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Development of Fetal Cardiac and Extracardiac Doppler Flows In Early Gestation (Yegal11)
Development of Fetal Cardiac and Extracardiac Doppler Flows In Early Gestation (Yegal11)
Cardiovascular Control Mechanisms
-must know cardiac cycle physiology (see pic)
Cardiac Cycle- Diastole
-in adult: passive and active phase
-passive phase w rapid filling till diastasis (plateau)
-initial rapid ventric inflow --> fall in atrial P --> Y descent in vn P
-active phase w atrial contraction bc of SA nd discharge
- --> rapid rise in atrial & veinous P (a wave)
-biphasic ventric inflow seen w E wave followed by A wave, w 90% inflow during E wave in adults
-if HR high, then atrial contraction can --> 40% of ventric filling, and E and A can reverse
-P atrial contraction, atrial P drops, so the P grade at AV vlv is reversed, causing AV vlvs to close
-ventric volume is now at its max at end diast... and this volume = ventric preload
Cardiac Cycle- Systole
-w ventric stim via AV nd, myocardial contraction starts
-incr intraventric P above atrial P --> close TV & MV, then rapid rise in intraventric P (isovol ctrctn) w some bulging of AV vlvs --> temporary incr in atrial P seen in veins; when ventric P > art P--> GA vlvs open, LV bld ejected to Ao, RV to PA, w rapid ejection phase. During rapid ejection, ventric shortening --> descent of AV ring --> atrial P falls below venous P = X wave) and atrial filling starts. This corresponds to the S wave in the venous flow velocity waveform.
-after rapid ejection, rate of ejection slows, at this pt the ventric fibers are shortened, are repolarizing, and cant contract forcefully anymore--> decrease the ventricular active tension and rate of ejection and rate of ventric emptying. WHen ventric P drops to 0, the intraventric P falls below the diastolic P in teh GA--> close GA vlvs. Then ventric relaxes more (isovol relax). The amt of blood in the ventricle at end syst is the end systolic volume. SV - end diast- end syst volume...
Cardiac Function Indices
-Cardiac Output
-Combined Cardiac Output (RV and LV CO)
-in fetus, bc there are parallel circs, RV CO might not = LV CO and changes w physiology/pathophys
-placental Q d/o BP made by the CCO, ventric contraction force, vessel wall resistance, downstream vasc resistance
-as w any organ, Q d/o P drop bn the arterial and venous ends of the organ
-Interacting factors:
-HR
-SV
-preload/filling state of the heart - PL = stretching of cardiac myocytes prior to contraction, related to sarcomere length
-afterload/downstream resistance
-myocardial contractility
-valvar competence
-bld viscosity/intertia of bld
-myocardial muscle mass
-Frank Starling mechanism- ability of myocardium to incr SV to respond to incr in PL, but efficiency of this is influenced by syst/diast myocardial props
-...Compliance- low --> incr P much for small incr vol...
-...
Fetal Circulation (lamb #s unless specified)
-DV carries 50% of the bld return to the heart bypassing the lungs, and does not incr in size as fetus grows so the Q velocity increases w GA
-...streaming in RA...
-LV SaO2 65%, 15-20% more than RV blood
-AL affects each ventricle differently, bc of the parallel circulation
-RV affected by resistance in MPA, DA, DescAo/organs, and fetoplacental circulation
-LV affected by resistance in Asc Ao, and brachiocephalic circulation
-PL also separate
-RV d/o IVC & SVC
-LV d/o PVns, L Hep Vn, & DV
-RV main generator of CO..., 1.8:1 ratio compared to LV in fetuses (see below)
-RV
-only 13% CO to lungs bc high PVR & bc DA orientation
-rest goes to Desc Ao
-2/3 of Q goes to placenta for oxygenation
-LV
-mainly to cor arts and brachiocephalic arts
-29% LV CO to Desc Ao. 2/3 of it goes to placenta
-in total (in lamb)- 41% CCO to placenta, 22% upper body, 8% lungs, 3% myocardium; by by term this changes to 35% to upper body, and only 30% to placenta
-at mid-Gestation, of Q thru Desc Ao 59% of Q goes to placenta, w 41% going to lower half of body, but by term only 33% to placenta, and 67% to lower body (in lambs)
-some differences in humans:
-RV--> 53% of CCO, ratio bn RV to LV CO is 1.2 fr 20wks GA onward. The diff in ppl is bc we have bigger brains... more LV CO...
-humans have less shunting by DV in liver than lambs
Structural & Functional Maturation of the Fetal Myocardium
-Immature fetal myocardium- decr contractility, decr compliance, slower contraction, slower relaxation
-Frank Starling mech- fxl by 20 week GA, but at upper limit
-resting fx is normally near maximum, so very Sn to changes in AL
-sharp decr in CO w minimal incr in AL
-only slight incr in CO if AL falls
-PL is important:
-CO does incr w incr volume load or w beta R stim as long as arterial P doesnt incr
-hard to regulate PL bc most of the blood is extracorporial, in the placenta, & bc shunting at FO equalizes the pressures of the 2 ventricles, so PL is affected equally at each lung
-Cellular contraction:
-beta R stim--> electrical impulse crosses sarc retic--> Ca release fr T-tubule syst--> bind Troponin at actin-myosin binding site. ATP converts to ADP by myosin bound ATPase--> energy release--> motion bn actin & myosin. Ca activation of tropnonin allows for the electromechanical coupling--> shorten sarcomere length & contract the muscle fiber.
-strength of contractility d/o maturity of these systems.
-contraction velocity d/o the reaction rate of myosin ATPase alone
-both contraction velocity & force are lower in fetus
Fetal Cardiac Conduction System & Autonomic Innervation
-Bn 21-23 days post conception, contractility begins w ventric contraction at caudal region of heart tube.
-Conduction syst dvps as folding/looping occurs,
-SA & AV nd are remnants of primary myocardium
-endocard cushions insulate atria fr ventricles, w AV nd --> pathway bn them...
-contraction starts as soon as there is turncoventricular fusion.. before rotation/septation
-Nl mean HR is 110bpm at 5 wks GA, then incr to 170 at 9-10wks gA, then decr to 150 at 14-15 wks GA w a gradual decline twd term GA.
-the incr inthe 1st tri is mainly bc of sinus venosus fusion w atria and ventricles & dvp of conduction tissue--> establish the SA nd as the primary pacer w highest intrinsic spont rate of rhythmicity
-the decr in HR aftwards is bc of increasing parasymp modulation, better ventric contractility, incr ventric muscle mass, better AV vlv fx.
-in ppl, parasymp inhib starts at 12-17 wks GA, then symp n stim at 22-24 wks GA
-may see pds of marked bradycardia until symp n stim dvpd
-AVnd complete at 12 wks GA
-HR variability increases bn 10 to 20 wk GA, reflecting maturation
-umb art pk syst velocity variability also increases
-variability = maturation of parasymp syst; peak velocity var = activation of a hemynamic feedback mech.
-incr HR assoc w decr umb art Q velocity--> seen as evidence of a Frank-Starling mech regulating CV ctrl, seen by late 1st/early 2nd tri
Doppler Investigation of CV System
-Quantitive analysis:
-diast & syst velocities
-TAV- time averaged velocity; can use it to calc volume of Q if know vessel diam
-TAMX- time avgd max velocity
-time to peak velocity
-Extracardiac analysis is usually qualitative, and based on angle independent indexes.
-systolic/diast ratio
-resistance index
-pulsatility index
-ea of above reflect downstream resistance & art bed filling pressure...
-incr in downstream resistance--> decr end-diast velocity ==> incr in each of the indexes...
-assess venous system w Doppler of IVC, DV, Hep vns, umbilical vn
-IVC more influenced by RV fx
-L Hep Vn & DV more influenced by LV fx
-see 2 pks and troughs (S & D waves)
-S wave - fr descent of AV ring during ventric syst, trough fr ascent of AV ring as ventric relax
-D fr passive ventric filling during early diast,
-A wave, seen after D wave, due to sudden incr RAP fr atrial contraction at late diast, w +/- Q reversal. amt of reversal d/o the individual vn (Nl in IVC/Hep vn, but not in DV)
-check:
-% Q reversal
-peak velocity index for vns
-pulsatility index for vns
-preload index
-all of above except preload index incr w a decr in antegrade Q (e.g. w atrial systole w flow reversal)...
-umbilical vn- doesn't change in 2nd/3rd tri; if pulsatile--> = elevated CVP
Development of Intracardiac Flow Velocity Waveforms
-Doppler AV vlvs for diastolic ventirc filling
-E & A waves of early diast and atrial systole
-prenatally, Nly E<A bc rely on atrial contraction for filling... bc of low compliance of ventricle
-usually monophasic AV flow until 8 wks GA
-RV has higher CO than LV, thus TV has more Q across it than LV...
-pk E increases w GA but little change in A, thus E/A gets to 0.9 by term, bc of decr AL and improved diast fx, and better myocard relax & compliance
Flow velocity waveforms in Outflow Tracts
-reflect systolic performance, bc d/o AL & contractility
-pk velocity increases w GA bn 13-20 wks as CO increases at both ventricles- fr 30cm/s at both initially to 60cm/s at Ao and 54cm/s at MPA. Then by term 60-120cm/s at Ao, and 50-110cm/s at MPA.
-check vlv area to calc CO at the vlv.
-CCO increases fr 100mL/min at 18wks GA to 1000mL/min at term
-TPV- time to peak velocity = acceleration time - of arterial flow velocity- d/o MAP & contractility to a lesser degree. higher MAP--> decr TPV
-?usefulness, controversial - some say higher in MPA, some Ao, some say equal
Flow velocity waveforms in ductus arteriosus
-after 26 wk GA, it has incr Sn to PGE
-PVP are mainly d/o DA resistance
-systolic pk Q velocity at DA increases fr 50cm/s at 15wk GA to 130-160cm/s at term
-end diast Q first seen at 13-14wk GA, but established by 17 wk GA
-pulsatility index of DA is high (2.46+/-0.5)
-constriction of DA--> incr arterial peak velocity, more marked in diastole--> decr in pulsatility index to <1.9 if mild and 1 if assoc w TR and severe constriction
-Nly, LV has longer filling time than RV, w shorter LV Eject Time than RV.
-w GA incr, cardiac cycle time incr as HR drops, w concurent incr in diast filling time w decr in isovol relax time and ejection time.
Extracardiac Arterial Doppler Indexes
-Ao doppler d/o mainly the carotid arteries
-changes in comm carotid arts reflect changes in cerebral vasc Q resistance (of ext & int carotid art & cerebral arts); many use middle cerbr art bc has similar characteristics as carotid arts
-RV AL d/o Q in pulm circ, DA, and vasc bed distal to DA (systemic organs/placenta)
Cerebral Circulation
-can be seen as early as 10 wks GA
-pulsatility index of intracereb vssla and ICA is near constant till 20wk GA, then it is decreased in cerebral arts near term. The PI in MCA is higher than in all other cereb arts
-many ppl see a modest incr in PI until 26 wk GA, then falls till term...
Pulmonary Circulation
-MPA and intrapulm arts connect bn 35-50 days p conception
-p 16 weeks --> incr pulm vasc tree arborization
-it's a low Q, high PVR vasc bed... bc of overall smaller cross sectional area of vasc bed
-See on Doppler a rapid early syst Q accel, then sharp mid syst deceleratoin, deep notch or Q reversal in early diastole, and low diastolic fwd Q
-distal PA branches have monophasic fwd Q w lower pulsatility and accel/decel velocities
-pk velocity & pulsatility of Q is decr in PA as you move the doppler fr prox to distal PAs
-some find decr in PI in PAs thru GA, others see decr at 20-30wk GA, then an incr till term
Descending Aorta & Fetal Visceral Blood Flow
-renal & adrenal arts- linear decr in PI after 20wk GA
-splenic art- initial rise in PI at mid GA then decr till term
-mesenteric/hep arts- high impedance vasc bed
-distal to ileac art bifurcation--> diff progression:
-fem arts - linear incr in PI w GA
-diastolic Q reversal at FA and ext iliac arts fr high resistance to Q
-iliac Q d/o placental and umb cd Q resistance, so changes w gestation
Uteroplacental Blood Flow
-see fall in placental resistance w GA
-diastolic notch in spiral arts disappears by 13 wk GA, then disappears in arcuate arts 2wks later
-intervillous Q fully dvps by 14 wks GA
-Umbil Artery-
-as tertiary villi form at vasc tree, placental resistance drops
-see end diast Q first at 13-15wks GA, w continuous rise in end diast velocities as the umb art PI falls linearly thru gestation.
Extracardiac Venous Doppler Indexes
Umbilical Vein
-umb vn volume incr linearly w fetal wt,
-1st tri UV is pulsatile w constant Doppler Q established by 13wk GA
-IVC & Hep Vns- see reverse Q w atrial contraction
-DV fwd Q even w atrial contraction, in part bc of much acceleration of Q in the DV Nly
-Doppler indexes decr w GA, bc of incr antegrae Q during atrial systole
-especially during 13-20wk GA
-improved cardiac diast fx and decr AL--> overall decr in intraventrc end diast P...
Pulmonary Veins
-biphasic w systolic pk and a second pk during early ventric diastole, incersely related to LAP pulsations
-unlike adults, there's continuous antegrade Q into LA in fetus (doesn't return to baseline)
-even during atrial systole (likely bc fetal pulm vns aren't very compliant)
-AFter 20wk GA, marked incr in pk velocities, w decr in S/D ratio
-bc of decr P grad twd LV (? bc better diastolic relaxn) --> thus a decr S/D in pulm vn vssl reflects improved LV diast fx and incr PL
Sequential Changes of Flow Velocity Waveforms
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