Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmit...Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients(BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case that non lung protective ventilator settings are applied. Measurement of respiratory mechanics in BD patients, as well as assessment of their evolution during mechanical ventilation, may lead to preclinical lung injury detection early enough, allowing thus the selection of the appropriate ventilator settings to avoid ventilatorinduced lung injury. The aim of this review is to explore the mechanical properties of the respiratory system in BD patients along with the underlying mechanisms, and to translate the evidence of animal and clinical studies into therapeutic implications regarding the mechanical ventilation of these critically ill patients.展开更多
Expiratory flow limitation(EFL), that is the inability of expiratory flow to increase in spite of an increase of the driving pressure, is a common and unrecognized occurrence during mechanical ventilation in a variety...Expiratory flow limitation(EFL), that is the inability of expiratory flow to increase in spite of an increase of the driving pressure, is a common and unrecognized occurrence during mechanical ventilation in a variety of intensive care unit conditions. Recent evidence suggests that the presence of EFL is associated with an increase in mortality, at least in acute respiratory distress syndrome(ARDS) patients, and in pulmonary complications in patients undergoing surgery. EFL is a major cause of intrinsic positive end-expiratory pressure(PEEPi), which in ARDS patients is heterogeneously distributed, with a consequent increase of ventilation/perfusion mismatch and reduction of arterial oxygenation. Airway collapse is frequently concomitant to the presence of EFL.When airways close and reopen during tidal ventilation, abnormally high stresses are generated that can damage the bronchiolar epithelium and uncouple small airways from the alveolar septa, possibly generating the small airways abnormalities detected at autopsy in ARDS. Finally, the high stresses and airway distortion generated downstream the choke points may contribute to parenchymal injury, but this possibility is still unproven. PEEP application can abolish EFL, decrease PEEPi heterogeneity, and limit recruitment/derecruitment.Whether increasing PEEP up to EFL disappearance is a useful criterion for PEEP titration can only be determined by future studies.展开更多
AIM:To investigate the prevalence of chronic dyspnea and its relationship to respiratory muscle function in end-stage liver disease.METHODS:Sixty-eight consecutive,ambulatory,Caucasian patients with end-stage liver di...AIM:To investigate the prevalence of chronic dyspnea and its relationship to respiratory muscle function in end-stage liver disease.METHODS:Sixty-eight consecutive,ambulatory,Caucasian patients with end-stage liver disease,candidates for liver transplantation,were referred for preoperative respiratory function assessment.Forty of these(29 men) were included in this preliminary study after applying strict inclusion and exclusion criteria.Seventeen of 40 patients(42%) had ascites,but none of them was cachectic.Fifteen of 40 patients(38%)had a history of hepatic encephalopathy,though none of them was symptomatic at study time.All patients with a known history and/or presence of co-morbidities were excluded.Chronic dyspnea was rated according to the modified medical research council(mMRC) 6-point scale.Liver disease severity was assessed according to the Model for end-stage liver disease(MELD).Routine lung function tests,maximum static expiratory(Pemax) and inspiratory(Pimax) mouth pressures were measured.Respiratory muscle strength(RMS) was calculated from Pimax and Pemax values.In addition,arterial blood gases and pattern of breathing(VE:minute ventilation;VT:tidal volume;VT/TI:mean inspiratory flow;TI:duration of inspiration) were measured.RESULTS:Thirty-five(88%) of 40 patients aged(mean ± SD) 52 ± 10 years reported various degrees of chronic dyspnea(mMRC),ranging from 0 to 4,with a mean value of 2.0 ± 1.2.MELD score was 14 ± 6.Pemax,percent of predicted(%pred) was 105 ± 35,Pimax,%pred was 90 ± 29,and RMS,%pred was 97 ± 30.These pressures were below the normal limits in 12(30%),15(38%),and 14(35%) patients,respectively.Furthermore,comparing the subgroups of ascites to non-ascites patients,all respiratory muscle indices measured were found significantly decreased in ascites patients.Patients with ascites also had a significantly worse MELD score compared to non-ascites ones(P = 0.006).Significant correlations were found between chronic dyspnea and respiratory muscle function indices in all patients.Specifically,mMRC score was significantly correlated with Pemax,Pimax,and RMS(r =-0.53,P < 0.001;r =-0.42,P < 0.01;r =-0.51,P < 0.001,respectively).These correlations were substantially closer in the non-ascites subgroup(r =-0.82,P < 0.0001;r =-0.61,P < 0.01;r =-0.79,P < 0.0001,respectively) compared to all patients.Similar results were found for the relationship between mMRC vs MELD score,and MELD score vs respiratory muscle strength indices.In all patients the sole predictor of mMRC score was RMS(r =-0.51,P < 0.001).In the subgroup of patients without ascites this relationship becomes closer(r =-0.79,P < 0.001),whilst this relationship breaks down in the subgroup of patients with ascites.The disappearance of such a correlation may be due to the fact that ascites acts as a "confounding" factor.PaCO2(4.4 ± 0.5 kPa) was increased,whereas pH(7.49 ± 0.04) was decreased in 26(65%) and 34(85%) patients,respectively.PaO2(12.3 ± 0.04 kPa) was within normal limits.VE(11.5 ± 3.5 L/min),VT(0.735 ± 0.287 L),and VT/TI(0.449±0.129 L/s) were increased signifying hyperventilation in both subgroups of patients.VT/TI was significantly higher in patients with ascites than without ascites.Significant correlations,albeit weak,were found for PaCO2 with VE and VT/TI(r =-0.44,P < 0.01;r =-0.41,P < 0.01,respectively).CONCLUSION:The prevalence of chronic dyspnea is 88% in end-stage liver disease.The mMRC score closely correlates with respiratory muscle strength.展开更多
Although asthma and chronic obstructive pulmonary disease(COPD) are distinct airway diseases characterized by chronic inflammation, in some cases distinguishing between them is puzzling. For example, chronic smoking l...Although asthma and chronic obstructive pulmonary disease(COPD) are distinct airway diseases characterized by chronic inflammation, in some cases distinguishing between them is puzzling. For example, chronic smoking leads asthmatic inflammation to a differentiated pattern resembling the COPD inflammation, and in some cases to fixed obstruction as in COPD, and on the other hand, few COPD patients may present with airway reversibility. ACOS is the condition sharing features encountered both in asthma and COPD. Asthma-COPD overlap syndrome(ACOS) represents a diagnostic challenge in the clinical practice, since there is lack of specific indicators to distinguish it from asthma or COPD, and moreover, genetic risk factors, underlying pathology and molecular pathways, clinical characteristics, therapeutic interventions, response to treatment and prognosis are poorly described. The management of ACOS is recommended to be individualized and should target on the maximum effectiveness with the least side effects. Combination therapy with ICS/LABA or LAMA, or newly developed specific anti-eosinophil therapies and treatments specifically targeting neutrophils might be of relevance in the management of ACOS, but studies are needed in order to assess the response and prognosis. Based on the current knowledge about ACOS thus far, it would be recommended that we approached chronic obstructive airway disease rather by describing than by classifying the disease; this would allow us to have a picture that better describes the disease and to implement an individualized therapeutic approach, according to the custom phenotype. Nevertheless, more studies are needed in order to clarify several important issues with regard to ACOS, such as the genetic risk factors for developing ACOS, the links between genotype and phenotype, the molecular pathways and underlying mechanisms of ACOS, the identification of possible specific biomarkers for diagnosis and targeted treatment, the optimal therapeutic interventions, and finally, the prognosis of ACOS.展开更多
文摘Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients(BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case that non lung protective ventilator settings are applied. Measurement of respiratory mechanics in BD patients, as well as assessment of their evolution during mechanical ventilation, may lead to preclinical lung injury detection early enough, allowing thus the selection of the appropriate ventilator settings to avoid ventilatorinduced lung injury. The aim of this review is to explore the mechanical properties of the respiratory system in BD patients along with the underlying mechanisms, and to translate the evidence of animal and clinical studies into therapeutic implications regarding the mechanical ventilation of these critically ill patients.
文摘Expiratory flow limitation(EFL), that is the inability of expiratory flow to increase in spite of an increase of the driving pressure, is a common and unrecognized occurrence during mechanical ventilation in a variety of intensive care unit conditions. Recent evidence suggests that the presence of EFL is associated with an increase in mortality, at least in acute respiratory distress syndrome(ARDS) patients, and in pulmonary complications in patients undergoing surgery. EFL is a major cause of intrinsic positive end-expiratory pressure(PEEPi), which in ARDS patients is heterogeneously distributed, with a consequent increase of ventilation/perfusion mismatch and reduction of arterial oxygenation. Airway collapse is frequently concomitant to the presence of EFL.When airways close and reopen during tidal ventilation, abnormally high stresses are generated that can damage the bronchiolar epithelium and uncouple small airways from the alveolar septa, possibly generating the small airways abnormalities detected at autopsy in ARDS. Finally, the high stresses and airway distortion generated downstream the choke points may contribute to parenchymal injury, but this possibility is still unproven. PEEP application can abolish EFL, decrease PEEPi heterogeneity, and limit recruitment/derecruitment.Whether increasing PEEP up to EFL disappearance is a useful criterion for PEEP titration can only be determined by future studies.
文摘AIM:To investigate the prevalence of chronic dyspnea and its relationship to respiratory muscle function in end-stage liver disease.METHODS:Sixty-eight consecutive,ambulatory,Caucasian patients with end-stage liver disease,candidates for liver transplantation,were referred for preoperative respiratory function assessment.Forty of these(29 men) were included in this preliminary study after applying strict inclusion and exclusion criteria.Seventeen of 40 patients(42%) had ascites,but none of them was cachectic.Fifteen of 40 patients(38%)had a history of hepatic encephalopathy,though none of them was symptomatic at study time.All patients with a known history and/or presence of co-morbidities were excluded.Chronic dyspnea was rated according to the modified medical research council(mMRC) 6-point scale.Liver disease severity was assessed according to the Model for end-stage liver disease(MELD).Routine lung function tests,maximum static expiratory(Pemax) and inspiratory(Pimax) mouth pressures were measured.Respiratory muscle strength(RMS) was calculated from Pimax and Pemax values.In addition,arterial blood gases and pattern of breathing(VE:minute ventilation;VT:tidal volume;VT/TI:mean inspiratory flow;TI:duration of inspiration) were measured.RESULTS:Thirty-five(88%) of 40 patients aged(mean ± SD) 52 ± 10 years reported various degrees of chronic dyspnea(mMRC),ranging from 0 to 4,with a mean value of 2.0 ± 1.2.MELD score was 14 ± 6.Pemax,percent of predicted(%pred) was 105 ± 35,Pimax,%pred was 90 ± 29,and RMS,%pred was 97 ± 30.These pressures were below the normal limits in 12(30%),15(38%),and 14(35%) patients,respectively.Furthermore,comparing the subgroups of ascites to non-ascites patients,all respiratory muscle indices measured were found significantly decreased in ascites patients.Patients with ascites also had a significantly worse MELD score compared to non-ascites ones(P = 0.006).Significant correlations were found between chronic dyspnea and respiratory muscle function indices in all patients.Specifically,mMRC score was significantly correlated with Pemax,Pimax,and RMS(r =-0.53,P < 0.001;r =-0.42,P < 0.01;r =-0.51,P < 0.001,respectively).These correlations were substantially closer in the non-ascites subgroup(r =-0.82,P < 0.0001;r =-0.61,P < 0.01;r =-0.79,P < 0.0001,respectively) compared to all patients.Similar results were found for the relationship between mMRC vs MELD score,and MELD score vs respiratory muscle strength indices.In all patients the sole predictor of mMRC score was RMS(r =-0.51,P < 0.001).In the subgroup of patients without ascites this relationship becomes closer(r =-0.79,P < 0.001),whilst this relationship breaks down in the subgroup of patients with ascites.The disappearance of such a correlation may be due to the fact that ascites acts as a "confounding" factor.PaCO2(4.4 ± 0.5 kPa) was increased,whereas pH(7.49 ± 0.04) was decreased in 26(65%) and 34(85%) patients,respectively.PaO2(12.3 ± 0.04 kPa) was within normal limits.VE(11.5 ± 3.5 L/min),VT(0.735 ± 0.287 L),and VT/TI(0.449±0.129 L/s) were increased signifying hyperventilation in both subgroups of patients.VT/TI was significantly higher in patients with ascites than without ascites.Significant correlations,albeit weak,were found for PaCO2 with VE and VT/TI(r =-0.44,P < 0.01;r =-0.41,P < 0.01,respectively).CONCLUSION:The prevalence of chronic dyspnea is 88% in end-stage liver disease.The mMRC score closely correlates with respiratory muscle strength.
文摘Although asthma and chronic obstructive pulmonary disease(COPD) are distinct airway diseases characterized by chronic inflammation, in some cases distinguishing between them is puzzling. For example, chronic smoking leads asthmatic inflammation to a differentiated pattern resembling the COPD inflammation, and in some cases to fixed obstruction as in COPD, and on the other hand, few COPD patients may present with airway reversibility. ACOS is the condition sharing features encountered both in asthma and COPD. Asthma-COPD overlap syndrome(ACOS) represents a diagnostic challenge in the clinical practice, since there is lack of specific indicators to distinguish it from asthma or COPD, and moreover, genetic risk factors, underlying pathology and molecular pathways, clinical characteristics, therapeutic interventions, response to treatment and prognosis are poorly described. The management of ACOS is recommended to be individualized and should target on the maximum effectiveness with the least side effects. Combination therapy with ICS/LABA or LAMA, or newly developed specific anti-eosinophil therapies and treatments specifically targeting neutrophils might be of relevance in the management of ACOS, but studies are needed in order to assess the response and prognosis. Based on the current knowledge about ACOS thus far, it would be recommended that we approached chronic obstructive airway disease rather by describing than by classifying the disease; this would allow us to have a picture that better describes the disease and to implement an individualized therapeutic approach, according to the custom phenotype. Nevertheless, more studies are needed in order to clarify several important issues with regard to ACOS, such as the genetic risk factors for developing ACOS, the links between genotype and phenotype, the molecular pathways and underlying mechanisms of ACOS, the identification of possible specific biomarkers for diagnosis and targeted treatment, the optimal therapeutic interventions, and finally, the prognosis of ACOS.
