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Preload-independent mechanisms contribute to increased stroke volume following large volume saline infusion in normal volunteers: a prospective interventional study.

AbstractINTRODUCTION: Resuscitation with saline is a standard initial response to hypotension or shock of almost any cause. Saline resuscitation is thought to generate an increase in cardiac output through a preload-dependent (increased end-diastolic volume) augmentation of stroke volume. We sought to confirm this to be the mechanism by which high-volume saline administration (comparable to that used in resuscitation of shock) results in improved cardiac output in normal healthy volunteers. METHODS: Using a standardized protocol, 24 healthy male (group 1) and 12 healthy mixed sex (group 2) volunteers were infused with 3 l normal (0.9%) saline over 3 hours in a prospective interventional study. Individuals were studied at baseline and following volume infusion using volumetric echocardiography (group 1) or a combination of pulmonary artery catheterization and radionuclide cineangiography (group 2). RESULTS: Saline infusion resulted in minor effects on heart rate and arterial pressures. Stroke volume index increased significantly (by approximately 15-25%; P < 0.0001). Biventricular end-diastolic volumes were only inconsistently increased, whereas end-systolic volumes decreased almost uniformly. Decreased end-systolic volume contributed as much as 40-90% to the stroke volume index response. Indices of ventricular contractility including ejection fraction, ventricular stroke work and peak systolic pressure/end-systolic volume index ratio all increased significantly (minimum P < 0.01). CONCLUSION: The increase in stroke volume associated with high-volume saline infusion into normal individuals is not only mediated by an increase in end-diastolic volume, as standard teaching suggests, but also involves a consistent and substantial decrease in end-systolic volumes and increases in basic indices of cardiac contractility. This phenomenon may be consistent with either an increase in biventricular contractility or a decrease in afterload.
AuthorsAnand Kumar, Ramon Anel, Eugene Bunnell, Sergio Zanotti, Kalim Habet, Cameron Haery, Stephanie Marshall, Mary Cheang, Alex Neumann, Amjad Ali, Clifford Kavinsky, Joseph E Parrillo (Affiliation: Division of Cardiovascular Diseases and Critical Care Medicine, Cooper Hospital/University Medical Center, Robert Wood Johnson Medical School, Camden, New Jersey, USA. akumar61 at yahoo.com)
JournalCritical care (London, England) (Crit Care) Vol. 8 Issue 3 Pg. R128-36 (Jun 2004) ISSN: 1466-609X England
PMID15153240 (Publication Type: Clinical Trial, Journal Article)
Chemical References
  • Sodium Chloride
Topics
  • Adolescent
  • Adult
  • Blood Pressure (drug effects)
  • Cardiac Volume (drug effects)
  • Catheterization, Swan-Ganz
  • Cineangiography (methods)
  • Echocardiography
  • Female
  • Gated Blood-Pool Imaging
  • Heart Rate (drug effects)
  • Humans
  • Infusions, Intravenous
  • Intervention Studies
  • Male
  • Myocardial Contraction (drug effects)
  • Prospective Studies
  • Resuscitation (methods)
  • Shock
  • Sodium Chloride (administration & dosage)
  • Stroke Volume (drug effects)
  • Ventricular Function, Left (drug effects)