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Journal Article
Research Support, Non-U.S. Gov't
Circulatory characteristics of normovolemia and normotension therapy after subarachnoid hemorrhage, focusing on pulmonary edema.
Acta Neurochirurgica 2012 December
BACKGROUND AND PURPOSE: Cardiopulmonary complications are common after subarachnoid hemorrhage (SAH), and include pulmonary edema (PE). The purpose of this study was to investigate circulatory characteristics of normovolemia and normotension therapy after SAH using pulse contour analysis, and to reveal the mechanisms of PE after SAH.
METHODS: Pulse contour analysis was performed from day 3 until day 12 after the onset of SAH in 49 patients.
RESULTS: Global end-diastolic volume index (GEDI) was normal, although net water balance was estimated to be negative and central venous pressure (CVP) was low in all patients. Seven patients (14 %) suffered from pulmonary edema. Cardiac function index (CFI) and global ejection fraction (GEF) were lower in patients with pulmonary edema (PE group) than in patients without PE (non-PE group) throughout the study period (CFI, P≤0.0119; GEF, P≤0.0348). The PE group showed higher GEDI from days 7 to 10, and higher extravascular lung water index (ELWI) throughout the entire study period compared to the non-PE group (GEDI, P≤0.0094; ELWI, P≤0.0077).
CONCLUSIONS: The appropriate preload was kept despite negative net water balance and low CVP. PE after SAH was biphasic, with cardiogenic PE caused by low cardiac contractility immediately after SAH, and hydrostatic PE caused by low cardiac contractility and hypervolemia on and after day 7 of SAH. Pulse contour analysis was useful to monitor this unique circulatory change and effective for detecting cardiopulmonary complications after SAH.
METHODS: Pulse contour analysis was performed from day 3 until day 12 after the onset of SAH in 49 patients.
RESULTS: Global end-diastolic volume index (GEDI) was normal, although net water balance was estimated to be negative and central venous pressure (CVP) was low in all patients. Seven patients (14 %) suffered from pulmonary edema. Cardiac function index (CFI) and global ejection fraction (GEF) were lower in patients with pulmonary edema (PE group) than in patients without PE (non-PE group) throughout the study period (CFI, P≤0.0119; GEF, P≤0.0348). The PE group showed higher GEDI from days 7 to 10, and higher extravascular lung water index (ELWI) throughout the entire study period compared to the non-PE group (GEDI, P≤0.0094; ELWI, P≤0.0077).
CONCLUSIONS: The appropriate preload was kept despite negative net water balance and low CVP. PE after SAH was biphasic, with cardiogenic PE caused by low cardiac contractility immediately after SAH, and hydrostatic PE caused by low cardiac contractility and hypervolemia on and after day 7 of SAH. Pulse contour analysis was useful to monitor this unique circulatory change and effective for detecting cardiopulmonary complications after SAH.
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