Topic: Retrospective or Prospective Cohort Study
CEREBRAL AUTOREGULATION IN COMATOSE SURVIVORS AFTER CARDIAC ARREST DURING HYPOTHERMIA
Ilaria Alice Crippa, J. Creteur, G. Citerio, J. Vincent, F. Taccone
Department of Health Science, Università degli Studi di Milano Bicocca, Monza, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Health Science, Università degli Studi di Milano Bicocca, Milan, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
Introduction:
Severe brain damage is frequent among survivors from cardiac arrest (CA). Thus, avoiding inadequate cerebral perfusion may contribute to avoid secondary brain damage in such patients [1]. Although targeted temperature management (TTM) remains the more effective neuroprotective intervention after CA, little is known about brain perfusion during cooling procedures [2].
Objectives: The aim of this study was to evaluate the autoregulation of cerebral blood flow (CAR) in CA patients treated by TTM.
Methods:
Adults (>18 years of age) comatose CA survivors undergoing TTM (32-34°C for 24 hours) were prospectively included in this study. Exclusion criteria were: traumatic CA; sepsis; previous neurological disease; drug overdose; irregular heart rhythm; severe hemodynamic instability, hypercapnia (45mmHg), extra-corporeal membrane oxygenation support. Left middle cerebral artery (LMCA) was insonated with a 2 MHz probe (DWL, Germany). Recordings were carried out at regular intervals throughout the hypothermic phase. LMCA velocity (FV) and blood pressure (BP) signal were recorded simultaneously through Doppler Box (DWL, Germany). Patients were maintained in steady state condition throughout the registration, avoiding any stimulus and manipulation of physiological or pharmacological variable. Collected data included: demographics, comorbidities, characteristics of CA, vital signs, biological and therapeutic variables. MATLAB (MathWorks, US) was used for CAR analysis. Mean BP and FV were calculated on a 10 seconds moving window with 50% overlap. Pearson's correlation coefficient between mean BP and FV (Mxa) was calculated. CAR was considered present if Mxa < 0,3 [3].
Results:
Seven patients were included until May 2015. All were males (age 69 [48-71] years). All recordings were carried out between 2 and 17 hours from the initiation of TTM. Mean temperature at CAR analysis was 33.0 [32.5-33.4] °C. Arterial carbon dioxide partial pressure (not adjusted for temperature) was 41 [35-42] mmHg. All patients but 1 (#6) were sedated and all patients but 2 (#4 and #6) were also paralysed. Mean insonating time was 6 [6-40] minutes. Four patients had intact CAR (Table 1). Further analysis of CAR at normothermia has been scheduled.
Conclusion:
CAR is deranged in half (3/7) of CA patients during the hypothermic phase of TTM. The impact of such alterations on brain function and neurological recovery needs to be further evaluated. Analysis of changes in CAR over time is on-going.
References:
1. Geocandin R et al. “Management of Brain Injury After Resuscitation From Cardiac Arrest” Neurologic Clinics 2008:487-506.
2. Sundgreen C et al. “Autoregulation of Cerebral Blood Flow in Patients Resuscitated From Cardiac Arrest” Stroke 2001:128-32.
3. Czosnyka M et al. “Monitoring of Cerebral Autoregulation in Head-Injured Patients” Stroke 1996:1829-34.
Topic: Retrospective or Prospective Cohort Study
CEREBRAL AUTOREGULATION IN COMATOSE SURVIVORS AFTER CARDIAC ARREST DURING HYPOTHERMIA
Ilaria Alice Crippa, J. Creteur, G. Citerio, J. Vincent, F. Taccone
Department of Health Science, Università degli Studi di Milano Bicocca, Monza, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Health Science, Università degli Studi di Milano Bicocca, Milan, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
Introduction:
Severe brain damage is frequent among survivors from cardiac arrest (CA). Thus, avoiding inadequate cerebral perfusion may contribute to avoid secondary brain damage in such patients [1]. Although targeted temperature management (TTM) remains the more effective neuroprotective intervention after CA, little is known about brain perfusion during cooling procedures [2].
Objectives: The aim of this study was to evaluate the autoregulation of cerebral blood flow (CAR) in CA patients treated by TTM.
Methods:
Adults (>18 years of age) comatose CA survivors undergoing TTM (32-34°C for 24 hours) were prospectively included in this study. Exclusion criteria were: traumatic CA; sepsis; previous neurological disease; drug overdose; irregular heart rhythm; severe hemodynamic instability, hypercapnia (45mmHg), extra-corporeal membrane oxygenation support. Left middle cerebral artery (LMCA) was insonated with a 2 MHz probe (DWL, Germany). Recordings were carried out at regular intervals throughout the hypothermic phase. LMCA velocity (FV) and blood pressure (BP) signal were recorded simultaneously through Doppler Box (DWL, Germany). Patients were maintained in steady state condition throughout the registration, avoiding any stimulus and manipulation of physiological or pharmacological variable. Collected data included: demographics, comorbidities, characteristics of CA, vital signs, biological and therapeutic variables. MATLAB (MathWorks, US) was used for CAR analysis. Mean BP and FV were calculated on a 10 seconds moving window with 50% overlap. Pearson's correlation coefficient between mean BP and FV (Mxa) was calculated. CAR was considered present if Mxa < 0,3 [3].
Results:
Seven patients were included until May 2015. All were males (age 69 [48-71] years). All recordings were carried out between 2 and 17 hours from the initiation of TTM. Mean temperature at CAR analysis was 33.0 [32.5-33.4] °C. Arterial carbon dioxide partial pressure (not adjusted for temperature) was 41 [35-42] mmHg. All patients but 1 (#6) were sedated and all patients but 2 (#4 and #6) were also paralysed. Mean insonating time was 6 [6-40] minutes. Four patients had intact CAR (Table 1). Further analysis of CAR at normothermia has been scheduled.
Conclusion:
CAR is deranged in half (3/7) of CA patients during the hypothermic phase of TTM. The impact of such alterations on brain function and neurological recovery needs to be further evaluated. Analysis of changes in CAR over time is on-going.
References:
1. Geocandin R et al. “Management of Brain Injury After Resuscitation From Cardiac Arrest” Neurologic Clinics 2008:487-506.
2. Sundgreen C et al. “Autoregulation of Cerebral Blood Flow in Patients Resuscitated From Cardiac Arrest” Stroke 2001:128-32.
3. Czosnyka M et al. “Monitoring of Cerebral Autoregulation in Head-Injured Patients” Stroke 1996:1829-34.
Topic: Retrospective or Prospective Cohort Study
CEREBRAL AUTOREGULATION IN COMATOSE SURVIVORS AFTER CARDIAC ARREST DURING HYPOTHERMIA
Ilaria Alice Crippa, J. Creteur, G. Citerio, J. Vincent, F. Taccone
Department of Health Science, Università degli Studi di Milano Bicocca, Monza, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Health Science, Università degli Studi di Milano Bicocca, Milan, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
Introduction:
Severe brain damage is frequent among survivors from cardiac arrest (CA). Thus, avoiding inadequate cerebral perfusion may contribute to avoid secondary brain damage in such patients [1]. Although targeted temperature management (TTM) remains the more effective neuroprotective intervention after CA, little is known about brain perfusion during cooling procedures [2].
Objectives: The aim of this study was to evaluate the autoregulation of cerebral blood flow (CAR) in CA patients treated by TTM.
Methods:
Adults (>18 years of age) comatose CA survivors undergoing TTM (32-34°C for 24 hours) were prospectively included in this study. Exclusion criteria were: traumatic CA; sepsis; previous neurological disease; drug overdose; irregular heart rhythm; severe hemodynamic instability, hypercapnia (45mmHg), extra-corporeal membrane oxygenation support. Left middle cerebral artery (LMCA) was insonated with a 2 MHz probe (DWL, Germany). Recordings were carried out at regular intervals throughout the hypothermic phase. LMCA velocity (FV) and blood pressure (BP) signal were recorded simultaneously through Doppler Box (DWL, Germany). Patients were maintained in steady state condition throughout the registration, avoiding any stimulus and manipulation of physiological or pharmacological variable. Collected data included: demographics, comorbidities, characteristics of CA, vital signs, biological and therapeutic variables. MATLAB (MathWorks, US) was used for CAR analysis. Mean BP and FV were calculated on a 10 seconds moving window with 50% overlap. Pearson's correlation coefficient between mean BP and FV (Mxa) was calculated. CAR was considered present if Mxa < 0,3 [3].
Results:
Seven patients were included until May 2015. All were males (age 69 [48-71] years). All recordings were carried out between 2 and 17 hours from the initiation of TTM. Mean temperature at CAR analysis was 33.0 [32.5-33.4] °C. Arterial carbon dioxide partial pressure (not adjusted for temperature) was 41 [35-42] mmHg. All patients but 1 (#6) were sedated and all patients but 2 (#4 and #6) were also paralysed. Mean insonating time was 6 [6-40] minutes. Four patients had intact CAR (Table 1). Further analysis of CAR at normothermia has been scheduled.
Conclusion:
CAR is deranged in half (3/7) of CA patients during the hypothermic phase of TTM. The impact of such alterations on brain function and neurological recovery needs to be further evaluated. Analysis of changes in CAR over time is on-going.
References:
1. Geocandin R et al. “Management of Brain Injury After Resuscitation From Cardiac Arrest” Neurologic Clinics 2008:487-506.
2. Sundgreen C et al. “Autoregulation of Cerebral Blood Flow in Patients Resuscitated From Cardiac Arrest” Stroke 2001:128-32.
3. Czosnyka M et al. “Monitoring of Cerebral Autoregulation in Head-Injured Patients” Stroke 1996:1829-34.
Topic: Retrospective or Prospective Cohort Study
CEREBRAL AUTOREGULATION IN COMATOSE SURVIVORS AFTER CARDIAC ARREST DURING HYPOTHERMIA
Ilaria Alice Crippa, J. Creteur, G. Citerio, J. Vincent, F. Taccone
Department of Health Science, Università degli Studi di Milano Bicocca, Monza, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Health Science, Università degli Studi di Milano Bicocca, Milan, Italy | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium | Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
Introduction:
Severe brain damage is frequent among survivors from cardiac arrest (CA). Thus, avoiding inadequate cerebral perfusion may contribute to avoid secondary brain damage in such patients [1]. Although targeted temperature management (TTM) remains the more effective neuroprotective intervention after CA, little is known about brain perfusion during cooling procedures [2].
Objectives: The aim of this study was to evaluate the autoregulation of cerebral blood flow (CAR) in CA patients treated by TTM.
Methods:
Adults (>18 years of age) comatose CA survivors undergoing TTM (32-34°C for 24 hours) were prospectively included in this study. Exclusion criteria were: traumatic CA; sepsis; previous neurological disease; drug overdose; irregular heart rhythm; severe hemodynamic instability, hypercapnia (45mmHg), extra-corporeal membrane oxygenation support. Left middle cerebral artery (LMCA) was insonated with a 2 MHz probe (DWL, Germany). Recordings were carried out at regular intervals throughout the hypothermic phase. LMCA velocity (FV) and blood pressure (BP) signal were recorded simultaneously through Doppler Box (DWL, Germany). Patients were maintained in steady state condition throughout the registration, avoiding any stimulus and manipulation of physiological or pharmacological variable. Collected data included: demographics, comorbidities, characteristics of CA, vital signs, biological and therapeutic variables. MATLAB (MathWorks, US) was used for CAR analysis. Mean BP and FV were calculated on a 10 seconds moving window with 50% overlap. Pearson's correlation coefficient between mean BP and FV (Mxa) was calculated. CAR was considered present if Mxa < 0,3 [3].
Results:
Seven patients were included until May 2015. All were males (age 69 [48-71] years). All recordings were carried out between 2 and 17 hours from the initiation of TTM. Mean temperature at CAR analysis was 33.0 [32.5-33.4] °C. Arterial carbon dioxide partial pressure (not adjusted for temperature) was 41 [35-42] mmHg. All patients but 1 (#6) were sedated and all patients but 2 (#4 and #6) were also paralysed. Mean insonating time was 6 [6-40] minutes. Four patients had intact CAR (Table 1). Further analysis of CAR at normothermia has been scheduled.
Conclusion:
CAR is deranged in half (3/7) of CA patients during the hypothermic phase of TTM. The impact of such alterations on brain function and neurological recovery needs to be further evaluated. Analysis of changes in CAR over time is on-going.
References:
1. Geocandin R et al. “Management of Brain Injury After Resuscitation From Cardiac Arrest” Neurologic Clinics 2008:487-506.
2. Sundgreen C et al. “Autoregulation of Cerebral Blood Flow in Patients Resuscitated From Cardiac Arrest” Stroke 2001:128-32.
3. Czosnyka M et al. “Monitoring of Cerebral Autoregulation in Head-Injured Patients” Stroke 1996:1829-34.
