Impact of carbon dioxide values after aortic impingement on postoperative morbimortality in pediatric patients undergoing cardiac surgery / Impacto de los valores de bióxido de carbono post-pinzamiento aórtico sobre la morbimortalidad postoperatoria en pacientes pediátricos sometidos a cirugía cardíaca

Abstract: Introduction: Inducing hypocapnia is a common practice during pediatric general anesthesia, even though it has not shown clear benefits. Objective: To compare the impact of carbon dioxide values after aortic impingement (< 32.7 vs ≥ 32.7 mmHg) on postoperative morbimortality among pediatric patients undergoing cardiac surgery. Material and methods: A case-control study included 90 pediatric patients undergoing cardiac surgery with cardiopulmonary bypass. The study cases consisted of 45 patients who died within 30 days of the postoperative period. Cases and controls were individually matched (1:1 ratio). Descriptive and inferential statistics (Mann-Whitney's U, Student's t and χ2 tests) were used to analyze the results. A p < 0.05 was considered significant. A univariate analysis was also carried out. The strength of association between morbimortality and carbon dioxide values after aortic impingement was determined using the odds ratio. The data were processed using SPSS v-24.0. Results: The group with carbon dioxide values of < 32.7 mmHg after aortic impingement was associated with greater morbidity (OR 24.75; 95% CI 4.92-124.32) and mortality (OR 22.47; 95% CI 4.85-10.17) at 30 days. Conclusion: Pediatric patients undergoing cardiac surgery with carbon dioxide values of < 32.7 mmHg after aortic impingement showed higher postoperative morbimortality than those with carbon dioxide values of ≥ 32.7 mmHg.

Resumen: Introducción: La hipocapnia es una práctica común durante la anestesia general pediátrica; sin embargo, a lo largo del tiempo no ha mostrado beneficios bien definidos. Objetivo: Comparar el impacto del bióxido de carbono post-pinzamiento aórtico (< 32.7 vs ≥ 32.7 mmHg) sobre la morbimortalidad postoperatoria en los pacientes pediátricos sometidos a cirugía cardíaca. Material y métodos: Se realizó un estudio de casos y controles que incluyó 90 pacientes pediátricos sometidos a cirugía cardíaca con derivación cardiopulmonar. Se consideraron casos 45 pacientes que fallecieron dentro de los 30 días del postoperatorio. Los controles fueron pareados en relación 1:1. Para su análisis se realizó estadística descriptiva e inferencial con U de Mann-Whitney, t de Student y χ2 según fue el caso. Una p < 0.05 fue significativa. Se realizó un análisis univariado. La fuerza de asociación entre la morbimortalidad y los valores de bióxido de carbono post-pinzamiento aórtico se obtuvo mediante el odds ratio. Los datos fueron procesados mediante SPSS v-24.0. Resultados: El grupo con valores de bióxido de carbono post-pinzamiento aórtico < 32.7 mmHg se asoció con una mayor morbilidad a los 30 días (OR 24.75; IC del 95% 4.92-124.32) y mortalidad (OR 22.47; IC del 95% 4.85-10.17). Conclusión: Los pacientes pediátricos sometidos a cirugía cardíaca con valores de bióxido de carbono post-pinzamiento aórtico < 32.7 mmHg tienen mayor morbimortalidad postoperatoria que los que tienen valores ≥ 32.7 mmHg.

Lung function and stress echocardiography in pulmonary arterial hypertension: a cross-sectional study

ABSTRACT BACKGROUND: The mechanism of exercise limitation in idiopathic pulmonary arterial hypertension (IPAH) is not fully understood. The role of hemodynamic alterations is well recognized, but mechanical, ventilatory and gasometric factors may also contribute to reduction of exercise capacity in these individuals. OBJECTIVE: To investigate whether there is an association between ventilatory pattern and stress Doppler echocardiography (SDE) variables in IPAH patients. DESIGN AND SETTING: Single-center prospective study conducted in a Brazilian university hospital. METHODS: We included 14 stable IPAH patients and 14 age and sex-matched controls. Volumetric capnography (VCap), spirometry, six-minute walk test and SDE were performed on both the patients and the control subjects. Arterial blood gases were collected only from the patients. The IPAH patients and control subjects were compared with regard to the abovementioned variables. RESULTS: The mean age of the patients was 38.4 years, and 78.6% were women. The patients showed hypocapnia, and in spirometry 42.9% presented forced vital capacity (FVC) below the lower limit of normality. In VCap, IPAH patients had higher respiratory rates (RR) and lower elimination of CO2 in each breath. There was a significant correlation between reduced FVC and the magnitude of increases in tricuspid regurgitation velocity (TRV). In IPAH patients, VCap showed similar tidal volumes and a higher RR, which at least partially explained the hypocapnia. CONCLUSIONS: The patients with IPAH showed hypocapnia, probably related to their higher respiratory rate with preserved tidal volumes; FVC was reduced and this reduction was positively correlated with cardiac output.

Analysis and prevention of hypocapnia caused by respiratory distress syndrome in premature infants treated with different mechanical ventilation modes / 中国基层医药

Objective To OxplorO thO rOlationship bOtwOOn diffOrOnt vOntilation modO and hypocapnia in prOtOrm infants.Methods From April 2014 to OctobOr 2017,a total of 302 prOtOrm infants with rOspiratory distrOss syndromO in Suining COntral Hospital who rOcOivOd diffOrOnt assistOd vOntilation wOrO sOlOctOd in this rOsOarch. According diffOrOnt vOntilation modO, thOy wOrO dividOd into convOntional mOchanical vOntilation(CMV) group( n=66),thO mOchanical vOntilation modO was CMV, continuous positivO airway prOssurO(CPAP) group(n=149),thO mOchanical vOntilation modO was CPAP, high frOquOncy vOntilation(HFOV) group(n=87),thO mOchanical vOntila-tion modO was HFOV. ThO morbidity of hypocapnia in diffOrOnt groups and prOvOntion mOthods wOrO analyzOd. Results Among 302 childrOn,52casOs had hypocarbonOmia,thO total morbidity of hypocapnia was 17.2%. ThO morbidity of hypocapnia in thO HFOV group was 37.9% (33/87),which in thO CMV group was 21.2% (14/66), which in thO CPAP group was 3.4% (5/149),thO diffOrOncO among thO thrOO groups was statistically significant(χ2 =47.013,P=0.000).Conclusion ThO incidOncO of invasivO vOntilation should bO carOfully considOrOd in prOtOrm infants, OspOcially high frOquOncy vOntilation. To prOvOnt and trOatmOnt of hypocapnia, timOly adjustmOnt of vOntilator paramOtOrs according to blood gas during diffOrOnt vOntilation modO should bO donO.

Hipocapnia en neuroanestesia: estado actual / Hypocapnia in Neuroanesthesia: Current Situation

Introducción: La hiperventilación ha sido una maniobra común en el manejo anestésico de procedimientos neuroquirúrgicos. Hace unos años había escepticismo entre los médicos sobre si esto resultaba en isquemia cerebral. Hoy sabemos que es perjudicial y deteriora el estado y el pronóstico del paciente. Objetivo: Hacer una revisión de los efectos adversos de la hipocapnia en diferentes órganos, principalmente el cerebro, e identificar las recomendaciones actuales de su utilidad. Métodos: Realizamos una búsqueda de la literatura en la base de datos de PubMed utilizando términos MeSH incluidos en las palabras clave; se amplió con la revisión de algunos textos y la bibliografía de los artículos más relevantes. Resultados: Con la revisión de la literatura, se ha demostrado que la hipocapnia es perjudicial tanto para el cerebro como para otros tejidos, y la recomendación actual es utilizarla sólo en dos situaciones (en caso de herniación inminente y para mejorar el campo quirúrgico) y por 20 min. Conclusiones: La hiperventilación no debe ser una intervención anestésica rutinaria en el manejo del paciente neuroquirúrgico; debe tener una indicación precisa y, una vez la indicación haya cesado, la intervención debe ser retirada lo más pronto posible.

Introduction: Hyperventilation has been a usual maneuver in the management of anesthesia in neurosurgical procedures. A few years back there used to be some medical skepticism about the potential of cerebral ischemia and today we know that it is detrimental and worsens the patient’s condition and prognosis. Objective: To review the adverse effects of hypocapnia on various organs -mainly the brain- and to identify the current recommendations about its use. Methodology: We conducted a PubMed literature search using MeSH terminology including the key words. The search was expanded to include a review of several texts and the bibliography of the most relevant articles. Results: The literature review showed that hypocapnia is harmful for the brain and for other tissues and the current recommendation is to use it for two situations only: in case of imminent herniation and to improve the surgical field, limited to 20 minutes. Conclusions: Hyperventilation should not be a routine anesthetic intervention for the management of the neurosurgical patient; there must be a precise indication and once the situation is corrected, the intervention must be immediately withdrawn.

Response of cerebral oximetry to increase in alveolar concentration of desflurane: effect of remifentanil and cerebrovascular CO2 reactivity / 대한마취과학회지

BACKGROUND: It is known that sympathetic stimulation and increase in cerebral blood flow velocity can be induced by desflurane. Cerebral oxygen balance could be disturbed during desflurane induction. Aim of this study was to elucidate that cerebral oxygen imbalance induced by desflurane mask induction can be reduced by combination of remifentanil and hypocapnia. METHODS: Twenty ASA 1-2 subjects were allocated randomly into 5 groups divided by concentration of remifentanil (0.0, 0.5, 1.0, 1.5, and 2.0 ng/ml). After confirmation of attaining proposed concentration of remifentanil, propofol and vecuronium were administered and mechanical ventilation was done with 8% desflurane with facial mask. Subsequently, changes in regional cerebral oxygen saturation (DeltarSO2), arterial blood pressure, heart rate, cardiac index, estimated alveolar concentration of desflurane (PDESF), and end-tidal concentration of carbon dioxide (PETCO2) were recorded for the following 10 minutes. According to concentration of desflurane and remifentanil, DeltarSO2 and hemodynamic factors were checked. RESULTS: During desflurane induction, changes in cerebral oximetry reached up to +10% (6 [first quartile], 13 [third quartile]). Arterial blood pressure, heart rate, and cardiac index were changed within clinical ranges. The DeltarSO2 showed S-shaped increasing pattern according to increasing PDESF. Hypocapnia and concentration of remifentanil reduced the maximum DeltarSO2 (P = 0.0046, P = 0.0060). Hypocapnia also shifted the curve to left (P = 0.0001). CONCLUSIONS: During 8% desflurane induction, regional cerebral oxygen saturation (rSO2) increases maximum +25%. Hypocapnia and use of remifentanil can reduce the increase in regional cerebral oxygen saturation.

The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder

OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. METHOD: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. DISCUSSION: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2) when the latent (metabolic) acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation) and catecholamine sensitivity begins to increase. CONCLUSION: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis.

OBJETIVO: Os autores apresentam um modelo de transtorno do pânico que se baseia nos efeitos da hiperventilação aguda e crônica, característicos do subtipo respiratório de transtorno do pânico. O modelo é generalizado a partir desses efeitos. Ele integra três características da hiperventilação: a hiperventilação é uma resposta fisiológica à hipercapnia; a hiperventilação pode induzir ataques de pânico; a hiperventilação crônica representa um mecanismo protetor contra os ataques de pânico. MÉTODO: Revisão seletiva da literatura a partir da base de dados Medline. Foram selecionados relatos referentes à inter-relação entre transtorno do pânico, hiperventilação, acidose, alcalose, liberação de catecolaminas e sensibilidade a catecolaminas, sendo os achados estruturados de modo a formar um modelo integrado. DISCUSSÃO: Os ataques de pânico do transtorno do pânico desenvolvem-se com base numa acidose metabólica, que é uma resposta compensatória à hiperventilação crônica. Os ataques são desencadeados por um súbito aumento da pressão parcial de dióxido de carbono (pCO2), quando a acidose (metabólica) latente se manifesta pela acidose hipercápnica. A condição acidótica induz liberação de catecolaminas. A simpaticotonia não pode manifestar-se durante a fase de hipercapnia, pois o baixo pH diminui a sensibilidade às catecolaminas. As catecolaminas podem provocar pânico quando a hipercapnia comuta para uma alcalose hipocápnica devido à supercompensação pela hiperventilação, situação na qual a sensibilidade às catecolaminas liberadas começa a aumentar. CONCLUSÃO: As abordagens terapêuticas deveriam voltar-se para a regulação em longo prazo do padrão respiratório e a eliminação da acidose metabólica.

Brain Injury and Neurodevelopmental Sequelae Following Mechanical Ventilation in Preterm Infants

In the care of neonates, complications from the use of mechanical ventilation and other treatment of respiratory problems have important effects on cardiac output, cerebral blood flow, cerebral oxygenation and cerebral venous return that at times result in brain injury. Hypercapnia or hypocapnia following mechanical ventilation during the first few days of life may result in adverse effect on the CNS in perterm and term infants. Hypocapnia, particularly at PaCO2 levels less than 25 to 30 mmHg, has been associated with periventricular leukomalcia, cerebral palsy and poor neurologic outcomes in preterm infants. Use of smaller tidal volumes combined with permissive hypercapnia to reduce ventilator-induced lung injury may protect against hypocapnia-induced brain injury. Recent randomized clinical studies have demonstrated the safety of mild permissive hypercapnia, but found only small clinical benefits. Several studies have reported that the use of postnatal dexamethasone for severe RDS evolving into BPD have adverse effects on growth and neurodevelopmental outcomes. The results of large long-term follow-up studies strongly suggest an association between use of postnatal dexamethasone and poor neurodevelopmental outcome including cerebral palsy. Further studies including an evaluation of neurodevelopmental outcome as a primary endpoint must be needed for postnatal use of systemic or inhaled steroid.

The Relation Between Hypocarbia and Periventricular Le ukomalacia in Preterm Infants / 中华围产医学杂志

0.05). The minimum PaCO 2 (minPaCO 2) within the first 72 h of life and duration of hypocarbia in PVL and control group were (23 0?1.2) mm Hg vs (31 0?7.6) mm Hg, and (26 .3 ?7.8) h vs (1.7?0.4) h, (P

Influences of the Intrapulmonary R-->L Shunt on PaO2 and PaCO2 after Instillation of Exogenous Pulmonary Surfactant to Premature Neonates with Respiratory Distress Syndrome

PURPOSE: We are inclined to analyze the relationship between the intrapulmonary right-to-left shunt and the PaO2/PaCO2 after endotracheal single-dose surfactant instillation to premature neonates with respiratory distress syndrome within 6 hours after birth. METHODS: From Jan. 1993 to Jun. 1995, we have conducted a clinical trial of surfactant replacement therapy to the premature neonates with respiratory distress syndrome at the neonatal intensive care unit of InHa University Hospital. The surfactant group (n=17) was given Surfactant-TA and mechanical ventilator care, but the control group (n=22) was treated with only mechanical ventilator. We analyzed umbilical arterial blood gases and estimated respiratoy indexes before and after treatment. RESULTS: 1) The QSP/QT decreased initially in the surfactant group, but significantly increased 24 hours after treatment in the control group (40.6+/-4.7%, P0.5) resulted in a decrease in PaO2 and also a significant relationship was found between the QSP/QT and the PaO2. However, there was no significant relationship between the QSP/QT and the PaCO2.

Effect of hypocapnia on extracellular glutamate and glycine concentrations during peri-ischemic period in the rabbit hippocampus

Glutamate (GLU) is a neurotransmitter. Massive release of GLU and glycine (GLY) into the brain's extracellular space may be triggered by ischemia, and may result in acute neuronal lysis or delayed neuronal death. The aim of this study was to evaluate the possible relationship between hyperventilation and the level of GLU and GLY during brain ischemia. Rabbits were anesthetized with halothane and oxygen. Group 1 was allowed to hyperventilate (PaCO2 25-35 mmHg). PaCO2 was maintained throughout the study. Group 2 was a normal control group that maintained normocapnia. Two global cerebral ischemic episodes were produced. Microdialysate was collected during the peri-ischemic and reperfusion periods from the dorsal hippocampus. GLU and GLY concentrations were determined using high-performance liquid chromatography. In the control group, GLU and GLY were significantly elevated during each episode of ischemia; these levels returned to baseline within 10 minutes after reperfusion. In contrast, in the hyperventilation group GLU and GLY concentrations increased during ischemia, but they were not statistically significant. We were able to demonstrate that hypocapnia during periischemic period lowered extracellular GLU and GLY concentrations. These results can explain a part of the protective action of hypocapnia during cerebral ischemia.