Maternal, Fetal, And Neonatal Circulations Flashcards

1
Q

Blood volume adaptations during pregnancy

A

. 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)

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2
Q

Pregnancy effect on HR

A

. 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

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3
Q

Pregnancy effect on stroke volume

A

. 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

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4
Q

Pregnancy effect on cardiac output

A

. 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

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5
Q

Pregnancy effect on systemic vascular resistance/ TPR

A

. Dec. early in pregnancy

. Mainly due to addition of low resistance uteroplacental circulation

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6
Q

Pregnancy effect in blood pressure

A

. 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

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7
Q

Uteroplacental blood flow

A

. 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.

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8
Q

Maternal vascular physiology in preeclampsia

A

. 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

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9
Q

Pregnancy effect on renal function

A

. 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

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10
Q

Volume and Na homeostasis during pregnancy

A

. 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

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11
Q

Shunts in fetal circulation

A

. Placenta
. Ductus venosus
. Foramen ovale
. Ductus arteriosus

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12
Q

Placenta as a shunt

A

. 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

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13
Q

Ductus venosus

A

. 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

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14
Q

Foramen ovale

A

. 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.

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15
Q

Ductus arteriosus

A

. 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

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16
Q

Fetal circulation characteristics

A

. Low resistance placenta receives 50% total fetal CO
. Placenta receives blood w/ PO2 of 23 mmHg and returns w/ pO2 of 30-35 mmHg
. Has relatively low resistance systemic circulation due to low PO2
. Fetal RV provides 2/3 CO (85% flows through ductus arteriosus)
. Fetal LV provides 1/3 CO mainly distributed to brain, heart, and upper extremities

17
Q

Loss of low-resistance placental circulation effect on infant after birth

A

. Causes large inc. in neonatal systemic vascular resistance
. Immediately after birth umbilical a. Vasoconstriction occurs due to stretching of aa. During birth and sudden rise in arteriolar PO2 w/ 1st breath
. Important to take 1st breath to reverse hypercapnia and hypoxemia that occurred during passage through birth canal from partial occlusion of umbilical circulation

18
Q

. What occurs in fetal circulation during first breath taken

A

. Breath inflates alveoli and immediately lowers pulmonary vascular resistance by loss of compressive forces on pulmonary aa. And vv.
. Inc. blood flow inc. pulmonary PO2 and removes hypoxic vasoconstriction
. Synthesis of prostacyclin (PGI2) and NO contribute to vasodilation
. Pulmonary vascular resistance dec. 5x from fetal levels
. Reassure in pulmonary a. Dec.

19
Q

Closure of foramen ovale

A

. Opening of pulmonary circulation inc. blood flow to LA raising LA pressure
. RA pressure dec. w/ opening and filing of pulmonary circulation so venous return to RA dec.
. Reversal fo atrial pressure gradient functional closes foramen ovale flap
. Gradually it becomes anatomically sealed
. May not be completely sealed in some adults but normally the high LA pressure prevents R to L shunting

20
Q

Closure of the ductus arteriosus

A

. W/ occlusion of the umbilical circulation, systemic resistance and arterial pressure rise above pulmonary arterial pressure
. Pulmonary pressure is also dec. due to the reduction in pulmonary vascular resistance
. W/ reversal of pressure gradient, blood flow verses so blood flows from aorta to he pulmonary artery (left to right shift)
. W/in 4 hours functional closure occurs due to vasoconstriction from inc. PO2 of blood coming from aorta and loss of vasodilatory prostaglandins
. All blood flow through here ceases in 1 week and undergoes anatomic closure w/in 1 month

21
Q

Closure of the ductus venosus

A

. At birth some blood flow still moves through ductus venosus skipping the liver
. W/in 1-3 hrs, venoconstriction in the DV inc. portal venous pressure moving blood into liver sinuses (normal pattern)
. It is functional closed by 2 weeks and structural closes after that to become ligamentum venosum

22
Q

Ventricular septal defect

A

. Most common congenital anomaly
. Causes left to right shunt
. Large defect can result in RV hypertrophy and pulmonary hypertension in infant that can result in irreversible obstructive pulmonary. Vascular disease and inc. pulmonary vascular resistance
. Small defects are often asymptomatic
. Small defect assoc. w/ loud pansystolic murmur while large defect do not have murmur

23
Q

Patent ductus arteriosus

A

. Results in blood flow from aorta to pulmonary a. (Left to right shunt)
. Inc. pulmonary a. And RV pressure
. Systemic blood remains normally oxygenated unless pulmonary congestion or right HF occurs
. Has continuous murmur (machinery murmur)
. NSAIDs promote close of this early in life, but surgical closure is recommended
. Can resul in exercise intolerance due to inability to inc. CO, pulmonary congestion and edema, right HF, left HF from chronic volume overloading, breath btw 20-40 if not corrected

24
Q

Tetralogy of Fallot

A

. Cause of blue baby syndrome
. 75% RV output is directly moved into left side of heart or into aorta bypassing pulmonary circulation
. Aorta originates from RV or straddles a VSD
. Fixed obstruction to RV outflow due to pulmonary stenosis so less blood sent to lungs, and more deoxygenated blood goes directly to aorta
. VSD that allows communication btw RV and LV
. RV hypertrophy bc it is pumping blood against pulmonary a. Resistance and against aortic pressure
. If left to right shunt occurs then the resultant volume overlaps of pulmonary circulation cause biventricular hypertrophy, LA enlargement, and signs of HF