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Light Seminars
May 24, 2017
L4H SEMINAR JANA KAINERSTORFER 'Blood Flow Autoregulation and Intracranial Pressure Influences on Cerebral Hemodynamic Signals Measured with Near Infrared Spectroscopy'

L4H SEMINAR JANA KAINERSTORFER 'Blood Flow Autoregulation and Intracranial Pressure Influences on Cerebral Hemodynamic Signals Measured with Near Infrared Spectroscopy'

JANA KAINERSTORFER
Seminar, May 24, 2017, 12:00. Seminar Room
JANA KAINERSTORFER
Carnegie Mellon University
Bedside monitoring of cerebral perfusion is desired for a variety of diseases, such as traumatic brain injury, hydrocephalus, sepsis, and stroke, where inadequate perfusion can lead to ischemia and neuronal damage. The healthy brain maintains a relatively constant blood flow even during episodes of changes in cerebral perfusion pressure (CPP), which is defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). The mechanism of preserving cerebral blood flow (CBF) is called cerebral autoregulation, which is known to be impaired in a variety of diseases and which is mediated by pressure reactivity. Within a certain range of CPP, pressure reactivity is implemented through a vasomotor adjustment in vascular resistance. How well CBF is maintained and how well the vasculature reacts and compensates changes in pressure is indicative of the level of autoregulation. While CBF changes and pressure reactivity are related, they are not the same and measurement methods vary. Using a pressure reactivity metric, by correlation analysis between blood pressure and intracranial pressure, to guide CPP management in traumatic brain injury patient has shown to improve patient outcome, while managing MAP alone does not. However, this requires ICP to be measured, which is currently only possible by placing a pressure sensor inside the brain. In order to overcome the invasiveness of ICP monitoring and in order to develop a bedside compatible autoregulation sensor, we are using hemodynamic changes as measured with near-infrared spectroscopy (NIRS) combined with a hemodynamic modeling approach. Our hemodynamic model translates changes in microvascular hemoglobin concentration into changes of cerebral blood volume and blood flow, allowing for an all optical tool for quantifying dynamic autoregulation. Results on human subjects will be presented, demonstrating the principles of NIRS based autoregulation quantification. For translating hemodynamic signals into ICP, we have conducted measurements on non-human primates, where controlled changes in ICP were induced. Results from the non-human primate study will be presented, which indicate a high temporal correlation between CPP and total hemoglobin concentration changes, demonstrating the potential for an all optical quantification of ICP without the need of invasive monitors.


Seminar, May 24, 2017, 12:00. Seminar Room

Hosted by Prof. Turgut Durduran
Light Seminars
May 24, 2017
L4H SEMINAR JANA KAINERSTORFER 'Blood Flow Autoregulation and Intracranial Pressure Influences on Cerebral Hemodynamic Signals Measured with Near Infrared Spectroscopy'

L4H SEMINAR JANA KAINERSTORFER 'Blood Flow Autoregulation and Intracranial Pressure Influences on Cerebral Hemodynamic Signals Measured with Near Infrared Spectroscopy'

JANA KAINERSTORFER
Seminar, May 24, 2017, 12:00. Seminar Room
JANA KAINERSTORFER
Carnegie Mellon University
Bedside monitoring of cerebral perfusion is desired for a variety of diseases, such as traumatic brain injury, hydrocephalus, sepsis, and stroke, where inadequate perfusion can lead to ischemia and neuronal damage. The healthy brain maintains a relatively constant blood flow even during episodes of changes in cerebral perfusion pressure (CPP), which is defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). The mechanism of preserving cerebral blood flow (CBF) is called cerebral autoregulation, which is known to be impaired in a variety of diseases and which is mediated by pressure reactivity. Within a certain range of CPP, pressure reactivity is implemented through a vasomotor adjustment in vascular resistance. How well CBF is maintained and how well the vasculature reacts and compensates changes in pressure is indicative of the level of autoregulation. While CBF changes and pressure reactivity are related, they are not the same and measurement methods vary. Using a pressure reactivity metric, by correlation analysis between blood pressure and intracranial pressure, to guide CPP management in traumatic brain injury patient has shown to improve patient outcome, while managing MAP alone does not. However, this requires ICP to be measured, which is currently only possible by placing a pressure sensor inside the brain. In order to overcome the invasiveness of ICP monitoring and in order to develop a bedside compatible autoregulation sensor, we are using hemodynamic changes as measured with near-infrared spectroscopy (NIRS) combined with a hemodynamic modeling approach. Our hemodynamic model translates changes in microvascular hemoglobin concentration into changes of cerebral blood volume and blood flow, allowing for an all optical tool for quantifying dynamic autoregulation. Results on human subjects will be presented, demonstrating the principles of NIRS based autoregulation quantification. For translating hemodynamic signals into ICP, we have conducted measurements on non-human primates, where controlled changes in ICP were induced. Results from the non-human primate study will be presented, which indicate a high temporal correlation between CPP and total hemoglobin concentration changes, demonstrating the potential for an all optical quantification of ICP without the need of invasive monitors.


Seminar, May 24, 2017, 12:00. Seminar Room

Hosted by Prof. Turgut Durduran

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