Advertisement

Intensive Care Medicine

, Volume 30, Issue 7, pp 1361–1369 | Cite as

Effect of large volume infusion on left ventricular volumes, performance and contractility parameters in normal volunteers

  • Anand Kumar
  • Ramon Anel
  • Eugene Bunnell
  • Kalim Habet
  • Alex Neumann
  • David Wolff
  • Robert Rosenson
  • Mary Cheang
  • Joseph E. Parrillo
Original

Abstract

Objective

Characterize the normal human cardiovascular response to large volume infusion of normal saline.

Design:

Prospective, interventional trial.

Setting

ICU procedure room.

Participants

Healthy male volunteers (n=32).

Interventions

Volumetric echocardiography during 4-L saline infusion (3 L over 3 h followed by 1 L over 2 h).

Measurements and results

Following 3-L saline infusion, stroke volume and cardiac output increased approximately 10% without a significant change in heart rate or blood pressure. A decrease in end-systolic volume contributed to the increase in stroke volume to an extent similar to that provided by the increase in end-diastolic volume. All contractility indices except end-systolic wall stress/end-systolic volume index were increased at 3 h post-initiation of saline infusion. Stroke volume but not cardiac output remained elevated at 5 h with persistence of ventricular volume responses; only ejection fraction was significantly elevated among the contractility indices. Afterload measures including total peripheral resistance and end-systolic wall stress were significantly decreased after 3-L infusion but were unchanged compared to baseline following infusion of an additional 1 L over 2 h. Modeled blood viscosity studies demonstrate that changes in apparent contractility after 3-L saline infusion can be explained solely by viscosity reduction associated with hypervolemic hemodilution.

Conclusion

The initial increase in stroke volume associated with high volume saline infusion in normal volunteers is associated with increases of most load-dependent and ostensibly load-independent parameters of left ventricular contractility. This phenomenon is unlikely to represent a true increase in contractility and appears to be caused by reduced afterload as a consequence of decreased blood viscosity. This decrease in blood viscosity may complicate analysis of some previous in vivo studies examining the effect of volume loading on cardiac function using low-viscosity solutions.

Keywords

Volunteers Saline Resuscitation Heart Cardiac output Contractility 

Supplementary material

supp.pdf (72 kb)
Supplementary Material (PDF 73 KB)

References

  1. 1.
    Patterson SW, Starling EH (1914) On the mechanical factors which determine the output of the ventricles. J Physiol 48:357–379Google Scholar
  2. 2.
    Stead EA, Warren JV (1947) Cardiac output in man: analysis of mechanisms of varying cardiac output based on recent clinical studies. Arch Intern Med 80:237Google Scholar
  3. 3.
    Kumar A, Anel R, Bunnell E, Zanotti S, Habet K, Haery C, Marshall S, Neumann A, Ali A, Kavinsky C, Parrillo JE (2004) Preload-independent mechanisms are partially responsible for improved cardiac output following large volume saline infusion in normal volunteers. Crit Care 8:R128–R136CrossRefGoogle Scholar
  4. 4.
    Carabello BA, Spann JF (1984) The uses and limitations of end-systolic indices of left ventricular function. Circulation 69:1058–1064PubMedGoogle Scholar
  5. 5.
    Carabello BA (1989) Ratio of end-systolic wall stress to end-systolic volume: Is it a useful clinical tool? J Am Coll Cardiol 14:496–498Google Scholar
  6. 6.
    Gordon EP, Schnittger I, Fitzgerald PJ, Williams P, Popp RL (1983) Reproducibility of left ventricular volumes by two-dimensional echocardiography. J Am Coll Cardiol 2:506–513PubMedGoogle Scholar
  7. 7.
    Weber KT, Janicki JS, Reeves RC, Hefner LL (1976) Factors influencing left ventricular shortening in isolated canine heart. Am J Physiol 230:419–426PubMedGoogle Scholar
  8. 8.
    Nixon JV, Murray RG, Leonard PD, Mitchell JH, Blomqvist CG (1982) Effect of large variations in preload on left ventricular performance characteristics in normal subjects. Circulation 65:698–703PubMedGoogle Scholar
  9. 9.
    Holt JP (1957) Regulation of the degree of emptying of the left ventricle by the force of ventricular contraction. Circ Res 5:281–287PubMedGoogle Scholar
  10. 10.
    Mahler F, Ross JJr, O’Rourke RA, Covell JW (1975) Effects of changes of preload, afterload, and inotropic state on ejection and isovolumic phase measures of contractility in the conscious dog. Am J Cardiol 35:626–634PubMedGoogle Scholar
  11. 11.
    Quinones MA, Gaasch WH, Cole JS, Alexander JK (1975) Echocardiographic determination of left ventricular stress-velocity relations in man: with reference to the effects of loading and contactility. Circulation 51:689–700PubMedGoogle Scholar
  12. 12.
    Rankin LS, Moss S, Grossman W (1975) Alterations in preload and ejection phase indices of left ventricular performance. Circulation 51:910–915PubMedGoogle Scholar
  13. 13.
    Sagawa K (1981) The end-systolic pressure-volume relation of the ventricle: definition, modifications and clinical use. Circulation 63:1223–1227Google Scholar
  14. 14.
    Carabello BA, Nolan SP, McGuire LB (1981) Assessment of preoperative left ventricular function in patients with mitral regurgitation: value of the end-systolic wall stress-end-systolic volume ratio. Circulation 64:1212–1217PubMedGoogle Scholar
  15. 15.
    Marsh JD, Green LH, Wynne J, Cohn PF, Grossman W (1979) Left ventricular end-systolic pressure-dimension and stress-length relations in normal human subjects. Am J Cardiol 44:1311–1317PubMedGoogle Scholar
  16. 16.
    Daughters GT, Derby GC, Alderman EL, Schwarzkopf A, Mead CW, Ingels NB, Miller DC (1985) Independence of left ventricular pressure-volume ratio from preload in man early after coronary artery bypass graft surgery. Circulation 71:945–950PubMedGoogle Scholar
  17. 17.
    Prewitt RM, Wood LDH (1982) Effect of altered resistive load on left ventricular systolic mechanics in dogs. Anesthesiology 56:195–202PubMedGoogle Scholar
  18. 18.
    Calvin JE, Driedger AA, Sibbald WJ (1981) The hemodynamic effect of rapid fluid infusion in critically ill patients. Surgery 90:61–76PubMedGoogle Scholar
  19. 19.
    Daele ME van, Trouwborst AD, Woerkens LC van, et al (1994) Transesophageal echocardiography monitoring of preoperative acute hypervolemic hemodilution. Anesthesiology 81:602–609PubMedGoogle Scholar
  20. 20.
    Urzua J, Zurick AM, Starr NJ, Cosgrove DM, Yared JP, Estafanous FG (1985) Enhanced cardiac performance following cardiopulmonary bypass. J Cardiovasc Surg 26:53–58Google Scholar
  21. 21.
    Fowler NO, Holmes JC (1975) Blood viscosity and cardiac output in acute experimental anemia. J Appl Physiol 9:453–456Google Scholar
  22. 22.
    Mangano DT, Van Dyke DC, Ellis RJ (1980) The effect of increasing preload on ventricular output and ejection in man: limitations of the Frank-Starling mechanism. Circulation 62:535–541PubMedGoogle Scholar
  23. 23.
    Ohki S, Ishikawa S, Ohtaki A, Takahashi T, Koyano T, Otani Y, Murakami J, Mohara J, Isa Y, Kunimoto F, Morishita Y (1999) Hemodynamic effects of alpha-human atrial natriuretic polypeptide on patients undergoing open-heart surgery. J Cardiovasc Surg 40:781–785Google Scholar
  24. 24.
    Legault L, van Nguyen P, Holliwell DL, Leenen FH (1992) Hemodynamic and plasma atrial natriuretic factor responses to cardiac volume loading in young versus older normotensive humans. Can J Physiol Pharmacol 70:1549–1554PubMedGoogle Scholar
  25. 25.
    McDowell RJS (1924) A vago-pressor reflex. J Physiol 59:41–53Google Scholar
  26. 26.
    Oberg B, Thoren P (1972) Studies on left ventricular receptors; signalling in non-medullated vagal afferents. Acta Physiol Scand 85:145–163PubMedGoogle Scholar

Copyright information

© Springer-Verlag 2004

Authors and Affiliations

  • Anand Kumar
    • 1
    • 5
  • Ramon Anel
    • 1
  • Eugene Bunnell
    • 1
  • Kalim Habet
    • 1
  • Alex Neumann
    • 1
  • David Wolff
    • 2
  • Robert Rosenson
    • 2
  • Mary Cheang
    • 3
  • Joseph E. Parrillo
    • 4
  1. 1.Division of Cardiovascular Disease and Critical Care MedicineRush-Presbyterian-St. Luke’s Medical CenterChicagoUSA
  2. 2.Section of Preventative Cardiology, Northwestern University Medical CenterNorthwestern University Medical SchoolChicagoUSA
  3. 3.Biostatistical Consulting Unit, Department of Community Health Sciences, Faculty of MedicineUniversity of ManitobaWinnipegCanada
  4. 4.Division of Cardiovascular Disease and Critical Care Medicine, Cooper Hospital/University Medical CenterRobert Wood Johnson Medical SchoolCamdenUSA
  5. 5.Section of Critical Care Medicine, GE-706Health Sciences CentreWinnipegCanada

Personalised recommendations