cannot overcome the increasing insulin resistanc.
• During pregnancy, there is insulin resistance, but fasting glucose levels are lower due to glycogen stores being built up, an increase in periphereal glucose absorbtion, decreased hepatic glucose production and more glucose consumption from the fetus

Glucose Consumption

• Compared to nonpregnant glucose homeostasis, transient hyperglycemia occurs after meals because of insulin resistant state
• The mother will preferentially use fats from fuel as well as preserve her glucose, amino acids, proteins and carbohydrates
• Means fasting glucose is 56mg/dL

Metabolic Adaptations and Lipids

• Triglycerides and cholesterol increase during pregnancy with triglycerides increasing 300% and cholesterol increasing 50%
• There is an increase in lg production
• The activities of the Lipoprotein lipase is suppressed, decreasing adipocyte catabolism
• Hih TG levels allow for more usage of maternal fuel and CHO sparing.
• High cholesterol will aid in placental steroidogenesis

Gastrointestinal Changes

• Pregnancy has little effect on GI secretion, absorption, but motility is slowed due to elevated progesterone.
• There is elevated progesterone and estrogen
• Bloating and constipation are common during pregnancy due to the increases
• Mechanical factors will compress the uterus
• Appendicitis can occur and presents unusually

GERD

• GERD occurs in 30-50% of pregnancies
• More common in first trimester
• Lower esophageal sphincter pressures fall with increased intraabdominal pressure
• Complications are reflux are uncommon.

Dermatologic Changes

• A hyperpigmentation in pregnant women occurs in 90% of pregnancies, including areolae
• Melanocyte-stimulating increases
• The linea alba becomes the hyperpigmented linea nigra.

Striae

• Striae are thin, atrophic scars on the abdomen, breasts and thighs that tend to appears in late second trimester around the abdomen. It usually affects 80-90% of women
• Striae is due to the growth of the fetus and tearing of the collagen matrix when the mother cannot produce the proper collagen
• Adrenocorticosteroids and estrogen can also promote tearing
• Many ointments claim to reduce the presence of striae but are unproven and of minimal benefit

Summary

• The pregnant woman undergoes dramatic changes in nearly every organ system
• Understanding normal physiology paramount to treating disease, which is an alteration in normal form and function