title: Serial assessment of the cardiovascular system in normal pregnancy. Role of arterial compliance and pulsatile arterial load.
abstract: BACKGROUND
  Temporal changes in systemic arterial compliance and wave propagation properties (pulsatile arterial load) and their role in ventricular-systemic arterial coupling during gestation have not been explored. Noninvasive methods combined with recently developed mathematical modeling techniques were used to characterize vascular and left ventricular (LV) mechanical adaptations during normal gestation.
  
  
  RESULTS
  Fourteen healthy women were studied at each trimester of pregnancy and again postpartum. Experimental measurements included instantaneous aortic pressure (subclavian pulse tracings) and flow (aortic Doppler velocities) and echocardiographic imaging of the LV. A small increase in LV muscle mass and end-diastolic chamber dimension occurred by late gestation, with no significant alterations in myocardial contractility. Cardiac output increased and the steady component of arterial load (total vascular resistance) decreased during pregnancy. Several changes in pulsatile arterial load were noted: Global arterial compliance increased (approximately 30%) during the first trimester and remained elevated thereafter. The magnitude of peripheral wave reflections at the aorta was reduced. The mathematical model-based analysis revealed that peripheral wave reflections at the aorta were delayed and that both conduit and peripheral vessels contributed to the increased arterial compliance. Finally, coordinated changes in the pulsatile arterial load and LV properties were responsible for maintaining the efficiency of LV-to-arterial system energy transfer.
  
  
  CONCLUSIONS
  The rapid time course of compliance changes and the involvement of both conduit and peripheral vessels are consistent with reduced vascular tone as being the main underlying mechanism. The pulsatile arterial load alterations during normal pregnancy are adaptive in that they help to accommodate the increased intravascular volume while maintaining the efficiency of ventricular-arterial coupling and diastolic perfusion pressure.
authors.affiliation: Department of Medicine, University of Chicago Medical Center, IL 60637, USA.
authors.forename: A
authors.initials: A
authors.lastname: Poppas
authors.forename: S G
authors.initials: SG
authors.lastname: Shroff
authors.forename: C E
authors.initials: CE
authors.lastname: Korcarz
authors.forename: J U
authors.initials: JU
authors.lastname: Hibbard
authors.forename: D S
authors.initials: DS
authors.lastname: Berger
authors.forename: M D
authors.initials: MD
authors.lastname: Lindheimer
authors.forename: R M
authors.initials: RM
authors.lastname: Lang
mesh_terms: D000328:Adult; D001011:Aorta / Q000000981:diagnostic imaging / Q000502:physiology; D001158:Arteries / Q000502:physiology*; D001783:Blood Flow Velocity; D001810:Blood Volume; D002320:Cardiovascular Physiological Phenomena; D003187:Compliance; D004452:Echocardiography; D005260:Female; D006801:Humans; D008955:Models, Cardiovascular; D011247:Pregnancy / Q000502:physiology*; D011673:Pulsatile Flow; D012016:Reference Values; D014666:Vasomotor System / Q000502:physiology*