Traumatic Brain InjuryPhase 2NCT01205607
IRB-HSR# 14299: The Use of the Intrathoracic Pressure Regulator (ITPR) to Improve Cerebral Perfusion Pressure in Patients With Altered Intracranial Elastance
A Phase 2 study testing ITPR -5 mm Hg then -9 mm Hg and ITPR -9 & then -5mm Hg in people with Traumatic Brain Injury, run by University of Virginia at 1 site in United States.
Trial 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 (i.e. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Traumatic Brain Injury
- What is being tested?
- ITPR -5 mm Hg then -9 mm Hg and ITPR -9 & then -5mm Hg
- Type of treatment
- Medical device
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 20 participants
- Where
- 1 siteUnited States
- Study dates
- May 2009to not given
- Phase
- Phase 2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- 1. 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 (i.e. in the NNICU)and have an arterial line in place, or are scheduled to undergo an operation or interventional neuroradiological procedure at the University of Virginia.
- 2. age 18 years of age and older 3. informed consent/ surrogate consent has been obtained
Who cannot join
- 1. pneumothorax 2. hemothroax 3. uncontrolled bleeding 4. uncontrolled hypertension defined as SBP > 180 mmHg at the time of surgery 5. known respiratory disease such as chronic emphysema, COPD, or Cystic Fibrosis
Trial locations and contacts
1 site in 1 country.
United States1 site
University of Virginia Health System
Charlottesville, Virginia, 22908
About this study
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 (i.e. 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, i.e. 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.
Read more
ABG's will be obtained before and during the use of the device at each setting.
This is a proof of concept/feasibility 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 (LVEDV/P), ejection fraction (EF), left ventricular end systolic volume and pressure (LVESV/P), fractional area change (FAC), all of which will be assessed by transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE).
Read the 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 LVESP/LVESV.1-8
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 34%9. Particularly interesting are the ITPR's 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 pressure)12-15. 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.
- Conditions
- Traumatic Brain Injury
- Being tested
- ITPR -5 mm Hg then -9 mm Hg, ITPR -9 & then -5mm Hg
- Keywords
- traumatic brain injury
- Medical subject headings
- Brain Injuries, Traumatic
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
ITPR -5 mm Hg then -9 mm HgDevice
the ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg
ITPR -9 & then -5mm HgDevice
the ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg
| Study group | Role | What they receive |
|---|---|---|
| ITPR -9 & then -5 mm Hg | Experimental | the ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg Receives: Device: ITPR -9 & then -5mm Hg |
| ITPR -5 & then _9 mm HG | Experimental | the ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg Receives: Device: ITPR -5 mm Hg then -9 mm Hg |
What is being measured
The primary outcome is the main question the study is designed to answer.
Hemodynamic variables
hemodynamic variables (systemic blood pressure, central venous pressure, ICP) will be collected at baseline, 5 minutes after device activation \& 5 minutes after device turned off
Measured: baseline, 5 minutes after device activation & 5 minutes after device turned off
Secondary outcomes (1)
cardiac performance
cardiac performance will also be examined. These include but are not limited estimates of ventricular end diastolic volume and pressure (LVEDV/P), ejection fraction (EF), left ventricular end systolic volume and pressure (LVESV/P), fractional area change (FAC)
Measured: baseline, 5 minutes after device activation & 5 minutes after device turned off
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted20 Sep 2010 (estimated)
- Study startMay 2009
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (15)Papers the sponsor has linked to this study.
- Other trials for Traumatic Brain InjuryStudies of the same condition, open and under way.
- More trials run by University of VirginiaThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 2
- Primary purpose
- Health services research
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind
- Who is masked
- Participant, Outcomes assessor
- Enrolment
- 20 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Virginia
- Sponsor type
- University, hospital or other
- Investigators
- Edward C Nemergfut, MD, Principal investigator, University of Virginia Anesthesiology
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01205607
- Sponsor's protocol ID
- 14299
- Status last verified
- Sep 2010
- First submitted
- 17 Sep 2010
- Last updated
- 20 Sep 2010
- Results posted
- No
- Data monitoring committee
- No
Publications
Lurie KG, Zielinski TM, McKnite SH, Idris AH, Yannopoulos D, Raedler CM, Sigurdsson G, Benditt DG, Voelckel WG. Treatment of hypotension in pigs with an inspiratory impedance threshold device: a feasibility study. Crit Care Med. 2004 Jul;32(7):1555-62. doi: 10.1097/01.ccm.0000131207.29081.a2.
PubMed 15241102Lurie KG, Zielinski T, McKnite S, Aufderheide T, Voelckel W. Use of an inspiratory impedance valve improves neurologically intact survival in a porcine model of ventricular fibrillation. Circulation. 2002 Jan 1;105(1):124-9. doi: 10.1161/hc0102.101391.
PubMed 11772887Lurie KG, Voelckel WG, Zielinski T, McKnite S, Lindstrom P, Peterson C, Wenzel V, Lindner KH, Samniah N, Benditt D. Improving standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve in a porcine model of cardiac arrest. Anesth Analg. 2001 Sep;93(3):649-55. doi: 10.1097/00000539-200109000-00024.
PubMed 11524335Lurie KG, Mulligan KA, McKnite S, Detloff B, Lindstrom P, Lindner KH. Optimizing standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve. Chest. 1998 Apr;113(4):1084-90. doi: 10.1378/chest.113.4.1084.
PubMed 9554651Yannopoulos D, McKnite S, Metzger A, Lurie KG. Intrathoracic pressure regulation improves 24-hour survival in a porcine model of hypovolemic shock. Anesth Analg. 2007 Jan;104(1):157-62. doi: 10.1213/01.ane.0000249047.80184.5a.
PubMed 17179262Yannopoulos D, McKnite SH, Metzger A, Lurie KG. Intrathoracic pressure regulation for intracranial pressure management in normovolemic and hypovolemic pigs. Crit Care Med. 2006 Dec;34(12 Suppl):S495-500. doi: 10.1097/01.CCM.0000246082.10422.7E.
PubMed 17114984Yannopoulos D, Metzger A, McKnite S, Nadkarni V, Aufderheide TP, Idris A, Dries D, Benditt DG, Lurie KG. Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs. Resuscitation. 2006 Sep;70(3):445-53. doi: 10.1016/j.resuscitation.2006.02.005. Epub 2006 Aug 9.
PubMed 16901611Yannopoulos D, Nadkarni VM, McKnite SH, Rao A, Kruger K, Metzger A, Benditt DG, Lurie KG. Intrathoracic pressure regulator during continuous-chest-compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest. Circulation. 2005 Aug 9;112(6):803-11. doi: 10.1161/CIRCULATIONAHA.105.541508. Epub 2005 Aug 1.
PubMed 16061732Jiang JY, Gao GY, Li WP, Yu MK, Zhu C. Early indicators of prognosis in 846 cases of severe traumatic brain injury. J Neurotrauma. 2002 Jul;19(7):869-74. doi: 10.1089/08977150260190456.
PubMed 12184856The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Hypotension. J Neurotrauma. 2000 Jun-Jul;17(6-7):591-5. doi: 10.1089/neu.2000.17.591.
PubMed 10937905Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS; Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW. Guidelines for the management of severe traumatic brain injury. I. Blood pressure and oxygenation. J Neurotrauma. 2007;24 Suppl 1:S7-13. doi: 10.1089/neu.2007.9995. No abstract available.
PubMed 17511549Pfister D, Strebel SP, Steiner LA. Effects of catecholamines on cerebral blood vessels in patients with traumatic brain injury. Eur J Anaesthesiol Suppl. 2008;42:98-103. doi: 10.1017/S0265021507003407.
PubMed 18289425Dudkiewicz M, Proctor KG. Tissue oxygenation during management of cerebral perfusion pressure with phenylephrine or vasopressin. Crit Care Med. 2008 Sep;36(9):2641-50. doi: 10.1097/CCM.0b013e3181847af3.
PubMed 18679110Myburgh JA. Driving cerebral perfusion pressure with pressors: how, which, when? Crit Care Resusc. 2005 Sep;7(3):200-5.
PubMed 16545046Alspaugh DM, Sartorelli K, Shackford SR, Okum EJ, Buckingham S, Osler T. Prehospital resuscitation with phenylephrine in uncontrolled hemorrhagic shock and brain injury. J Trauma. 2000 May;48(5):851-63; discussion 863-4. doi: 10.1097/00005373-200005000-00008.
PubMed 10823528
Study at a glance
From the registry record, last updated by the sponsor on 20 Sep 2010. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- IRB-HSR# 14299: The Use of the Intrathoracic Pressure Regulator (ITPR) to Improve Cerebral Perfusion Pressure in Patients With Altered Intracranial Elastance
- ClinicalTrials.gov ID
- NCT01205607
- Acronym / sponsor ID
- 14299
- Conditions
- Traumatic Brain Injury
- Keywords
- traumatic brain injury
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 20 participants (estimated)
- Lead sponsor
- University of VirginiaUniversity, hospital or other
- Study start
- May 2009
- First posted
- 20 Sep 2010 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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 (i.e. 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, i.e. 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.
ABG's will be obtained before and during the use of the device at each setting.
This is a proof of concept/feasibility 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 (LVEDV/P), ejection fraction (EF), left ventricular end systolic volume and pressure (LVESV/P), 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 LVESP/LVESV.1-8
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 34%9. Particularly interesting are the ITPR's 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 pressure)12-15. 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 design
- Primary purpose
- Health services research
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind (participant, outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| ITPR -9 & then -5 mm Hg | Experimental | Device: ITPR -9 & then -5mm Hgthe ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg |
| ITPR -5 & then _9 mm HG | Experimental | Device: ITPR -5 mm Hg then -9 mm Hgthe ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (2 listed)
- 1. 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 (i.e. in the NNICU)and have an arterial line in place, or are scheduled to undergo an operation or interventional neuroradiological procedure at the University of Virginia.
- 2. age 18 years of age and older 3. informed consent/ surrogate consent has been obtained
Key exclusion criteria (1 listed)
- 1. pneumothorax 2. hemothroax 3. uncontrolled bleeding 4. uncontrolled hypertension defined as SBP > 180 mmHg at the time of surgery 5. known respiratory disease such as chronic emphysema, COPD, or Cystic Fibrosis
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| ITPR -5 mm Hg then -9 mm Hgthe ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg | Device | ITPR -5 & then _9 mm HG |
| ITPR -9 & then -5mm Hgthe ITPR will be inserted in the ventilator circuit and activated to provide either -5 mm Hg or -9 mm Hg endotracheal tube pressure (ETP) Each subject will have all measurements recorded at both -5 \& -9 mm Hg | Device | ITPR -9 & then -5 mm Hg |
Primary outcome
Hemodynamic variables
Time frame: baseline, 5 minutes after device activation & 5 minutes after device turned off
hemodynamic variables (systemic blood pressure, central venous pressure, ICP) will be collected at baseline, 5 minutes after device activation \& 5 minutes after device turned off
1 secondary outcome
cardiac performance
Time frame: baseline, 5 minutes after device activation & 5 minutes after device turned off
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 20 Sep 2010.
- Background: PubMed 15241102Lurie KG, Zielinski TM, McKnite SH, Idris AH, Yannopoulos D, Raedler CM, Sigurdsson G, Benditt DG, Voelckel WG. Treatment of hypotension in pigs with an inspiratory impedance threshold device: a feasibility study. Crit Care Med. 2004 Jul;32(7):1555-62. doi: 10.1097/01.ccm.0000131207.29081.a2.
- Background: PubMed 11772887Lurie KG, Zielinski T, McKnite S, Aufderheide T, Voelckel W. Use of an inspiratory impedance valve improves neurologically intact survival in a porcine model of ventricular fibrillation. Circulation. 2002 Jan 1;105(1):124-9. doi: 10.1161/hc0102.101391.
- Background: PubMed 11524335Lurie KG, Voelckel WG, Zielinski T, McKnite S, Lindstrom P, Peterson C, Wenzel V, Lindner KH, Samniah N, Benditt D. Improving standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve in a porcine model of cardiac arrest. Anesth Analg. 2001 Sep;93(3):649-55. doi: 10.1097/00000539-200109000-00024.
- Background: PubMed 9554651Lurie KG, Mulligan KA, McKnite S, Detloff B, Lindstrom P, Lindner KH. Optimizing standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve. Chest. 1998 Apr;113(4):1084-90. doi: 10.1378/chest.113.4.1084.
- Background: PubMed 17179262Yannopoulos D, McKnite S, Metzger A, Lurie KG. Intrathoracic pressure regulation improves 24-hour survival in a porcine model of hypovolemic shock. Anesth Analg. 2007 Jan;104(1):157-62. doi: 10.1213/01.ane.0000249047.80184.5a.
- Background: PubMed 17114984Yannopoulos D, McKnite SH, Metzger A, Lurie KG. Intrathoracic pressure regulation for intracranial pressure management in normovolemic and hypovolemic pigs. Crit Care Med. 2006 Dec;34(12 Suppl):S495-500. doi: 10.1097/01.CCM.0000246082.10422.7E.
- Background: PubMed 16901611Yannopoulos D, Metzger A, McKnite S, Nadkarni V, Aufderheide TP, Idris A, Dries D, Benditt DG, Lurie KG. Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs. Resuscitation. 2006 Sep;70(3):445-53. doi: 10.1016/j.resuscitation.2006.02.005. Epub 2006 Aug 9.
- Background: PubMed 16061732Yannopoulos D, Nadkarni VM, McKnite SH, Rao A, Kruger K, Metzger A, Benditt DG, Lurie KG. Intrathoracic pressure regulator during continuous-chest-compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest. Circulation. 2005 Aug 9;112(6):803-11. doi: 10.1161/CIRCULATIONAHA.105.541508. Epub 2005 Aug 1.
- Background: PubMed 12184856Jiang JY, Gao GY, Li WP, Yu MK, Zhu C. Early indicators of prognosis in 846 cases of severe traumatic brain injury. J Neurotrauma. 2002 Jul;19(7):869-74. doi: 10.1089/08977150260190456.
- Background: PubMed 10937905The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Hypotension. J Neurotrauma. 2000 Jun-Jul;17(6-7):591-5. doi: 10.1089/neu.2000.17.591.
- Background: PubMed 17511549Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS; Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW. Guidelines for the management of severe traumatic brain injury. I. Blood pressure and oxygenation. J Neurotrauma. 2007;24 Suppl 1:S7-13. doi: 10.1089/neu.2007.9995. No abstract available.
- Background: PubMed 18289425Pfister D, Strebel SP, Steiner LA. Effects of catecholamines on cerebral blood vessels in patients with traumatic brain injury. Eur J Anaesthesiol Suppl. 2008;42:98-103. doi: 10.1017/S0265021507003407.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Edward C Nemergfut, MD principal investigator
University of Virginia Anesthesiology
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing ITPR -5 mm Hg then -9 mm Hg and ITPR -9 & then -5mm Hg in people with Traumatic Brain Injury, run by University of Virginia at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 20 Sep 2010. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Hemodynamic variables (time frame: baseline, 5 minutes after device activation & 5 minutes after device turned off). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT01205607, which also lists 15 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 20 Sep 2010.