Ignite Creation Date:
2024-05-05 @ 10:53 PM
Last Modification Date:
2024-10-26 @ 10:25 AM
Study NCT ID:
NCT01205607
Status:
UNKNOWN
Last Update Posted:
2010-09-20
First Post:
2010-09-17
Brief Title:
IRB-HSR 14299 The Use of the Intrathoracic Pressure Regulator ITPR to Improve Cerebral Perfusion Pressure in Patients With Altered Intracranial Elastance
Sponsor:
University of Virginia
Organization:
University of Virginia
Study Overview
Official Title:
IRB-HSR 14299 The Use of the Intrathoracic Pressure Regulator ITPR to Improve Cerebral Perfusion Pressure in Patients With Altered Intracranial Elastance
Status:
UNKNOWN
Status Verified Date:
2010-09
Last Known Status:
ENROLLING_BY_INVITATION
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Patients who have a functioning intracranial pressure-monitoring device either a subarachnoid bolt or an intraventricular catheter in place and are either sedated intubated and mechanically ventilated ie in the NNICU or are scheduled to undergo an operation or interventional neuroradiological procedure at the University of Virginia Patients with a contraindication to TTE will be excluded
For patients in the NNICU basic hemodynamic variables systemic blood pressure central venous pressure etc will be collected In addition left ventricular performance including estimates of LVEDV LVESV EF FAC and SV will be assessed using TTE Once these baseline data are recorded the ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal rube pressure ETP based on a randomization scheme After the ITPR has been active for at least five minutes the same intracranial hemodynamic and TTE data obtained above will be gathered The ITPR will then be turned off for five minutes and intracranial hemodynamic and TTE data will again be recorded The ITPR will be activated a second time -9 mm Hg or -5 mm Hg ETP ie whichever value was not used previously and after five minutes of use data will be recorded again The ITPR will then be disconnected data will be collected after waiting two minutes and no further interventions will be made
ABGs will be obtained before and during the use of the device at each setting
This is a proof of conceptfeasibility study designed to test the primary hypothesis that use of the ITPR will result in decreased intracranial pressure and increased cerebral perfusion pressure The effect of the ITPR on secondary indicators of cardiac performance will also be examined These include but are not limited estimates of ventricular end diastolic volume and pressure LVEDVP ejection fraction EF left ventricular end systolic volume and pressure LVESVP fractional area change FAC all of which will be assessed by transthoracic echocardiography TTE or transesophageal echocardiography TEE
For patients in the NNICU basic hemodynamic variables systemic blood pressure central venous pressure etc will be collected In addition left ventricular performance including estimates of LVEDV LVESV EF FAC and SV will be assessed using TTE Once these baseline data are recorded the ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal rube pressure ETP based on a randomization scheme After the ITPR has been active for at least five minutes the same intracranial hemodynamic and TTE data obtained above will be gathered The ITPR will then be turned off for five minutes and intracranial hemodynamic and TTE data will again be recorded The ITPR will be activated a second time -9 mm Hg or -5 mm Hg ETP ie whichever value was not used previously and after five minutes of use data will be recorded again The ITPR will then be disconnected data will be collected after waiting two minutes and no further interventions will be made
ABGs will be obtained before and during the use of the device at each setting
This is a proof of conceptfeasibility study designed to test the primary hypothesis that use of the ITPR will result in decreased intracranial pressure and increased cerebral perfusion pressure The effect of the ITPR on secondary indicators of cardiac performance will also be examined These include but are not limited estimates of ventricular end diastolic volume and pressure LVEDVP ejection fraction EF left ventricular end systolic volume and pressure LVESVP fractional area change FAC all of which will be assessed by transthoracic echocardiography TTE or transesophageal echocardiography TEE
Detailed Description:
The ITPR is an FDA-approved device intended to increase circulation and blood pressure in hypovolemic and cardiogenic shock The device is inserted within a standard respiratory circuit between the patient and the ventilator It functions by decreasing intrathoracic pressure during the expiratory phase to subatmospheric levels after each positive pressure ventilation This decrease in intrathoracic pressure creates a vacuum within the thorax relative to the rest of the body thereby enhancing venous return to the heart and consequently increasing cardiac output and blood pressure Activation of the device is also accompanied by a decrease in SVR The end result is a device that simultaneously improves cardiac output by increasing LVEDV and decreasing SVR while increasing coronary perfusion pressure by increasing blood pressure and decreasing LVESPLVESV1-8
Interestingly while the ITPR was developed as a non-invasive mechanism to increase preload in hypovolemic patients its mechanism of action generation of subatmospheric intrathoracic pressure has been shown to reduce intracranial pressure6 This is critical in brain-injured patients because elevated intracranial pressure is strongly associated with poor outcome in traumatic brain injury TBI patients - in a recent study of 846 TBI patients those with ICP 20 mm Hg by 48 hours had a mortality rate of 14 whereas those with ICP 20 mm Hg had a mortality rate of 349 Particularly interesting are the ITPRs combined benefits of increased MAP and decreased ICP as hypotension is a well-known poor prognostic indicator in this patient population
In fact according to the Brain Trauma Foundation Guidelines Hypotension occurring at any time from injury through the acute intensive care course has been found to be a primary predictor of outcome from severe head injury for the health care delivery systems within which prognostic variables have been best studied Hypotension is repeatedly found to be one of the five most powerful predictors of outcome and is generally the only one of these five that is amenable to therapeutic modification A single recording of a hypotensive episode is generally associated with a doubling of mortality and a marked increase in morbidity from a given head injury10
Importantly cerebral perfusion pressure mean arterial pressure - the greater of ICP or CVP is only a surrogate marker for cerebral blood flow The function of hypotension as a useful clinical variable is dependent on two factors - first its correlation with the true variable of interest cerebral blood flow and second the ability of clinicians to manipulate the underlying variable of interest cerebral blood flow based on the surrogate marker cerebral perfusion pressure
The acceptable level of hypotension in patients with brain injuries has not been determined and the Brain Trauma Foundation BTF Guidelines recommend maintaining systolic blood pressures 90 mm Hg but acknowledge that this number is relatively arbitrary and not based on any high-level studies thus assigning it a designation of Level II evidence 11 The BTF Guidelines further state that because hypotension is such a poor prognostic variable it would be unethical to randomize patients to various blood pressure goals and therefore Level I evidence is not forthcoming Further complicating the situation is the lack of agreement on how to increase blood pressure with the hopes of increasing cerebral perfusion pressure12-15 Many of the pharmacologic agents used to increase mean arterial pressure have significant vasoconstrictive effects which could counteract any increase blood pressure and lead to unchanged or even reduced cerebral blood flow
Interestingly while the ITPR was developed as a non-invasive mechanism to increase preload in hypovolemic patients its mechanism of action generation of subatmospheric intrathoracic pressure has been shown to reduce intracranial pressure6 This is critical in brain-injured patients because elevated intracranial pressure is strongly associated with poor outcome in traumatic brain injury TBI patients - in a recent study of 846 TBI patients those with ICP 20 mm Hg by 48 hours had a mortality rate of 14 whereas those with ICP 20 mm Hg had a mortality rate of 349 Particularly interesting are the ITPRs combined benefits of increased MAP and decreased ICP as hypotension is a well-known poor prognostic indicator in this patient population
In fact according to the Brain Trauma Foundation Guidelines Hypotension occurring at any time from injury through the acute intensive care course has been found to be a primary predictor of outcome from severe head injury for the health care delivery systems within which prognostic variables have been best studied Hypotension is repeatedly found to be one of the five most powerful predictors of outcome and is generally the only one of these five that is amenable to therapeutic modification A single recording of a hypotensive episode is generally associated with a doubling of mortality and a marked increase in morbidity from a given head injury10
Importantly cerebral perfusion pressure mean arterial pressure - the greater of ICP or CVP is only a surrogate marker for cerebral blood flow The function of hypotension as a useful clinical variable is dependent on two factors - first its correlation with the true variable of interest cerebral blood flow and second the ability of clinicians to manipulate the underlying variable of interest cerebral blood flow based on the surrogate marker cerebral perfusion pressure
The acceptable level of hypotension in patients with brain injuries has not been determined and the Brain Trauma Foundation BTF Guidelines recommend maintaining systolic blood pressures 90 mm Hg but acknowledge that this number is relatively arbitrary and not based on any high-level studies thus assigning it a designation of Level II evidence 11 The BTF Guidelines further state that because hypotension is such a poor prognostic variable it would be unethical to randomize patients to various blood pressure goals and therefore Level I evidence is not forthcoming Further complicating the situation is the lack of agreement on how to increase blood pressure with the hopes of increasing cerebral perfusion pressure12-15 Many of the pharmacologic agents used to increase mean arterial pressure have significant vasoconstrictive effects which could counteract any increase blood pressure and lead to unchanged or even reduced cerebral blood flow
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None