Maternal, Fetal, And Neonatal Circulations Flashcards
Blood volume adaptations during pregnancy
. Begins to inc. at 6-8 weeks gestation
. 40-50% inc. in total BV (peak in 2nd trimester)
. Plasma volume inc.75% due to inc. in salt Nd water retention by kidney
. EBC volume inc. 33%
. Hematocrit dec. from 40 to 35% (physiologic anemia of pregnancy)
Pregnancy effect on HR
. Inc. early in 1st trimester and peaks late in 2nd trimester (15-20 bpm inc. at rest representing 20-30% inc.)
. May dec. slightly at term
Pregnancy effect on stroke volume
. Inc. progressively for 1st 2 trimesters by 30% and then declines somewhat during 3rd rimester
. Elevated CO at term is supported more by HR than SV
. Contractility may go up a little
. Remodeling of ventricle causes enlarged ventricular size and LVEDV
. Cardiac filling pressures are not elevated despite inc. in blood volume
Pregnancy effect on cardiac output
. Inc. early (by 8 weeks) and is elevated 30-50% by end of 2nd trimester
. Elevated CO well maintained into 3rd trimester
. Inc. due to inc. HR, SV, and look volume
. Early inc. in CO is not related to metabolic requirements of the mother or fetus
Pregnancy effect on systemic vascular resistance/ TPR
. Dec. early in pregnancy
. Mainly due to addition of low resistance uteroplacental circulation
Pregnancy effect in blood pressure
. MAP falls in 1st trimester and peaks at mid-pregnancy
. falls due to dec. in TPR despite the inc. in CO
. gradually returns to the nonpregnant value by term
Uteroplacental blood flow
. By term 20-25% of the elevated maternal CO is sent to the uteroplacental circulation
. Maternal uteroplacental blood flow is 50 ml/min at 10 weeks and inc. further to 500-600 ml/min at term
. Resistance to flow is very low in uteroplacental circuit, accomplished by remodeling of maternal uterine spiral aa.
Maternal vascular physiology in preeclampsia
. Reproductive vascular bed uteroplacental aa. Have incomplete remodeling and impaired reactivity -> dec. uteroplacental perfusion -> dec. fetal growth
. Nonreproductive vasular beds and systemic resistance aa. That have impaired reactivity -> inc. peripheral vascular resistance -> inc. maternal hypertension and proteinuria
Pregnancy effect on renal function
. Renal blood flow inc. early in gestation and peals at 30% above pre-pregnancy levels
. Stays stable until parturition
. GFR inc. soon after conception and peaks at 40-50% over pre-pregnancy levels
. Stays stable until parturition
Volume and Na homeostasis during pregnancy
. Accumulation of 6.2-8.5 L of water occurs
. Interstitial fluid levels start to inc. at 6 weeks and accelerate during 2nd half of pregnancy (accumulation over 1.5L = edema)
. Total body Na levels elevated by 900-950 mOsm, 60% of extra Na used by fetus and placenta
. Total plasma osmolality dec. to 272 mOsm/kg
. Hypo-osmolality is normal adaptation and maintained bc relationship btw plasma osmolality and ADH secretion is reset
Shunts in fetal circulation
. Placenta
. Ductus venosus
. Foramen ovale
. Ductus arteriosus
Placenta as a shunt
. Low resistance path that shunts blood away from lower trunk
. Umbilical aa. Move deoxygenated blood into placenta
. Umbilical vv. Returns oxygenated blood to ductus venosus that dumps into IVC of fetus
Ductus venosus
. Allows blood to skip liver and dump newly oxygenated blood into IVC
. IVC received a lot of oxygenated blood from placenta and deoxygenated blood from lower body and liver
Foramen ovale
. Opening in atrial septum (w/ valve-like flap on left side)
. Allows blood flow from RA to LA bc atrial pressure is higher in right in a fetus
. RA pressure is higher due to 27$ blood that enters RA from IVC shifts directly to left side of heart and bypasses the nonfunctional fetal lungs
. Most of blood from SVC and some form IVC goes directly into RA and moves into RV to go to pulmonary a.
Ductus arteriosus
. Muscular, vasoactive vessel
. Moves oxygenated blood from Pulmonary a. To aorta (R to L shift) bypassing nonfunctional lungs
. Lungs only receive 7% of total CO
. Shunted blood mixes w/ smaller output from LV that did not make it up to head and moves in descending aorta to perfuse trunk, viscera, and legs
. Resistance to pulmonary circulation high bc lung is collapsed and from hypoxic vasoconstriction
. Ductus arteriosus is dilated bc of fetal production of PGE2 and other vasodilatory prostaglandins