Cerebral Vasospasm and Concurrent Left Ventricular Outflow Tract Obstruction: Requirement for Modification of Hyperdynamic Therapy Regimen

Abstract

Medical treatment for cerebral vasospasm with inotropic pressor agents may result in paradoxical decreases in hemodynamic parameters and cerebral perfusion in patients with LVOT obstruction. While HOCM is the most likely structural abnormality to cause this phenomenon, it can be induced by several physiological conditions encountered in the neurocritical care setting. Modifications in triple H therapy regimens may be required in order to optimize cerebral perfusion and prevent cerebral ischemia and stroke in these patients.

Early Intensive Versus Minimally Invasive Approach to Postoperative Hemodynamic Management After Subarachnoid Hemorrhage

“…Ideal fluid management for the treatment of DCI involves knowing how much hydration patients will tolerate and Difficulty in fluid optimization and higher risks of DCI and poor outcome have been observed in patients with cardiac dysfunction 16,45,46 and pulmonary edema. 7,13,17,19,47,48 In these subsets of patients, EGDT guided by the transpulmonary thermodilution algorithm allows estimation of current hypovolemia based on decreased cardiac preload (GEDI) and of effective functional/dynamic hypovolemia based on continuous CO monitoring, as well as quantification of pulmonary edema based on extravascular lung water index, all of which help to enable rapid responses to the various hemodynamic changes after SAH.…”

Hemodynamic Management of Subarachnoid Hemorrhage

“…In general, because it is important to maintain adequate cardiac output in the management of patients with vasospasm following SAH, case reports have been published on the use of levosimendan [35], discontinuation of dobutamine in situations of left ventricular outflow tract obstruction [36], and insertion of intra-aortic balloon pump counterpulsation [37,38] with the intent of maximizing cardiac function in situations of ventricular failure.…”

Continuous Cardiac Output and Near-Infrared Spectroscopy Monitoring to Assist in Management of Symptomatic Cerebral Vasospasm After Subarachnoid Hemorrhage

“…We prospectively enrolled all patients with SAH admitted to the Research Institute for Brain and Blood Vessels-Akita from October 2009 until December 2009 who underwent surgical clipping within 24 h of onset (designated study day 0) and met the following inclusion criteria: 1) at least 18 years of age; 2) aneurysmal cause of SAH; and 3) sudden clinical deterioration attributable to vasospasm within 14 days after hemorrhage. Exclusion criteria were 1) cardiac failure or arrhythmia that can limit correct APCO tracking [10]; 2) hemoglobin concentrations >9 g/dl associated with an increased incidence of brain hypoxia and cell energy dysfunction [11]; 3) contraindications to DOB-induced hemodynamic treatment (e.g., neurogenic pulmonary edema, Tako-tsubo cardiomyopathy, and left ventricular outflow tract obstruction) [12][13][14][15]; and 4) technical difficulties in establishing safe, stable monitoring or sufficient signal-to-noise ratios in recordings due to patient characteristics (e.g., difficulty in securing a radial arterial line, patient agitation or restlessness, or increased bone thickness or subdural fluid/ hematoma collection at the recording site) [16][17][18].…”