13. Physiological Adaptations in Pregnancy Flashcards
How does RBC volume, plasma volume, total blood volume and cardiac output change during pregnancy?
How does Hb concentration change during pregnancy?
RBC blood volume decreases in first 10 weeks and then increases, although not as much as the other factors. Plasma volume may increase as much as 45% (rises most in 1st trimester). Total blood volume starts to increase in 1st trimester and expands rapidly during 2nd trimester, before rising at a lower rate in 3rd trimeseter. CO: Increases (mainly in 1st trimester).
Hb concentrations fall from around 150g/l pre-pregnancy to 120g/l during the 3rd trimester (physiological anaemia of pregnancy - dilutional anaemia)
Why does plasma volume increase in early pregnancy?
Why do erythrocyte numbers increase?
Why does cardiac output increase?
Where is most of the cardiac output distributed to in a pregnant woman as opposed to a non-pregnant woman?
Vasodilation leads to decreased peripheral vascular resistance. Activation of RAAS: retention of Na and total increase in body water.
Increase in erythropoiesis via increased renal EPO production. Red cell mass can increase by 20%
Due to increased stroke volume and heart rate.
Pregnant: mainly to uterus (metabolic demands of foetus), a little more to skin and a little less to renal.
How does blood pressure change in pregnancy and why?
What causes a drop in peripheral vascular resistance?
What effect does this have on the heart rate?
Dip in blood pressure around 17-24w due to decrease in peripheral vascular resistance (falls by 50% in early pregnancy). Returns to normal in late 2nd trimester.
Oestrogen, progesterone, NO, relaxin and calcitonin gene-related peptide are all implicated.
Systolic and diastolic BP falls resulting in increased heart rate.
What is pre-eclampsia?
How does posture affect cardiac output and blood pressure measurements in the pregnant woman?
Characterised by high blood pressure with oedema and proteinuria. It’s normal for arterial BP to rise a little towards end of 3rd trimester, usually monitored closely for significant increases as indicator for PE. Life threatening.
Enlarged uterus can compress vena cava and impede venous return causing reduced CO and BP (maternal hypotension) and dizziness. Pregnant women should not be supine for BP measurements.
How does pregnancy affect haemostasis and why?
How does this occur?
How are platelets and tPA affected by pregnancy?
Pregnancy induced a hypercoaguable state: increased tendency towards blood clotting. Important to maintain placental function during pregnancy and as preparation for haemostatic challenge (prevent excessive bleeding) during delivery.
Increase in concentration of clotting factors and decrease in coagulation inhibitors.
Increased platelet production and decreased platelet count (reflects increased activity and consumption), inihbition of fibrinolysis via decreases in tPA.
What risk does the pregnany woman’s hypercoaguable state create?
How does oxygen consumption change during pregnancy and why?
How does pregnancy affect alveolar ventilation, minute ventialtion, tidal volume and respiratory rate?
Thrombosis (localised blood clot) and venous thromboembolism. More common >35 (2.5/1000 compared to 1/1000). Thrombophilia can be inherited. 10-20% of VTEs are PEs.
Increases (250 -> 300ml/min resting) to maintain foetal metabolic requirements.
Alveolar ventilation increases, minute ventilation increases, tidal volume increases and respiratory rate slightly increases.
Why does ventilation increase?
What is a major physical change in pregnancy that affects the heart?
How does pregnancy affect arterial blood gases and why?
Progesterone stimulates the respiratory centre directly to increase sensitivity to CO2.
Elevation of the diaphragm causes the heart axis to deviate left. The expanding uterus also decreases residual volume, expiratory reserve volume and total lung capacity, and increases tidal volume.
Increased ventilation results in a fall in PaCO2 and a slight rise in PaO2.
Why doesn’t hyperventilation and removal of CO2 lead to chronic respiratory alkalosis in pregnancy?
What changes occur in the kidney during pregnancy?
How does renal function change?
Renal compensation (HCO3- loss, H+ retention)
Increase in length, dilation of renal calyces, pelvis and ureter mainly due to action of progesterone to relax SM, increased CO -> increased renal plasma flow and GFR.
Increase in urea, creatinine, urate clearance and excretion of bicarbonate causing a slight decrease in the plasma concentrations.
What is the role of the RAAS during pregnancy?
How is RAAS regulated during pregnancy?
How does pregnancy affect liver function?
Increased activity of RAAS -> water retention and decrease in plasma osmolarity. High levels of angiotensin II are important for maintaining blood volume, blood pressure and uteroplacental blood flow. IRT fall in systemic BP.
Potentially direct action of progesterone and oestrogen in kidney, oestrogen thought to increase renin secretion from granular cells, and upregulate angiotensinogen production in liver. Increase in aldosterone secretion during pregnancy which favours reabsorption of salt and water.
High normal or elevated but clinically insignificant levels of liver enzymes (markers).
Why does pregnancy make the diagosis of liver disease more difficult?
How does pregnancy affect GI function and why?
Clinical signs of liver disease e.g. spider naevi and palmar erythema may occur in pregnancy, as well as increased plasma concentrations of alkaline phosphatase (from placental production).
Heartburn/reflux common, partly due to increased intra-abdominal pressure which is aggravated in the supine position. Progesterone-mediated reduction in lower oesophageal sphinter tone (NB UOS not affected b/c it’s striated). Predisposition to regurgitation and aspiration during anaesthesia.
Also decrease in motility of small and large bowel, 60% water absorption = constipation, haemorrhoid formation.
How does pregnancy affect pancreatic function?
What is glycosuria and why does it happen?
What are the 3 stages of labour?
Islets of Langerhands beta cell hyperplasia (insulin-producing cells), increased insulin production, early pregnancy tissues show increased insulin sensitivity and plasma glucose may fall, late pregnancy insulin response blunted by placental hormones and plasma glucose may rise. Increased placental glucose uptake.
Decrease in re-absorption of glucose, prob due to increase in filtered load of glucose which is > than ability of PCT to reabsorb glucose. Common in pregnancy.
Dilation of cervix/uterine contractions. Foetal expulsion. Placental expulsion.
What changes in cardiac output occur during labour?
How long does it take the physiolgical adaptations in pregnacy to return to normal?
Cardiac output increases most during contractions. Increases in autotransfusion from contracting uterus, further increase in blood may be autotransfused as placenta delivered. Pain/anxiety and sympathetic nerve stimulation also increases HR and poss BP.
CDV changes quite quick: blood volume (72hrs), HR and CO (2wks), proteins and lipids (2-3w). Structural changes take longer (e.g. urinary system takes > or 3 months to shrink back down to normal).
Describe the three physiological changes in preparation for lactation.
Describe the milk ejection reflex.
1. Initial development of mammary gland: initiated at start of puberty, regulated by progesterone and oestrogen in non-pregnant adult. Lactiferious ducts and alveoli (lobes) develop but breast incapable of lactogenesis.
2. Development of mammary gland during pregnancy: lobular ductal-alveolar system undergoes hypertrophy, duct proliferation, alveoli mature, deposition of adipose tissue between lobules of gland, controlled by placental steroids: estradiol, progesterone, placental peptide hormone (hPL), and possibly pituitary prolactin (growth hormone).
3. Lactogenesis: breast fully dev for milk prod by mid-pregnancy, prolactin = primary lactogenic hormone, oestrogen and progesterone may inihibit secretory activity of breast, lactogenesis triggered post delivery by fall in placental steroid secretion.
Oxytocin released IRT suckling. Contraction of myoepithelial cells - release milk from alveoli and small ducts into large ducts and sinuses.
