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- W2189493873 abstract "SUlMMARY Toassesstheeffects ofanatural volume overload state (pregnancy) onleft ventricular function werecorded echocardiograms eachtrimester (TM)andfour to12weekspostpartum. Heartrate increased from77± 2(SEM)to88± 2 heats/min (TM IvsTM 3,P < 0.01) anddeclined to69± 2.0beats/min postpartum (P< 0.05 vsTM 3).Despite these changes, end-diastolic dimension increased from46.3 ± 0.7to50.7 0.7mm (TM I vsTM 3,P < 0.01) anddecreased postpartum to47.5 ± 0.7mm (P< 0.01 vsTM 3).Calculated stroke volume andcardiac index changed correspondingly, butejection fraction, percent offractional shortening andmean normalized rateofinternal diameter shortening werenot significantly altered. Leftventricular wall mass increased during gestation butdecreased between TM 3andpostpartum 162± 8.3vs 143± 6.2g,P < 0.05). Theratio ofposterior wallthickness toleft ventricular radius decreased from 0.32 ± 0.01to0.29 ± 0.01(TM IvsTM 3,P <0.05), indicating progressive eccentric left ventricular enlargement. We conclude that a temporary volume overload state innormalhumansresults inhemodynamic adjustments often observed in cardiac decompensation (increased heart rateandsize). However, left ventricular function, although notaugmented, iswellpreserved, thereby leading toan increase inminute output. Thus,despite progressive left ventricular enlargement the shortening characteristics oftheleft ventricle remain unimpaired. THE OPTIMAL MANAGEMENT ofpregnancy, especially forwomenwithheart disease, requires an understanding ofthebasic hemodynamic stresses that occurduring gestation. Themostimportant hemodynamic change inthematernal circulation during pregnancy isanincrease incardiac output of30-40%.' Thisalteration hasseveral unique features: 1)the augmentation occurs relatively early inpregnancy (20-24 weeks), 2)itcannot beexplained entirely on thebasis offetal needs, and3)fluctuations incardiac output occurwithchanges inbodyposition asthe gravid uterus impinges invarying degree ontheinferior venacava, thus altering systemic venous return.2 A second fundamental hemodynamic change isa decrease inperipheral vascular resistance asaconsequence ofthecreation ofa low-resistance circuit (placenta). Thisalteration ismanifest asawidened pulse pressure duetoadecline inlevels ofdiastolic arterial bloodpressure anda fall inmeanblood pressure.3 A third hemodynamically important shift during pregnancy isadramatic increase inmaternal bloodvolumeapproaching 40%abovenonpregnant values.4 Whiletheeffects oncardiac output havebeenwelldocumented, there isconflicting information concerningleft ventricular performance during pregnancy. Normal, augmented anddepressed function havebeen reported atvarious stages ofgestation.' Inaddition, normal gestation provides theopportunity tostudy a naturally occurring volume overload state innormal humansubjects. Thisstudy wasdesigned toprovide quantitative information regarding serial alterations inleftventricular performance duringnormal pregnancy." @default.
- W2189493873 created "2016-06-24" @default.
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- W2189493873 date "1978-01-01" @default.
- W2189493873 modified "2023-09-27" @default.
- W2189493873 title "Effects ofa Natural VolumeOverload State(Pregnancy) on LeftVentricular Performance inNormalHumanSubjects" @default.
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