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Brian P. Kavanagh - One of the best experts on this subject based on the ideXlab platform.
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Hypocapnia and the injured brain more harm than benefit
Critical Care Medicine, 2010Co-Authors: Gerard F Curley, Brian P. Kavanagh, John G. LaffeyAbstract:Objectives: Hypocapnia is used in the management of acute brain injury and may be life-saving in specific circumstances, but it can produce neuronal ischemia and injury, potentially worsening outcome. This review re-examines the rationale for the use of Hypocapnia in acute brain injury and evaluates the evidence for therapeutic and deleterious effects in this context. Data Sources and Study Selection: A MEDLINE/PubMed search from 1966 to August 1, 2009, was conducted using the search terms "hyperventilation," "Hypocapnia," "alkalosis," "carbon dioxide," "brain," "lung," and "myocardium," alone and in combination. Bibliographies of retrieved articles were also reviewed. Data Extraction and Synthesis: Hypocapnia—often for prolonged periods of time—remains prevalent in the management of severely brain-injured children and adults. Despite this, there is no proof beyond clinical experience with incipient herniation that Hypocapnia improves neurologic outcome in any context. On the contrary, Hypocapnia can cause or worsen cerebral ischemia. The effect of sustained Hypocapnia on cerebral blood flow decreases progressively because of buffering; subsequent normocapnia can cause rebound cerebral hyperemia and increase intracranial pressure. Hypocapnia may also injure other organs. Accidental Hypocapnia should always be avoided and prophylactic Hypocapnia has no current role. Conclusions: Hypocapnia can cause harm and should be strictly limited to the emergent management of life-threatening intracranial hypertension pending definitive measures or to facilitate intraoperative neurosurgery. When it is used, PaCO 2 should be normalized as soon as is feasible. Outside these settings Hypocapnia is likely to produce more harm than benefit.
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Bench-to-bedside review: Carbon dioxide
Critical Care, 2010Co-Authors: Gerard Curley, John G. Laffey, Brian P. KavanaghAbstract:Carbon dioxide is a waste product of aerobic cellular respiration in all aerobic life forms. PaCO_2 represents the balance between the carbon dioxide produced and that eliminated. Hypocapnia remains a common - and generally underappreciated - component of many disease states, including early asthma, high-altitude pulmonary edema, and acute lung injury. Induction of Hypocapnia remains a common, if controversial, practice in both adults and children with acute brain injury. In contrast, hypercapnia has traditionally been avoided in order to keep parameters normal. More recently, advances in our understanding of the role of excessive tidal volume has prompted clinicians to use ventilation strategies that result in hypercapnia. Consequently, hypercapnia has become increasingly prevalent in the critically ill patient. Hypercapnia may play a beneficial role in the pathogenesis of inflammation and tissue injury, but may hinder the host response to sepsis and reduce repair. In contrast, Hypocapnia may be a pathogenic entity in the setting of critical illness. The present paper reviews the current clinical status of low and high PaCO_2 in the critically ill patient, discusses the insights gained to date from studies of carbon dioxide, identifies key concerns regarding Hypocapnia and hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.
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Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation.
Critical Care Medicine, 2003Co-Authors: John G. Laffey, Ruud A. W. Veldhuizen, James F. Lewis, Michelle Duggan, Doreen Engelberts, Brian P. KavanaghAbstract:Objective: Deliberate elevation of PaCO 2 (therapeutic hypercapnia) protects against lung injury induced by lung reperfusion and severe lung stretch. Conversely, hypocapnic alkalosis causes lung injury and worsens lung reperfusion injury. Alterations in lung surfactant may contribute to ventilator-associated lung injury. The potential for CO 2 to contribute to the pathogenesis of ventilator-associated lung injury at clinically relevant tidal volumes is unknown. We hypothesized that: 1) Hypocapnia would worsen ventilator-associated lung injury, 2) therapeutic hypercapnia would attenuate ventilator-associated lung injury; and 3) the mechanisms of impaired compliance would be via alteration of surfactant biochemistry. Design: Randomized, prospective animal study. Setting: Research laboratory of university-affiliated hospital. Subjects: Anesthetized, male New Zealand Rabbits. Interventions: All animals received the same ventilation strategy (tidal volume, 12 mUkg; positive end-expiratory pressure, 0 cm H 2 O; rate, 42 breaths/min) and were randomized to receive FiCO 2 of 0.00, 0.05, or 0.12 to produce Hypocapnia, normocapnia, and hypercapnia, respectively. Measurements and Main Results: Alveolar-arterial oxygen gradient was significantly lower with therapeutic hypercapnia, and peak airway pressure was significantly higher with hypocapnic alkalosis. However, neither static lung compliance nor surfactant chemistry (total surfactant, aggregates, or composition) differed among the groups. Conclusions: At clinically relevant tidal volume, CO 2 modulates key physiologic indices of lung injury, including alveolar-arterial oxygen gradient and airway pressure, indicating a potential role in the pathogenesis of ventilator-associated lung injury. These effects are surfactant independent.
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injurious effects of hypocapnic alkalosis in the isolated lung
American Journal of Respiratory and Critical Care Medicine, 2000Co-Authors: John G. Laffey, Doreen Engelberts, Brian P. KavanaghAbstract:Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in Hypocapnia. Although Hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether Hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that Hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia–reperfusion. We utilized the isolated buffer-perfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (Fi CO2 = 0.06) or groups with Hypocapnia (Fi CO2 = 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchan...
Shuichi Miura - One of the best experts on this subject based on the ideXlab platform.
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changes in the arterial fraction of human cerebral blood volume during hypercapnia and Hypocapnia measured by positron emission tomography
Journal of Cerebral Blood Flow and Metabolism, 2005Co-Authors: Hiroshi Ito, Iwao Kanno, Masanobu Ibaraki, Hiroshi Fukuda, Shuichi MiuraAbstract:Hypercapnia induces cerebral vasodilation and increases cerebral blood volume (CBV), and Hypocapnia induces cerebral vasoconstriction and decreases CBV. Cerebral blood volume measured by positron emission tomography (PET) is the sum of three components, that is, arterial, capillary, and venous blood volumes. Changes in arterial blood volume (V(a)) and CBV during hypercapnia and Hypocapnia were investigated in humans using PET with H(2)(15)O and (11)CO. Arterial blood volume was determined from H(2)(15)O PET data by means of a two-compartment model that takes V(a) into account. Baseline CBV and values during hypercapnia and Hypocapnia in the cerebral cortex were 0.034+/-0.003, 0.038+/-0.003, and 0.031+/-0.003 mL/mL (mean+/-s.d.), respectively. Baseline V(a) and values during hypercapnia and Hypocapnia were 0.015+/-0.003, 0.025+/-0.011, and 0.007+/-0.003 mL/mL, respectively. Cerebral blood volume changed significantly owing to changes in PaCO(2), and V(a) changed significantly in the direction of CBV changes. However, no significant change was observed in venous plus capillary blood volume (=CBV-V(a)). This indicates that changes in CBV during hypercapnia and Hypocapnia are caused by changes in arterial blood volume without changes in venous and capillary blood volume.
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changes in human cerebral blood flow and cerebral blood volume during hypercapnia and Hypocapnia measured by positron emission tomography
Journal of Cerebral Blood Flow and Metabolism, 2003Co-Authors: Hiroshi Ito, Iwao Kanno, Masanobu Ibaraki, Jun Hatazawa, Shuichi MiuraAbstract:Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and Hypocapnia induces cerebral vasoconstriction and decreases CBF. The relation between changes in CBF and cerebral blood volume (CBV) during hypercapnia and Hypocapnia in humans, however, is not clear. Both CBF and CBV were measured at rest and during hypercapnia and Hypocapnia in nine healthy subjects by positron emission tomography. The vascular responses to hypercapnia in terms of CBF and CBV were 6.0 +/- 2.6%/mm Hg and 1.8 +/- 1.3%/mm Hg, respectively, and those to Hypocapnia were -3.5 +/- 0.6%/mm Hg and -1.3 +/- 1.0%/mm Hg, respectively. The relation between CBF and CBV was CBV = 1.09 CBF0.29. The increase in CBF was greater than that in CBV during hypercapnia, indicating an increase in vascular blood velocity. The degree of decrease in CBF during Hypocapnia was greater than that in CBV, indicating a decrease in vascular blood velocity. The relation between changes in CBF and CBV during hypercapnia was similar to that during neural activation; however, the relation during Hypocapnia was different from that during neural deactivation observed in crossed cerebellar diaschisis. This suggests that augmentation of CBF and CBV might be governed by a similar microcirculatory mechanism between neural activation and hypercapnia, but diminution of CBF and CBV might be governed by a different mechanism between neural deactivation and Hypocapnia.
John G. Laffey - One of the best experts on this subject based on the ideXlab platform.
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Hypocapnia and the injured brain more harm than benefit
Critical Care Medicine, 2010Co-Authors: Gerard F Curley, Brian P. Kavanagh, John G. LaffeyAbstract:Objectives: Hypocapnia is used in the management of acute brain injury and may be life-saving in specific circumstances, but it can produce neuronal ischemia and injury, potentially worsening outcome. This review re-examines the rationale for the use of Hypocapnia in acute brain injury and evaluates the evidence for therapeutic and deleterious effects in this context. Data Sources and Study Selection: A MEDLINE/PubMed search from 1966 to August 1, 2009, was conducted using the search terms "hyperventilation," "Hypocapnia," "alkalosis," "carbon dioxide," "brain," "lung," and "myocardium," alone and in combination. Bibliographies of retrieved articles were also reviewed. Data Extraction and Synthesis: Hypocapnia—often for prolonged periods of time—remains prevalent in the management of severely brain-injured children and adults. Despite this, there is no proof beyond clinical experience with incipient herniation that Hypocapnia improves neurologic outcome in any context. On the contrary, Hypocapnia can cause or worsen cerebral ischemia. The effect of sustained Hypocapnia on cerebral blood flow decreases progressively because of buffering; subsequent normocapnia can cause rebound cerebral hyperemia and increase intracranial pressure. Hypocapnia may also injure other organs. Accidental Hypocapnia should always be avoided and prophylactic Hypocapnia has no current role. Conclusions: Hypocapnia can cause harm and should be strictly limited to the emergent management of life-threatening intracranial hypertension pending definitive measures or to facilitate intraoperative neurosurgery. When it is used, PaCO 2 should be normalized as soon as is feasible. Outside these settings Hypocapnia is likely to produce more harm than benefit.
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Bench-to-bedside review: Carbon dioxide
Critical Care, 2010Co-Authors: Gerard Curley, John G. Laffey, Brian P. KavanaghAbstract:Carbon dioxide is a waste product of aerobic cellular respiration in all aerobic life forms. PaCO_2 represents the balance between the carbon dioxide produced and that eliminated. Hypocapnia remains a common - and generally underappreciated - component of many disease states, including early asthma, high-altitude pulmonary edema, and acute lung injury. Induction of Hypocapnia remains a common, if controversial, practice in both adults and children with acute brain injury. In contrast, hypercapnia has traditionally been avoided in order to keep parameters normal. More recently, advances in our understanding of the role of excessive tidal volume has prompted clinicians to use ventilation strategies that result in hypercapnia. Consequently, hypercapnia has become increasingly prevalent in the critically ill patient. Hypercapnia may play a beneficial role in the pathogenesis of inflammation and tissue injury, but may hinder the host response to sepsis and reduce repair. In contrast, Hypocapnia may be a pathogenic entity in the setting of critical illness. The present paper reviews the current clinical status of low and high PaCO_2 in the critically ill patient, discusses the insights gained to date from studies of carbon dioxide, identifies key concerns regarding Hypocapnia and hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.
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Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation.
Critical Care Medicine, 2003Co-Authors: John G. Laffey, Ruud A. W. Veldhuizen, James F. Lewis, Michelle Duggan, Doreen Engelberts, Brian P. KavanaghAbstract:Objective: Deliberate elevation of PaCO 2 (therapeutic hypercapnia) protects against lung injury induced by lung reperfusion and severe lung stretch. Conversely, hypocapnic alkalosis causes lung injury and worsens lung reperfusion injury. Alterations in lung surfactant may contribute to ventilator-associated lung injury. The potential for CO 2 to contribute to the pathogenesis of ventilator-associated lung injury at clinically relevant tidal volumes is unknown. We hypothesized that: 1) Hypocapnia would worsen ventilator-associated lung injury, 2) therapeutic hypercapnia would attenuate ventilator-associated lung injury; and 3) the mechanisms of impaired compliance would be via alteration of surfactant biochemistry. Design: Randomized, prospective animal study. Setting: Research laboratory of university-affiliated hospital. Subjects: Anesthetized, male New Zealand Rabbits. Interventions: All animals received the same ventilation strategy (tidal volume, 12 mUkg; positive end-expiratory pressure, 0 cm H 2 O; rate, 42 breaths/min) and were randomized to receive FiCO 2 of 0.00, 0.05, or 0.12 to produce Hypocapnia, normocapnia, and hypercapnia, respectively. Measurements and Main Results: Alveolar-arterial oxygen gradient was significantly lower with therapeutic hypercapnia, and peak airway pressure was significantly higher with hypocapnic alkalosis. However, neither static lung compliance nor surfactant chemistry (total surfactant, aggregates, or composition) differed among the groups. Conclusions: At clinically relevant tidal volume, CO 2 modulates key physiologic indices of lung injury, including alveolar-arterial oxygen gradient and airway pressure, indicating a potential role in the pathogenesis of ventilator-associated lung injury. These effects are surfactant independent.
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injurious effects of hypocapnic alkalosis in the isolated lung
American Journal of Respiratory and Critical Care Medicine, 2000Co-Authors: John G. Laffey, Doreen Engelberts, Brian P. KavanaghAbstract:Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in Hypocapnia. Although Hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether Hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that Hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia–reperfusion. We utilized the isolated buffer-perfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (Fi CO2 = 0.06) or groups with Hypocapnia (Fi CO2 = 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchan...
Hiroshi Ito - One of the best experts on this subject based on the ideXlab platform.
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changes in the arterial fraction of human cerebral blood volume during hypercapnia and Hypocapnia measured by positron emission tomography
Journal of Cerebral Blood Flow and Metabolism, 2005Co-Authors: Hiroshi Ito, Iwao Kanno, Masanobu Ibaraki, Hiroshi Fukuda, Shuichi MiuraAbstract:Hypercapnia induces cerebral vasodilation and increases cerebral blood volume (CBV), and Hypocapnia induces cerebral vasoconstriction and decreases CBV. Cerebral blood volume measured by positron emission tomography (PET) is the sum of three components, that is, arterial, capillary, and venous blood volumes. Changes in arterial blood volume (V(a)) and CBV during hypercapnia and Hypocapnia were investigated in humans using PET with H(2)(15)O and (11)CO. Arterial blood volume was determined from H(2)(15)O PET data by means of a two-compartment model that takes V(a) into account. Baseline CBV and values during hypercapnia and Hypocapnia in the cerebral cortex were 0.034+/-0.003, 0.038+/-0.003, and 0.031+/-0.003 mL/mL (mean+/-s.d.), respectively. Baseline V(a) and values during hypercapnia and Hypocapnia were 0.015+/-0.003, 0.025+/-0.011, and 0.007+/-0.003 mL/mL, respectively. Cerebral blood volume changed significantly owing to changes in PaCO(2), and V(a) changed significantly in the direction of CBV changes. However, no significant change was observed in venous plus capillary blood volume (=CBV-V(a)). This indicates that changes in CBV during hypercapnia and Hypocapnia are caused by changes in arterial blood volume without changes in venous and capillary blood volume.
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changes in human cerebral blood flow and cerebral blood volume during hypercapnia and Hypocapnia measured by positron emission tomography
Journal of Cerebral Blood Flow and Metabolism, 2003Co-Authors: Hiroshi Ito, Iwao Kanno, Masanobu Ibaraki, Jun Hatazawa, Shuichi MiuraAbstract:Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and Hypocapnia induces cerebral vasoconstriction and decreases CBF. The relation between changes in CBF and cerebral blood volume (CBV) during hypercapnia and Hypocapnia in humans, however, is not clear. Both CBF and CBV were measured at rest and during hypercapnia and Hypocapnia in nine healthy subjects by positron emission tomography. The vascular responses to hypercapnia in terms of CBF and CBV were 6.0 +/- 2.6%/mm Hg and 1.8 +/- 1.3%/mm Hg, respectively, and those to Hypocapnia were -3.5 +/- 0.6%/mm Hg and -1.3 +/- 1.0%/mm Hg, respectively. The relation between CBF and CBV was CBV = 1.09 CBF0.29. The increase in CBF was greater than that in CBV during hypercapnia, indicating an increase in vascular blood velocity. The degree of decrease in CBF during Hypocapnia was greater than that in CBV, indicating a decrease in vascular blood velocity. The relation between changes in CBF and CBV during hypercapnia was similar to that during neural activation; however, the relation during Hypocapnia was different from that during neural deactivation observed in crossed cerebellar diaschisis. This suggests that augmentation of CBF and CBV might be governed by a similar microcirculatory mechanism between neural activation and hypercapnia, but diminution of CBF and CBV might be governed by a different mechanism between neural deactivation and Hypocapnia.
Angel Carrillo Alvarez - One of the best experts on this subject based on the ideXlab platform.
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hyperoxia Hypocapnia and hypercapnia as outcome factors after cardiac arrest in children
Resuscitation, 2012Co-Authors: Jimena Del Castillo, Jesus Lopezherce, Martha Matamoros, Sonia Canadas, Ana Rodriguezcalvo, Corrado Cechetti, Antonio Rodrigueznunez, Angel Carrillo AlvarezAbstract:Abstract Purpose Arterial hyperoxia after resuscitation has been associated with increased mortality in adults. The aim of this study was to test the hypothesis that post-resuscitation hyperoxia and Hypocapnia are associated with increased mortality after resuscitation in pediatric patients. Methods We performed a prospective observational multicenter hospital-based study including 223 children aged between 1 month and 18 years who achieved return of spontaneous circulation after in-hospital cardiac arrest and for whom arterial blood gas analysis data were available. Results After return of spontaneous circulation, 8.5% of patients had hyperoxia (defined as PaO 2 >300mmHg) and 26.5% hypoxia (defined as PaO 2 p =0.61). Hypocapnia (defined as PaCO 2 2 >50mmHg) in 27.6%. Patients with hypercapnia or Hypocapnia had significantly higher mortality (59.0% and 50.0%, respectively) than patients with normocapnia (33.1%) ( p =0.002). At 24h after return of spontaneous circulation, neither PaO 2 nor PaCO 2 values were associated with mortality. Multiple logistic regression analysis showed that hypercapnia (OR, 3.27; 95% CI, 1.62–6.61; p =0.001) and Hypocapnia (OR, 2.71; 95% CI, 1.04–7.05; p =0.04) after return of spontaneous circulation were significant mortality factors. Conclusions In children resuscitated from cardiac arrest, hyperoxemia after return of spontaneous circulation or 24h later was not associated with mortality. On the other hand, hypercapnia and Hypocapnia were associated with higher mortality than normocapnia.
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hyperoxia Hypocapnia and hypercapnia as outcome factors after cardiac arrest in children
Resuscitation, 2012Co-Authors: Jimena Del Castillo, Jesus Lopezherce, Martha Matamoros, Sonia Canadas, Ana Rodriguezcalvo, Corrado Cechetti, Antonio Rodrigueznunez, Angel Carrillo AlvarezAbstract:PURPOSE: Arterial hyperoxia after resuscitation has been associated with increased mortality in adults. The aim of this study was to test the hypothesis that post-resuscitation hyperoxia and Hypocapnia are associated with increased mortality after resuscitation in pediatric patients. METHODS: We performed a prospective observational multicenter hospital-based study including 223 children aged between 1 month and 18 years who achieved return of spontaneous circulation after in-hospital cardiac arrest and for whom arterial blood gas analysis data were available. RESULTS: After return of spontaneous circulation, 8.5% of patients had hyperoxia (defined as PaO(2)>300 mm Hg) and 26.5% hypoxia (defined as PaO(2) 50 mm Hg) in 27.6%. Patients with hypercapnia or Hypocapnia had significantly higher mortality (59.0% and 50.0%, respectively) than patients with normocapnia (33.1%) (p=0.002). At 24h after return of spontaneous circulation, neither PaO(2) nor PaCO(2) values were associated with mortality. Multiple logistic regression analysis showed that hypercapnia (OR, 3.27; 95% CI, 1.62-6.61; p=0.001) and Hypocapnia (OR, 2.71; 95% CI, 1.04-7.05; p=0.04) after return of spontaneous circulation were significant mortality factors. CONCLUSIONS: In children resuscitated from cardiac arrest, hyperoxemia after return of spontaneous circulation or 24h later was not associated with mortality. On the other hand, hypercapnia and Hypocapnia were associated with higher mortality than normocapnia.