The female body undergoes complex changes during pregnancy in order to nurture and adapt to the growing fetus. The changes in each system will be discussed below.
General Metabolism and Endocrine System:
During pregnancy there are increased caloric and nutritional requirements, including increased requirements for protein, iron, calcium, folate, and other vitamins and minerals.
In early pregnancy, maternal insulin sensitivity increases, followed by resistance in the second and third trimesters. This insulin resistance along with increased insulin production is mediated by human placental lactogen (HPL) produced by the placenta. HPL acts to supply nutrition to the fetus by inducing lipolysis to increase free fatty acids to be preferentially used by the pregnant mother; thus, diverting glucose to the fetus.
There is also an increase in production of cortisol, adrenocorticotropic hormone (ACTH), corticosteroid-binding globulin (CGB), and deoxycorticosterone by the adrenal glands. This results in a hyper cortisol state which reaches 3 times that of non-pregnant women by the end of the third trimester.
In addition to the above, raised levels of estrogen and estradiol in pregnancy are also associated with an increase in the production of thyroid hormones, parathyroid hormone, prolactin and oxytocin, which increase throughout pregnancy and peak at term.
Respiratory System:
During pregnancy, the progressive enlargement of the gravid uterus causes elevation of diaphragm resulting in a 5% decrease in total lung capacity. In addition to this there are many hormone mediated changes to accommodate increasing demand of pregnancy. Increasing levels of serum progesterone leads to progesterone-induced relaxation of the bronchial and tracheal smooth muscles resulting in decreased airway resistance and increased respiratory air volume. The minute ventilation is increased by 30 to 40%, which is thought to be due to enhanced sensitivity to CO2 mediated by progesterone. This will also lead to a reduction in maternal PaCO2. These changes result in dyspnea of pregnancy which is a subjective breathlessness without hypoxia.
Cardiovascular System:
The cardiac output increases 30-50%, with the sharpest increase being in the first trimester and peak being between 20 and 24 weeks. This is initially due to an increase in stroke volume but towards the end of the third trimester, an increase in heart rate acts to maintain the increased cardiac output.
There is a substantial decrease in peripheral vascular resistance starting from the first trimester, which decreases to a nadir during the middle of the second trimester at which point it plateaus or slowly increases. This is due to the elevated progesterone levels present during pregnancy that leads to smooth muscle relaxation. The decrease in systemic vascular resistance results in decreased arterial blood pressure, systolic decreasing by approximately 5 to 10 mm Hg, and diastolic by 10 to 15 mm Hg.
Heart rate also increases progressively throughout the pregnancy by 10 to 20 bpm, reaching a maximum heart rate in the third trimester unlike many of the prior parameters which reach maximum in the second trimester.
By 2 weeks after delivery, maternal hemodynamics will have mostly returned to non-pregnant levels.
Hematological Changes:
An increase of 30–45% in the blood volume occurs, with changes starting at 6–8 weeks and peaking at 28–34 weeks. This is because of the substantial activation of the renin-angiotensin-aldosterone system in early pregnancy. The RBC volume increases by 20% to 30% due to increased erythropoiesis stimulated by high levels of erythropoietin. This disproportionate volume increase leads to dilutional anemia with decreased hematocrit.
Pregnancy induces a hypercoagulable state with a higher risk of thromboembolic events due to an intrinsic activation of the coagulation system in the uteroplacental circulation because of venous stasis and damaged vessel endothelium. The coagulation factors that are increased mainly include Factors I, VII, VIII, X, XII, pre-kallikrein and the von Willebrand factor (VWF). This hypercoagulable state starts in the first trimester and continues at least 12 weeks postpartum.
Gastrointestinal System:
A combination of increased progesterone levels induced smooth muscle relaxation leading to prolonged gastric emptying time, decreased gastroesophageal sphincter tone and increased abdominal pressure due to the growing fetus results in reflux in around 80% of pregnant women. This usually occurs during the third trimester around 36 weeks.
Another change that occurs is intestinal villus hypertrophy and increased absorptive capacity of fluids and nutrients. Together with decreased motility in the large bowel, increased absorption will result in constipation.
Raised levels of estrogen, progesterone, and human chorionic gonadotropin (hCG) combine to bring about nausea and vomiting, which is usually termed as morning sickness.
Renal System:
Vasodilation of the renal vessels results in a 40-65% increase in renal plasma flow and glomerular filtration rates by the end of the first trimester. Consequently, there will be increased clearance of creatinine, urea, and uric acid and excretion of bicarbonate leading to reduction of serum level of these solutes.
The direct effects of the gravid uterus on the bladder lead to urinary frequency. In addition, it also causes urinary stasis, and this combined with progesterone-mediated ureteric smooth muscle relaxation result in increased risk of urinary tract infections.
Female Reproductive System:
To accommodate a growing fetus, the uterus undergoes extreme structural changes and cellular hypertrophy. During early pregnancy, the uterine growth process is initiated by estrogen. Throughout the pregnancy, the uterus must maintain a passive non-contractile state; this is achieved progesterone mediated smooth muscle relaxation. As fetal growth rate begins to accelerate around 20 weeks, the uterus rapidly elongates, and the walls become thinner.
Musculoskeletal and Integumentary System:
As a result of weight gain and a shift in the point of gravity, progressive lordosis (increased lumbar curvature) may ensue. Relaxin hormone softens ligaments, affecting joint stability and flexibility making the joints laxer.
Elevated melanocyte-stimulating hormones and steroid hormones during pregnancy lead to hyperpigmentation of the face, nipples, perineum, abdominal line (Linea nigra), and umbilicus.
References
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