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


CONCLUSIONS
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.
Kumar
Anand
A
Division of Cardiovascular Diseases and Critical Care Medicine, Cooper Hospital/University Medical Center, Robert Wood Johnson Medical School, Camden, New Jersey, USA. akumar61@yahoo.com
Anel
Ramon
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Bunnell
Eugene
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Zanotti
Sergio
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Habet
Kalim
K
Haery
Cameron
C
Marshall
Stephanie
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Cheang
Mary
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Neumann
Alex
A
Ali
Amjad
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Kavinsky
Clifford
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Parrillo
Joseph E
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D000293:Adolescent; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002306:Cardiac Volume / Q000187:drug effects*; D002407:Catheterization, Swan-Ganz; D002932:Cineangiography / Q000379:methods; D004452:Echocardiography; D005260:Female; D015637:Gated Blood-Pool Imaging; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D011446:Prospective Studies; D012151:Resuscitation / Q000379:methods; D012769:Shock; D012965:Sodium Chloride / Q000008:administration & dosage*; D013318:Stroke Volume / Q000187:drug effects*; D016277:Ventricular Function, Left / Q000187:drug effects
D012965:Sodium Chloride