physiological changes during pregnancy 2010

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Physiological Changes During PregnancyDr Che Badariah Ab Aziz Dept of Physiology

Contents Introduction Cardiovascular System Haematology Respiratory System Gastrointestinal System Endocrine System Renal Function Central Nervous System

Introduction:Relative Uterus Size During Pregnancy

IntroductionThe physiological changes during pregnancy maintain a healthy environment for the fetus without compromising the mother's health. However, sometimes the changes will give discomfort to the mother. Many complex physiological changes are observed in the mother during pregnancy and, for the most part, they are brought about by the physical presence of the placenta (i.e. the large low pressure vascular space created) and gravid uterus placental secretions other endocrine changes

Effects of Pregnancy: Metabolic Changes The placenta secretes human placental lactogen (hPL), also called human chorionic somatomammotropin (hCS), which stimulates the maturation of the breasts hPL promotes growth of the fetus and exerts a maternal glucose-sparing effect Human chorionic thyrotropin (hCT) increases maternal metabolism Parathyroid hormone levels are high, ensuring a positive calcium balance

Effects of Pregnancy: Physiological Changes GI tract morning sickness occurs due to elevated levels of estrogen and progesterone Urinary system urine production increases to handle the additional fetal wastes Respiratory system edematous and nasal congestion may occur Dyspnea (difficult breathing) may develop late in pregnancy

Cardiovascular System Multiple changes, many of which are compensatory designed to cope with growing fetus, uterus and placenta Increased cardiac output is main overall result of changes

Cardiovascular System Position and Size of Heart As the uterus enlarges and the diaphragm becomes elevated, the heart is displaced upward and somewhat to the left with rotation on its long axis, so that the apex beat is moved laterally. Cardiac capacity increases by 70-80mL; this may be due to increased volume or hypertrophy of cardiac muscle. The size of the heart appears to increase by about 12%

Cardiac Output (CO) CO increase approximately 40% during pregnancy, reaching its maximum at 20-24 weeks gestation and continuing at this level until term. The increase in CO can be as much as 1.5L/min over the non pregnant level. (4.5L/min to 6 L/min). The major part is due to increases in stroke volume. The basal heart rate increases by about 10 beats per minute, which accounts for a small part of the increased CO.

Factors increasing CO during pregnancyPlacenta ------> large and low resistance A-V shunt

progesterone vasodilatation

systemic resistance

BP

blood volume

venous return

BP

metabolism

CO HR SV

BP

perfusion

Blood Pressure Systemic blood pressure declines slightly during pregnancy. There is a little change in systolic blood pressure, but diastolic pressure is reduced (510mmHg) from about 1226 weeks. Diastolic pressure increases thereafter to prepregnancy levels by about 36 weeks.

Blood Pressure BP = PR x CO Because blood pressure either decreases or remain the same during pregnancy and cardiac output increases appreciably, there is good evidence that peripheral resistance declines markedly.

Venous pressure Pressure of pregnant uterus on femoral vein and inferior vena cava impedes the blood flow from the legs Venous pressure rises and forces the fluid out and causes oedema Distensibility of the veins ** also decreases the venous return to the heart Lateral recumbent position relieves the pressure on the femoral veins/IVC and venous pressure is reduced to normal ** 1) Progesterone decreases intrinsic vascular tone by renderingthe vessel walls less responsive to angiotensin II, norepinephrine and epinephrine. 2) Endothelial cells increase production of vasodilatory prostaglandins (e.g., PGI2) which decreases sensitivity of arterioles to angiotensin II and nor-epinephrine.

Hematological SystemBlood Volume Total plasma volume increases in early pregnancy and continues to increase throughout pregnancy. The magnitude of the increase varies greatly between individuals, ranging between a 40-90% increase. Average increases amount to 12501800 ml.

Blood Volume Increased blood flow to the uterus, increased perfusion of others organs, especially kidneys and extra metabolic needs of the fetus Extra volume also compensate for maternal blood loss delivery. The average blood loss with vaginal delivery is 500-600ml, and with cesarean section is 1000ml. Plasma protein concentration falls dramatically in early pregnancy due to expansion in blood volume. Serum albumin concentration falls from a non-pregnant value of 4 gms/100 ml to 2.5-3.0 gms/100 ml. As a result oncotic pressure falls which favors filtration at the capillary, often leading to a general edema, especially in lower limbs.

Mechanism of increased blood volume during pregnancy

PLACENTAL STEROIDS Plasma volume ALDOSTERONE

Na+ and water retention BV haemodilution

HPL erythropoietin ESTROGEN

RBC production

Effects of increased blood volume during pregnancy physiological anemia plasma volume dilution RBC count Hb concentration Haematocrit BV RBC mass plasma protein concentration

oedema plasma osmolarity

Red Blood Cells Red cell volume also increases about 33%, but frequently lags behind the plasma volume, resulting in a reduced hematocrit and hemoglobin concentration. This has sometimes been referred to as the physiologic anemia of pregnancy. The total amount of hemoglobin is greater during pregnancy The oxygen carrying capacity of the blood is higher and this matches the increase in oxygen consumption. **Progestrone, hPL, PRL stimulate erythropoiesis

Iron requirement Iron requirement increases with the increase in red blood cells (Hb production) If supplemental iron is not added to the diet, iron deficiency anemia will result. Maternal requirements can reach 5-6mg/d in the latter half of pregnancy. If iron is not readily available, the fetus uses iron from maternal stores. Thus, the production of fetal hemoglobin is usually adequate even if the mother is severely iron deficient. Therefore anemia in the newborn is rarely a problem; instead, maternal iron deficiency more commonly may cause preterm labour and late spontaneous abortion, increasing the incidence of infant wastage and morbidity

Plasma and Erythrocyte volume changes during pregnancy Pitkin RM: Nutrtional support in obstetrics and gynecology. Clin Obstet Gynecol 19:489-513, 1976.

White Blood Cells The total WBC count increases during pregnancy from a prepregnancy level of 4300-4500/mL to 5000-12000/mL in the last trimester. Lymphocyte and monocyte numbers stay essentially the same throughout pregnancy; polymorphonuclear leucocytes are the primary contributors to the increase.

Clotting Factors During pregnancy, levels of several essential coagulation factors is increased. There are marked increase in fibrinogen and factor 8. Factors VII, IX, X, and XII also increased but to a lesser extent. (Estrogen effect) Fibrinolytic activity is depressed during pregnancy and labor, although the precise mechanism is unknown. The placenta may be partially responsible for this alteration in fibrinolytic status. Plasminogen levels increase concomitantly with fibrinogens levels, causing an equilibration of clotting and lysing activity. Holmes & Wallacet (2005)

Pulmonary System Anatomic and Physiologic Changes Early in pregnancy, capillary dilatations occurs throughout the respiratory tract, leading to engorgement of the nasopharynx, larynx, trachea, and bronchi. This causes the voice to change and makes breathing though the nose difficult. Chest X-rays reveal increased vascular makings in the lungs. As the uterus enlarges, the diaphragm is elevated as much as 4cm, and the rib cage is displaced upward and widens, increasing the lower thoracic diameter by 2cm and the thoracic circumference by up to 6cm. Elevation of the diaphragm does not impede its movement. Abdominal muscles have less tone and are less active during the pregnancy.

Respiratory System Lung Mechanics and Volumes Tidal volume increases by up to 45% at term FRC is decreased by 20 30% at term due to reduction in expiratory reserve volume and residual volume Closing capacity can become greater than FRC causing V/Q mismatch and ready occurrence of hypoxia Minute Volume increased by up to 50%, this is stimulated by high progesterone levels and increased carbon dioxide production

Respiratory System - Blood Gases pCO2 decreases secondary to alveolar hyperventilation (3.7 4.2kPa) Metabolic compensation reduces bicarbonate level to about 18-21mmol/l (kidney excretes more HCO3-) pO2 rises to approx 14kPa whilst upright, may fall when supine

Respiratory System Pulmonary circulation Pulmonary vascular resistance reduced Pulmonary blood flow increased Pulmonary blood volume increased Oxygen consumption increased by 30 60 % due to metabolic demands of fetus, uterus and placenta. (therefore hypoxia can develop rapidly)

Lung Volumes and CapacitiesDead volumes increases owing to relaxation of the musculature of conducting airways. Tidal volumes increases gradually (35-50%) as pregnancy progresses. Total lung capacity is reduced (45%) by the elevation of the diaphragm. Functional residual capacity, residual volume, and respiratory reserve volume all decrease by about 20%. Larger tidal volume and smaller residual volume cause increased alveolar ventilation (about 65%) during pregnancy. Inspiratory capacity increases 510%.

Functional respiratory changes include a slight increase in respiratory rate, a 40% increase in tidal volume, a 50% increase in minute ventilation, and a progressive increase in oxygen consumption of up to 15-20% above nonpregnant levels by term. As the respiratory minute volume increases, hyperventilation of pregnancy occurs, causing a decrease in alveolar CO2. This decrease lowers the maternal blood CO2 tension; however alveolar O2 tension is maintained within normal limits. Maternal hyperventilation is considered a protective measure that prevents the fetus from the exposure to excessive levels of CO2. The high circulating levels of progesterone that occur during pregnancy increase the sensitivity of the hypothalamic respiratory centers to small increases in PCO2, and also lowers the "set-point."

Urinary System Renal Dilatation During pregnancy, each kidney increases in length by 1-1.5cm, with a concomitant increase in weight. The renal pelvis is dilated. The ureters are dilated above the brim of the bony pelvis, elongated, widen, and become more curved. Thus, increase in urinary stasis, this may lead to infection and may make tests of renal function difficult to interpret. The absolute cause of hydonephrosis and hydroureter in pregnancy is unknown, there may be several contributing factors: 1-Elevated progesterone levels may contribute to hypotonia of the smooth muscle in the ureter. 2-The ovarian vein complex in the suspensory ligament of the ovary may enlarge enough to compress the ureter at the brim of the bony pelvis, thus causing dilatation above that level. 3-Dextrorotation of the uterus during pregnancy, may explain why the right ureter is usually more dilated than the left. 4-Hyperplasia of smooth muscle in distal one-third of the ureter may cause reduction in the luminal size.

Renal Function The renal plasma flow rate increases by as much as 25-50%; from 600 ml/min to 1200 ml/min in the first trimester which then returns to the nongravid flow at term The glomerular filtration rate (GFR) increases during pregnancy by about 50%; normally about 120 ml/min and in pregnancy increases to 150-180 ml/min. Even thought the GFR increased dramatically during pregnancy, the volume of the urine passed each day is not increased. Thus, the urinary system appears to be even more efficient during pregnancy. With the increase in GFR, there is an increase in endogenous clearance of creatinine. The concentration of creatinine in serum is reduced in proportion to increase in GFR, and concentration of blood urea nitrogen is similarly reduced.

Glucosuria during pregnancy is not necessarily abnormal, may be explained by the increase in GFR with impairment of tubular reabsorption capacity for filtered glucose. Increased levels of urinary glucose also contribute to increased susceptibility of pregnant women to urinary tract infection. Proteinuria changes little during pregnancy and if more than 500mg/24h is lost, a disease process shoud be suspected Levels of the enzyme renin, which is produced in kidney, increase early in the first trimester, and continue to arise until term. This enzyme acts on its substrate angiotensinogen, to first form angiotensin 1 and then angiotensin 2, which acts as a vasoconstrictor. Normal pregnant are resistant to the pressor effect of elevated levels of angiotensin 2 but those suffering from preeclampsia are not resistant, this is one of the some theories to explain this disease.

Bladder As the uterus enlarges, the urinary bladder is displaced upward and flattened in the anterior-posterior or diameter. Pressure from the uterus leads to increased in urinary frequency. Bladder vascularity increases and muscle tone decreases, increasing capacity up to 1500ml.

Gastointestinal Motility Gastrointestinal motility may be reduced during pregnancy due to increased levels of progesterone, which in turn decrease the production of motilin, a hormonal peptide that is known to stimulate smooth muscle in the gut. Transit time of food throughout the gastrointestinal tract may be so much slower that more water than normal is reabsorbed, leading to constipation.

Stomach and Esophagus Gastric production of hydrochloric acid is variable and sometimes exaggerated, especially during the first trimester. More commonly, gastric acidity is reduced. Production of the hormone gastrin increases significantly, resulting in increased stomach volume and decreased stomach pH. Gastric production of mucus may be increased. Gastric reflux occurs because of Increased intraabdominal pressure increases intragastric pressure the slower stomach emptying time relaxation of the cardiac sphincter (progesterone decreases the sphincter tone)

Gastrointestinal system During pregnancy, nutritional requirements, including those for vitamins and minerals, are increased, and several maternal alterations occur to meet this demand. The mother's appetite usually increases, so that food intake is greater, some women have a decreased appetite or experience nausea and vomiting. These symptoms may be related to relative levels of human chorionic gonadotrophin (hCG). Oral Cavity Salivation may seem to increase due to swallowing difficulty associated with nausea, and, if the pH of the oral cavity decreases, tooth decay may occur. Tooth decay during pregnancy, however, is not due to lack of calcium in the teeth. Indeed, dental calcium is stable and not mobilized during pregnancy as is bone calcium. The gums may become hypertrophy, hyperemic and friable; this maybe due to increased systemic estrogen. Vitamin C deficiency also can cause tenderness and bleeding of the gums. The gums should return to normal in the early puerperium

Small and Large Bowel and Appendix The large and small bowel move upward and laterally, the appendix is displaced superiorly in the right flank area. These organs return to the normal positions in the early puerperium. As noted previously, motility is generally decreased an gastrointestinal tone is decreased.

Gallbladder Gallbladder function is also altered during pregnancy because of the hypotonia of the smooth muscle wall. Emptying time is slowed and often incomplete. Bile can become thick, and bile stasis may lead to gallstone formation.

Liver There are no apparent morphologic changes in the liver during normal pregnancy, but there are functional alterations. Serum alkaline phosphatase activity can double, probably because of increased placental alkaline phosphatase isoenzymes. Thus, a decrease in the albumin/globulin ratio occurs normally in pregnancy.

Reproductive System By six to eight weeks of gestation Softening of the cervix on pelvic examination (Goodell,s sign), A purple hue of the vagina and cervix (Chadwick,s sign) and Compressibility and softening of the isthmus (Hegar,s sign) Uterine hypertrophy of the myocytes Hypertrophy can cause venous compression Can result in fall in venous return Furthermore a fall in CO Physiologic compensation Rise in peripheral resistance to minimize fall in blood pressure

Endocrine systemAnti-insulin environment is aided by: Placental Lactogen Similar to growth hormone Increases lipolysis and FFA Increases tissue resistance to insulin

Increased unbound cortisol Estrogen and Progesterone may also exert some anti-insulin effects

Thyroid Estrogen stimulates Increase in TBG Total T3 and T4 are increased However the active hormones remains unchanged

hCG stimulates thyroid TSH is reduced

Iodine deficient state Due to Increased renal clearance

Metabolism Weight gain is due not only to the uterus and its contents but also to increase breast tissue, blood and water volume in the form of extravascular and extracellular fluid. Deposition of fat and protein and increased cellular water are added to the maternal stores. The average weight gain during pregnancy is 12.5Kg. During normal pregnancy, approximately 1000g of weight gain is attributable to protein. Half of this is found in the fetus and the placenta, with the rest being distribute as uterine contractile protein, breast glandular tissue, plasma protein, and hemoglobin. Total body fat increases during pregnancy, but the amount varies with total weight gain. During the second half of pregnancy, plasma lipids increase, but triglycerides, cholesterol and lipoproteins decrease soon after delivery. The ratio of low density lipoproteins to high density lipoproteins increases during pregnancy.

CVS Estrogen increased in RAA Progestrone, hPL, PRL stimulate erythropoiesis CVS changes due to a-v shunt through placenta (late pregnancy)

Pulm Growing fetus and uterus increases intraabdominal pressure and forces the diaphragm upward High BMR of growing fetus increases maternal O2 consumption and CO2 production Progesterone acts on CNS to lower the set-point for regulation of respiration by CO2 increase ventilation

Renal RAA increase due to decrease in BP (Uterus also produces renin in pregnancy) Estrogen stimulates liver synthesis of angiotensinogen Estrogen and progesterone increase angiotensin converting enzyme Placental Deoxycorticosterone (DOC) synthesis increases during pregnancy. DOC stimulates renal salt and water retention The increased in mineralocorticoids, aldosterone and DOC is important for the maternal volume expansion seen during pregnancy.

Central Nervous SystemPARAMETERSensitivity to PaCO2 Volume of epidural space Pressure of epidural space CSF volume CSF pressure Sensitivity to local anaesthetics Local anaesthetic dose

CHANGEIncreases Decrease Increase Decrease Increase Increase Decrease