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J Neurosurg Anesthesiol · Jan 2012
Changes in left ventricular preload, afterload, and cardiac output in response to a single dose of mannitol in neurosurgical patients undergoing craniotomy: a transesophageal echocardiographic study.
- Nilay Chatterjee, Thomas Koshy, Satyajeet Misra, and Balethbail Suparna.
- Department of Anesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India.
- J Neurosurg Anesthesiol. 2012 Jan 1;24(1):25-9.
BackgroundMannitol increases intravascular volume by withdrawing water from the brain and causes significant changes in stroke volume, cardiac output (CO), systemic vascular resistance, central venous pressure (CVP), and blood pressure. No previous studies have demonstrated changes in left ventricular (LV) preload, afterload, and CO using transesophageal echocardiography (TEE).MethodsFifteen adult patients undergoing elective supratentorial craniotomy received 20% mannitol 1.0 gm/kg over 15 minutes before dural opening. The following hemodynamic and TEE-derived parameters were recorded before and after the administration of mannitol: heart rate (HR), mean arterial pressure (MAP), CVP, LV end diastolic area (EDA), end systolic area, fractional area change, stroke volume, and CO.ResultsEDA and CVP significantly increased at 5 minutes (P=0.002 and <0.001) after mannitol infusion and remained insignificantly elevated till 15 minutes, thereafter returning to baseline values. CO also increased significantly at 5 and 15 minutes (P=0.001 and 0.013) and remained insignificantly elevated till 25 minutes, and thereafter returned to baseline values. A concomitant significant decline in systemic vascular resistance was observed at 5 and 15 minutes (P=0.002 and 0.008 at 5 and 15 min, respectively). Although EDA increased significantly at 5 minutes, there were no appreciable changes in MAP and HR throughout the study period.ConclusionsIn conclusion, in patients undergoing craniotomy, TEE demonstrated that a single bolus dose of 20% mannitol (1.0 gm/kg) caused significant but short-duration alterations in LV preload, afterload, and CO without concomitant changes in hemodynamic variables (MAP/HR).
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