Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2007;38:3218-3224
Published online before print November 8, 2007, doi: 10.1161/STROKEAHA.107.484634
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
38/12/3218    most recent
STROKEAHA.107.484634v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mutoh, T.
Right arrow Articles by Terasaka, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mutoh, T.
Right arrow Articles by Terasaka, S.
Related Collections
Right arrow Other Stroke Treatment - Medical
Right arrow Cardiovascular Pharmacology
Right arrow Cerebral Aneurysm, AVM, & Subarachnoid hemorrhage

(Stroke. 2007;38:3218.)
© 2007 American Heart Association, Inc.


Original Contributions

Goal-Directed Fluid Management by Bedside Transpulmonary Hemodynamic Monitoring After Subarachnoid Hemorrhage

Tatsushi Mutoh, MD, DVM, PhD; Ken Kazumata, MD; Minoru Ajiki, MD; Satoshi Ushikoshi, MD Shunsuke Terasaka, MD

From the Department of Neurosurgery, Teine Keijinkai Medical Center, Sapporo, Japan.

Correspondence to Tatsushi Mutoh, MD, DVM, PhD, Department of Strokology, Research Institute of Brain and Blood Vessels, Akita, 6-10 Senshu-Kubota-machi, Akita 010-0874, Japan. E-mail tmutoh{at}tiara.ocn.ne.jp

Background and Purpose— Optimal monitoring of cardiac output and intravascular volume is of paramount importance for good fluid management of patients with subarachnoid hemorrhage (SAH). The aim of this study was to demonstrate the feasibility of advanced hemodynamic monitoring with transpulmonary thermodilution and to provide descriptive data early after SAH.

Methods— Forty-six patients with SAH treated within 24 hours of the ictus were investigated. Specific targets for cardiac index (≥3.0 L · min–1 · m–2), global end-diastolic volume index (700 to 900 mL/m2), and extravascular lung water index (≤14 mL/kg) were established by the single-indicator transpulmonary thermodilution technique, and a fluid management protocol emphasizing supplemental colloid administration was used to attain these targets. Plasma hormones related to stress and fluid regulation were also measured.

Results— A higher cardiac index (mean value of 5.3 L · min–1 · m–2) and a lower global end-diastolic volume index (555 mL/m2) were observed on initial measurement, for which elevations of plasma adrenaline, noradrenaline, and cortisol were also detected. Cardiac index was progressively decreased (3.5 L · min–1 · m–2) and global end-diastolic volume index was normalized by fluid administration aimed at normovolemia. The extent of the initial hemodynamic and hormonal profile was greater in patients with a poor clinical status (P<0.05). The extravascular lung water index was mildly elevated but within the target range throughout the study period. No patients developed pulmonary edema or congestive heart failure.

Conclusions— The impact of sympathetic hyperactivity after SAH predisposes patients to a hyperdynamic and hypovolemic state, especially in those whose clinical status is poor. Bedside monitoring with the transpulmonary thermodilution system may be a powerful tool for the systemic management of such patients.

Supplemental Material