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Circulation In the Normal Fetus & Cardiovascular Adaptations to Birth (Yegal10)
Circulation In the Normal Fetus & Cardiovascular Adaptations to Birth (Yegal10)
Fetal Circulation
-postnatal circ: O2/CO2 exchange thru lungs & energy abs thru GI followed by liver via portal syst b4 entering gen circ
-prenatal circ: O2/CO2 exchange thru placenta & energy abs via diffusion or active transport via placenta w 1/2 of the blood bypassing the liver via ductus venosus to directly enter fetal gen circ.
Circulation Course
-Postnatal circ is in series, so no mixing of pulm/systemic Q
-Fetaly, umb vn returns oxygenated bld to fetus, where it mixes w systemic venous bld (fr SVC/IVC/hep vns, at IVC/RA) prior to getting to the ventricles
-Umb Vein--> enters Porta Hepatis--> branches to LEFT liver lobe, then (distal to these branches), it gives off the ductus venosus. The DV passes post'ly then sup'ly to connect to IVC. Umb Vn then arches to RIGHT liver lobe to join portal vn and then branches to right liver… The L Hep Vns drain to IVC near the DV. The R Hep Vn drains into the R post aspect of IVC, partly covered orifice by a valve like membrane.
-Blood thru the DV flowed to LA via the FO
-Nearly all (except for some portal Q) of DV Q is fr Umb Vn (95%)
-About half (range 20-90%) of the Umb Vn Q passes thru DV
-DV Q goes mainly to FO then LA/LV, abdominal IVC Q goes mainly to TV/RV, thru streaming effects (including L hep Q to FO and R hep Q to TV…)
-?Selective streaming bc of valves at DV entrance to IVC, and IVC entrance to RA, but these vlvs are less well defined in human fetus vs sheep fetus, so ? other mech:
-Crista Dividens- crescent edge of sup part of atrial septum- overlies the IVC so that the post-left part of IVC connects directly thru the FO to the LA
-Eustachian Valve and lower part of atrial septum move in unison thru the cardiac cyclegoing either left to allow Q thru FO or R to allow Q to TV (net--> Q at L aspect of IVC goes to FO)
-Diff in velocities of ea stream in the IVC (abd IVC Q is slower than DV Q)
-SVC Q- nearly all goes to TV, w <5% to FO- this bld gets their bc it first is diverted into IVC during atrial systole, then enters FO during the rapid inflow phase fr IVC…
-RV Q to PA, and most goes to the DA to Desc Ao (none goes retrograde across Ao isthmus to asc Ao)
-LA gets Q fr FO and PVns--> LV--> Asc Ao--> mainly to coronary circ, head/neck vessels, w only small amt crossing Ao isthmus to Desc Ao.
-Desc Ao Q to abd organs/lower trunk/LE & a large amt to umb artery to placenta…
Admixture of O2 & Systemic Venous Blood
-Mixing occurs at:
-UV + Portal Vn @ R hep vn
-DV + L & R Hep Vns + abd IVC @ thoracic IVC
-IVC to FO Q + PVn Q @ LA
-RV to PA Q + Asc Ao Q (some) @Desc Ao
-Some UV Q goes to placenta w/o first getting to fetal tissues = inefficient bc --> extra wk on fetal heart…
-Q via SVC and IVC that goes to fetal body w/o getting O2 first also inefficent…
-in fetal sheep, 45% SVC and 53% IVC Q go to fetal tissue w/o first getting O2 fr placenta & about 22% of UV Q goes back to placenta w/o first going to fetal tissue to give its O2
==> net 33% of combined ventricular output of fetal heart is 'waisted'
Fetal Vascular Pressures
-we relate the fetal BP to the amniotic fluid pressure
-Fetal BP rises w intra-abd maternal P- straining, gas, feeding, uterine contraction
-In the sheep, amniotic P is about 10mmHg above atm P
-Umb Vn P is 8-10mmHg at umb ring, and 2-3mmHg lower by the placenta
-Nly, pressure in UV is NOT pulsatile (no change w atrial or ventric systole); same seen in porta hepatis, w a mena P 5-6mmHg
-DDx- IVC and SVC have variations of BP thru cardiac cycle
-LA postnatally has higher BP than RA, w a RA contour having dominant a-wave, and LA having dominant v-wave
-In Fetus, SVC/IVC/RA mean BP is 2-3mmHg, and a and v waves are both 4-5mmHg in RA, while LA pressure is less- 1-2mmHg less than RA.
-RV and LV systolic BP and EDP are similar
-lamb- RV and pulm art systolic BP is > LV and Ao BP by 5-8mmHg, likely bc of mild DA constriction
-Ao BP increases w GA in lamb fetus
Blood Gases & Oxygen Saturation
-big PO2 gradient between maternal and UV PO2, not much diff in PCO2
-P50 (PO2 w 50% Hgb saturation) is lower than that of adult blood, so that at a PO2 of 35mmHg (the Nl PO2 of UV), the blood is 90% saturated
-see diagram for diff sats throughout the fetus
-Asc Ao is 65%, vs Desc Ao is 55%
Effects of Maternal O2 Administration
-in ewe, SaO2 is 100% and PO2 incr to >400mmHg on 100%FiO2
-UV incr PO2 incr fr 35 to 50, sats reach 95-100%
-fetal art PO2 only increases to 30-35mmHg, and sats to 80% SaO2
-the reason PO2 is >400 in mom, but only 50 in fetus is bc of diffusion limitation across the placental membrane, ?may be lower in human fetus bc we dont have a syndesmochorial placenta
Cardiac Output & Its Distribution
-Unlike postnatally, fetal ventricles pump diff amts of bld
-So, discuss the CO as a combined ventricular output (CVO)
=Nl CVO = 450mL/min per kg fetal body wt
-RV ejects 2/3 and LV 1/3 of the CVO in fetal lamb
-Umbilical-Placental Q is 200mL/min/kgBW
-Fetal Body Q is 250mL/min/kgBW
-so UV Q is 40-45% of CVO
-55% of UV Q passes thru DV, and rest to hepatic circ
-IVC Q at RA jct = 75% of CVO
-35% of CVO passes thru FO to the LA (mainly fr the DV Q)
-SVC Q at RA jct = 21% of CVO
-Only 10-15% of RV Q goes to pulm circ (this = 8% of the CVO) the rest goes thru the DA to the Desc Ao
-LA gets 33% of CVO (fr FO and PVns)
-<33% of LV Q goes across the Ao isthmus to the Desc Ao (this =10% of CVO), rest goes to head/neck arts
Human Fetal Circulation
-similar circulation course as lamb, but diff Q distrib to body parts bc diff weights of ea organ…, e.g. more Q to brain bc bigger brains
…
see pic **
Flow Velocity Contours
……
Determinants of Cardiac Output
-HR, SV{PL, AL, Contractility….
-PL: determines amt of ventric muscle stretch just prior to contraction- EDV determines the length of the cardiac myocytes, thus determines the sarcomere length (longer sarc, up to the optimal level--> greater force created in contraction. Incr in EDV--> incr force of contraction--> incr SV
-AL: the load on the heart determines the degree of sarc shortening, thus determines volume ejected in syst
-if the ventricle contracts w the same Force, the volume ejected will be greater at a lower AL
-d/o art BP, arterial compliance, SVR
-Contractility: intrinsic force of contraction of the muscle (incr Contractility--> incr Force made--> incr SV)
-HR
-in adults major changes in HR--> little change in CO, and incr HR might actually decr CO bc decr diast filling
-at slow HR, SV incr to --> same CO
-but at max diast filling reached, then slower HR --> decr CO
-in fetal sheep, incr HR does incr CVO and decr HR does decr CVO
-?if it was the HR that did it, or if the item that increased HR also affected contractility…
-above 300bpm, CVO dropped much, bc low diastolic filling time (?)
-PL & AL
-usually interact w ea other
-incr AL--> decr SV so residual ventric vol is greater--> next PL is greater than prior (if ventric filling is the same)
-after dropping PL bc of removal of blood, it was increased rapidly by infusing a bolus. When atrial P was incr by 2-4mmHg, the CVO increased, but beyond that it did not increase more, unlike in postnatal, where increasing atrial P to 15-20mmHg is assoc w progressive incr in CVO. => maybe fetal heart is Nly at the near top of ventric fx curve, so more PL isn't going to help incr CVO, because the contractility (myocardial performance) is low.
-one problem w the experiment is that the bolus also increases BP, so AL was increased too…
-another experiment using a constant BP- incr in LAP --> incr LV SV even at atrial P of 10-12mmHg ==> fetal heart DOES respond to incr PL w incr CVO
-Myocardial Performance
-less active tension than that of adult, and max force generated is lower than in adults
-?bc less sarcomeres
-?bc Sarc Retic's T tubule system that relates it to contractile elements is is less dvpd, and there is impaired fetal Ca uptake into the SR…
-NE locally is important to incr contractility
-symp nerves are sparse in fetus
-beta adrenergic R' [ ] is lower in fetus
Regulation of Fetal Circulation
-in adults, each ventricle has diff AL and PL, but bc of Frank Starling mech they have similar CO in the short term (bc decr CO left--> back up Q onto right…)
-In fetus, FO --> near = LA and RA P, and DA--> near = Ao and PA P.
-diff in CO bn the ventricles is mainly due to AL diff
-Ao Isthmus is narrower than Asc and Desc Ap, so ~separates UE and LE Q
-LV ejects into Asc Ao/head/neck - poor compliance, high resistance
-RV ejects to pulm trunk then to DA then to Desc Ao- higher compliance, lower resist. bc placenta
-Reflex Regulation
-Chemoreflexes
-conflicting results on their impact; do have importance in 3rd Tri
-stim by hypoxemia
-heart responds w bradycardia, immediate hypotension, resp gasps too
-likely due to vagal stim
-in adults, stim to chemoR --> reflex periph vasoconstriction; likely w fetus gets periph vasoconstrict p hypoxemia too via chemoR….
-Baroreflexes
-in adults, BP range is kept narrow
-in fetus, fx early on, ?importance, ….
Birth Associated Changes in Circulation
-Delivery--> lose umb-placental circ & lungs fx for O2/CO2 exchange; postnatal change to incr Qp
-Circulation changes to series
-FO and DA close
-Delivery--> fluid in fetal airways removed w expulsion thru mouth fr chest compression & thru absorption into pulm circ w breathing onset.
-Regular ventilation starts--> incr Alveolar oxygen [ ] , expand lungs and remove fluid in alveoli
-Umb-placental circ stops w clamping the cord
-Incr Q to LA fr PVns--> incr LAP >RAP--> close FO
-Total CVO no change, but now LV CO is >RV CO (bc PDA still open… gets 10% of CVO)
-PAP's gradually decr to below Ao levels
-Clamping cord--> no umb Q--> modest incr in syst art BP, small incr in shunt thru the DA fr teh Ao to the PA
Perinatal Changes in Pulmonary Circulation
-Rhythmic physical expansion of the lungs & incr O2 in the vented gas --> pulm vasodilation
-rhythmic lung expansion--> release PGI1 (prostacylcin) & prostaglandin fr endothel cells (?)
-? physical removal of fluid fr alveoli helps drop PVR; no longer have compression fr amniotic pressure transmitted to alveoli via fluid in the lungs…
-?effect of negative P ventilation
-incr PO2--> local vasodilation…
……
Persistent Pulmonary Hypertension of the Newborn
-if PVR doesn't drop--> decr Qp to < needed…
…
Ductus Arteriosus Closure after Birth
-DA wall is different- has sm muscle and not elastic tissue in the media layer
-in gestation, no P gradient across DA bc it's so patent, until last few weeks when it constricts mildly then rapidly constricts postnatally. Usually closed by 12-15 hrs postnatal in ppl
-first few hrs- bidirectional Q, then at 6hrs old only sm L to right, until 15hrs when no Q…
-responds to decr in PO2 by dilating…
...
Postnatal Changes in CO
-major increase in CO, twice that of fetus, and the LV and RV CO equalize
-LV CO increases to 3x fetal, RV CO increases to 1.5x fetal amt
-theory: the positive P of the amniotic environment limits SV bc high pericardial pressure. W spont vent postnatally and negative intrapleural P relative to atm--> better fill the ventricles--> incr SV--> incr CO
-catecholamines incr at delivery--> incr CO w vaginal delivery --> incr contractility (?)
-cortisol incr in sheep--> mature the myocardium, incr prtn [ ] in myocytes… ?facilitate incr CO
-Thyroid hormone- ?affect incr beta R's in myocardium --> better respond to NE/E ??
Morphological Changes in Myocardium after Birth
-incr in myocyte size… in sheep…
Postnatal Changes in Hepatic and Ductus Venosus Blood Flow after Birth
-portal vn flow in fetal lamb is low, most goes to R lobe w <10% going thru DV
-liver gets a lot of bld. post birth, UV Q stops, and hep flow is gotten only fr portal vn + some small hep art Q, and Q to liver increases w newborn feeding…
-DV reacts passively to intraluminal P (?)- but prostaglandin is in part responsible to maint DV patency. so removal of prostaglandins postnatally and stopping umb Q --> close the DV
-In postnatal pd, a good amt of portal Q may go thru DV, but by 3-4 days old it is nill, and by 6-10 days old, the DV closes.
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