Study of the relationship between regional cerebral saturation and pCO2 changes during mechanical ventilation to evaluate modifications in cerebral perfusion in a newborn piglet model.

Near-infrared spectroscopy (NIRS) could be a useful continuous, non-invasive technique for monitoring the effect of partial pressure of carbon dioxide (PaCO2) fluctuations in the cerebral circulation during ventilation. The aim of this study was to examine the efficacy of NIRS to detect acute changes in cerebral blood flow following PaCO2 fluctuations after confirming the autoregulation physiology in piglets. Fourteen piglets (<72 h of life) were studied. Mean arterial blood pressure, oxygen saturation, pH, glycemia, hemoglobin, electrolytes, and temperature were monitored. Eight animals were used to evaluate brain autoregulation, assessing superior cava vein Doppler as a proxy of cerebral blood flow changing mean arterial blood pressure. Another 6 animals were used to assess hypercapnia generated by decreasing ventilatory settings and complementary CO2 through the ventilator circuit and hypocapnia due to increasing ventilatory settings. Cerebral blood flow was determined by jugular vein blood flow by Doppler and continuously monitored with NIRS. A decrease in PaCO2 was observed after hyperventilation (47.6±2.4 to 29.0±4.9 mmHg). An increase in PaCO2 was observed after hypoventilation (48.5±5.5 to 90.4±25.1 mmHg). A decrease in cerebral blood flow after hyperventilation (21.8±10.4 to 15.1±11.0 mL/min) and an increase after hypoventilation (23.4±8.4 to 38.3±10.5 mL/min) were detected by Doppler ultrasound. A significant correlation was found between cerebral oxygenation and Doppler-derived parameters of blood flow and PaCO2. Although cerebral NIRS monitoring is mainly used to detect changes in regional brain oxygenation, modifications in cerebral blood flow following experimental PaCO2 changes were detected in newborn piglets when no other important variables were modified.

Prevalence of cerebral edema among diabetic ketoacidosis patients. / Prevalencia de edema cerebral en pacientes con cetoacidosis diabética.

Introduction: Cerebral edema (CE) is the most severe complication of diabetic ketoacidosis (DKA) in children. There is no accurate knowledge of CE pathogenesis and its onset has been related to intravenous rehydration therapy during the initial treatment. Objectives: To estimate the prevalence of CE among DKA patients treated at Hospital General de Niños Pedro de Elizalde with intravenous rehydration and analyze potential risk factors for the development of CE. Materials and methods: Cross-sectional prevalence study and exploratory analysis to compare clinical and laboratory characteristics between patients with and without CE. Patients aged 1-18 years hospitalized with the diagnosis of DKA between January 1st, 2005 and December 31st, 2014 were included. Results: A total of 693 DKA events from 561 medical records were analyzed. Ten patients had evidence of CE (1.44 %; 95 % confidence interval: 0.8-2.6). Patients with CE had higher serum urea levels (p < 0.001), lower carbon dioxide pressure (p < 0.001), and lower serum sodium levels (p < 0.001) than those without CE. Conclusion: The prevalence of CE among DKA patients was 1.44 %, smaller than that reported in our country (1.8 %). The risk factors at admission associated with CE development were high serum urea levels, hyponatremia, and hypocapnia.

Introducción. El edema cerebral (EC) es la complicación más grave de la cetoacidosis diabética (CAD) en niños. La patogénesis del EC no se conoce con exactitud y su aparición ha sido relacionada con la terapia de rehidratación endovenosa en el tratamiento inicial. Objetivos. Estimar la prevalencia de EC en pacientes con CAD tratados en el Hospital General de Niños Pedro de Elizalde mediante rehidratación endovenosa y analizar potenciales factores de riesgo para el desarrollo de EC. Materiales y método. Estudio de diseño transversal para prevalencia y un análisis exploratorio para comparar las características clínicas y de laboratorio entre los pacientes con y sin EC. Se incluyeron pacientes de 1 a 18 años hospitalizados con diagnóstico de CAD desde el 1 de enero de 2005 hasta el 31 de diciembre de 2014. Resultados. Se analizaron 693 episodios de CAD en 561 historias clínicas. En 10 pacientes, se evidenció EC (el 1,44 %; intervalo de confianza del 95 %: 0,8-2,6). Los pacientes con EC presentaron mayor uremia (p < 0,001), menor presión de dióxido de carbono (p < 0,001) y menor natremia (p < 0,001) que aquellos pacientes sin EC. Conclusión. La prevalencia de EC en pacientes con CAD fue del 1,44 %, menor que la reportada en nuestro país (del 1,8 %). Los factores de riesgo al ingresar asociados a su desarrollo fueron la presencia de uremia elevada, hiponatremia e hipocapnia.

Hypocapnia after traumatic brain injury: how does it affect the time constant of the cerebral circulation?

The time constant of the cerebral arterial bed ("tau") estimates how fast the blood entering the brain fills the arterial vascular sector. Analogous to an electrical resistor-capacitor circuit, it is expressed as the product of arterial compliance (Ca) and cerebrovascular resistance (CVR). Hypocapnia increases the time constant in healthy volunteers and decreases arterial compliance in head trauma. How the combination of hyocapnia and trauma affects this parameter has yet to be studied. We hypothesized that in TBI patients the intense vasoconstrictive action of hypocapnia would dominate over the decrease in compliance seen after hyperventilation. The predominant vasoconstrictive response would maintain an incoming blood volume in the arterial circulation, thereby lengthening tau. We retrospectively analyzed recordings of intracranial pressure (ICP), arterial blood pressure (ABP), and blood flow velocity (FV) obtained from a cohort of 27 severe TBI patients [(39/30 years (median/IQR), 5 women; admission GCS 6/5 (median/IQR)] studied during a standard clinical CO2 reactivity test. The reactivity test was performed by means of a 50-min increase in ventilation (20% increase in respiratory minute volume). CVR and Ca were estimated from these recordings, and their product calculated to find the time constant. CVR significantly increased [median CVR pre-hypocapnia/during hypocapnia: 1.05/1.35 mmHg/(cm3/s)]. Ca decreased (median Ca pre-hypocapnia/during hypocapnia: 0.130/0.124 arbitrary units) to statistical significance (p = 0.005). The product of these two parameters resulted in a significant prolongation of the time constant (median tau pre-hypocapnia/during hypocapnia: 0.136 s/0.152 s, p ˂ .001). Overall, the increase in CVR dominated over the decrease in compliance, hence tau was longer. We demonstrate a significant increase in the time constant of the cerebral circulation during hypocapnia after severe TBI, and attribute this to an increase in cerebrovascular resistance which outweighs the decrease in cerebral arterial bed compliance.

Do acute stroke patients develop hypocapnia? A systematic review and meta-analysis.

PURPOSE: Carbon dioxide (CO2) is a potent cerebral vasomotor agent. Despite reduction in CO2 levels (hypocapnia) being described in several acute diseases, there is no clear data on baseline CO2 values in acute stroke. The aim of the study was to systematically assess CO2 levels in acute stroke. MATERIAL AND METHODS: Four online databases, Web of Science, MEDLINE, EMBASE and CENTRAL, were searched for articles that described either partial pressure of arterial CO2 (PaCO2) and end-tidal CO2 (EtCO2) in acute stroke. RESULTS: After screening, based on predefined inclusion and exclusion criteria, 20 studies were retained. There were 5 studies in intracerebral hemorrhage and 15 in ischemic stroke, totalling 660 stroke participants. Acute stroke was associated with a significant decrease in CO2 levels compared to controls. Cerebral haemodynamic studies using transcranial Doppler ultrasonography demonstrated a significant reduction in cerebral blood flow velocities and cerebral autoregulation in acute stroke patients. CONCLUSION: The evidence from this review suggests that acute stroke patients are significantly more likely than controls to be hypocapnic, supporting the value of routine CO2 assessment in the acute stroke setting. Further studies are required in order to evaluate the clinical impact of these findings.

Theoretical perspectives on central chemosensitivity: CO2/H+-sensitive neurons in the locus coeruleus.

Central chemoreceptors are highly sensitive neurons that respond to changes in pH and CO2 levels. An increase in CO2/H+ typically reflects a rise in the firing rate of these neurons, which stimulates an increase in ventilation. Here, we present an ionic current model that reproduces the basic electrophysiological activity of individual CO2/H+-sensitive neurons from the locus coeruleus (LC). We used this model to explore chemoreceptor discharge patterns in response to electrical and chemical stimuli. The modeled neurons showed both stimulus-evoked activity and spontaneous activity under physiological parameters. Neuronal responses to electrical and chemical stimulation showed specific firing patterns of spike frequency adaptation, postinhibitory rebound, and post-stimulation recovery. Conversely, the response to chemical stimulation alone (based on physiological CO2/H+ changes), in the absence of external depolarizing stimulation, showed no signs of postinhibitory rebound or post-stimulation recovery, and no depolarizing sag. A sensitivity analysis for the firing-rate response to the different stimuli revealed that the contribution of an applied stimulus current exceeded that of the chemical signals. The firing-rate response increased indefinitely with injected depolarizing current, but reached saturation with chemical stimuli. Our computational model reproduced the regular pacemaker-like spiking pattern, action potential shape, and most of the membrane properties that characterize CO2/H+-sensitive neurons from the locus coeruleus. This validates the model and highlights its potential as a tool for studying the cellular mechanisms underlying the altered central chemosensitivity present in a variety of disorders such as sudden infant death syndrome, depression, and anxiety. In addition, the model results suggest that small external electrical signals play a greater role in determining the chemosensitive response to changes in CO2/H+ than previously thought. This highlights the importance of considering electrical synaptic transmission in studies of intrinsic chemosensitivity.

Metodología físico-matemática de evaluación del pH y la presión de dióxido de carbono arteriales y venosos en la unidad de cuidados intensivos / Physical-mathematical assessment methodology ph dioxide pressure and arterial and venous carbon in the intensive care unit

ResumenIntroducción:La dinámica cardíaca ha sido caracterizada a partir de la teoría de los sistemas dinámicos y la geometría fractal, permitiendo generar metodologías de aplicación clínica.Objetivo:desde los sistemas dinámicos, se desarrollará una metodología de evaluación de los pH y presiones de dióxido de carbono arteriales y venosos para pacientes de la Unidad de Cuidados Intensivos.Materiales y Métodos:se escogieron 10 pacientes con diversas patologías de la Unidad de Cuidados Intensivos Postqui rúrgicos del Hospital Militar Central, registrando pH y presiones de dióxido de carbono arteriales y venosas durante su tiempo de estancia; posteriormente se construyeron atractores, determinando su tipo de trayectoria y estableciendo los valores máximos y mínimos de estas variables en el mapa de retardo.Resultados:se encontró un comportamiento caótico de las variables evaluadas, hallando valores mínimos y máximos de 7,01 y 7,59 para pH arterial, 6,97 y 7,53 para pH venoso, 14,40 y 73,70 para presión arterial de dióxido de carbono, y 19,20 y 97,90 para presión venosa de dióxido de carbono.Conclusiones:La evaluación de los valores máximos y mínimos del atractor en el mapa de retardo constituye un nuevo método, objetivo y reproducible, para la evaluación matemática de cada una de las variables estudiadas, de utilidad para el seguimiento de pacientes en UCI.

SummaryIntroduction:Cardiac dynamics has been characterized from the theory of dynamical systems and fractal geometry, allowing to generate methodologies with clinical application. Objective: from dynamic systems, a methodology for evaluating the arterial and venous pH and dioxide of carbon pressures for patient in Intensive Care Unit will be developed.Materials and Methods:10 patients with various pathologies were selected from Post-surgical Intensive Care Unit of the Central Military Hospital, recording arterial and venous pH and dioxide of carbon pressures of during its stay; attractors were built subsequently, determining the type of path and setting the maximum and minimum values of these variables on the delay map.Results:chaotic behavior of the variables evaluated was found, finding maximum and minimum values of 7,01 and 7,59 for arterial pH values, 6,97 and 7,53 for venous pH, 14,40 and 73,70 for arterial dioxide of carbon pressure, and 19,20 and 97,90 for venous dioxide of carbon pressure.Conclusions:The evaluation of the maximum and minimum values of the attractor on the delay map is a new method, objective and reproducible for the mathematical evaluation of each of the variables studied, useful for monitoring patients in Intensive Care Unit.

Alteraciones electrocardiográficas en personas sanas con Síndrome de Apnea Hipopnea del Sueño inducido, predictoras de arritmias ventriculares y muerte súbita / Electrocardiographic alterations in healthy people with hypopnea Apnea syndrome of induced sleep, predictors of ventricular arrhythmias and sudden death

Antecedentes: El Síndrome de Apnea Hipopnea durante el sueño puede producir trastornos de la conducción cardiaca que pueden conducir a la muerte súbita. Objetivo: Determinar las alteraciones electrocardiográficas y del ritmo cardíaco en sujetos con Síndrome de Apnea-Hipopnea del Sueño (SAHS) y apnea central inducida. Métodos: Evaluación clínica y electrocardiográfica de 50 sujetos aparentemente sanos con SAHS, mediante maniobra de Mueller y con apnea central postespiratoria. Se comparan resultados basales, durante y después de la maniobra mediante análisis de varianza para mediciones repetidas. Resultados: El 60 por ciento de casos fueron varones y 40 por ciento mujeres, con edades promedio de 36 años para varones y de 35,55 años para mujeres (p>0,05). Con la maniobra de Mueller no hubo efecto sobre la duración de la onda P (101,5 ms antes y durante la maniobra, 101,6 ms luego; p>0,05). El complejo QRS tampoco se afectó de manera significativa (90,7 ms antes, 90,9 ms durante y 90,6 ms después; p>0,05). El intervalo QTc aumentó de 413,3 ms antes, a 423,3 ms durante y 423,1 ms después de la maniobra (p0,05), pero la PAM descendió de 89,7 mmHg en el basal a 88,2 mmHg durante el procedimiento y ascendió a 93,6 mmHg después de la misma (p<0,05); no hubo efecto sobre la frecuencia cardiaca y no hubo contracciones supraventriculares...

Background: Obstructive Sleep Apnea can cause cardiac conduction disorders that can lead to sudden death. Objective: To determine the electrocardiographic changes and heart rate in subjects with Obstructive Sleep Apnea and central apnea induced. Methods: Clinical and electrocardiographic evaluation of 50 apparent1y healthy subjects with OSA, using Mueller maneuver and central apnea post-expiratory. Baseline values are compared, during and after the maneuver by analysis of variance for repeated measurements. Results: 60 per cent of cases were male and 40 per cent female mean age of 36 years for males and 35.55 years for females (p>0.05). With Mueller maneuver had no effect on P-wave duration (101.5 msec before and during the maneuver, 101.6 msec following, P>0.05). The QRS wave is not significantly affected (90.7 msec before and 90.6 msec, 90.9 msec after, P>0.05). The QTc raised from 413.3 to 423.3 msec before and 423.1 msec after the maneuver msec (p0.05), but MAP decreased from 89.7 mmHg at baseline to 88.2 mmHg during the procedure and amounted to 93.6 mmHg (p<0.05), there was no effect on heart rate and no supraventricular or ventricular premature contractions with the maneuver. Conclusions: Patients with SAHS QT prolongation and Tp-Tec, and increase in MAP with Mueller maneuver, and only affected the PAM with central apnea postespiratory.

Hypocarbia and adverse outcome in neonatal hypoxic-ischemic encephalopathy.

OBJECTIVE: To evaluate the association between early hypocarbia and 18- to 22-month outcome among neonates with hypoxic-ischemic encephalopathy. STUDY DESIGN: Data from the National Institute of Child Health and Human Development Neonatal Research Network randomized, controlled trial of whole-body hypothermia for neonatal hypoxic-ischemic encephalopathy were used for this secondary observational study. Infants (n = 204) had multiple blood gases recorded from birth to 12 hours of study intervention (hypothermia versus intensive care alone). The relationship between hypocarbia and outcome (death/disability at 18 to 22 months) was evaluated by unadjusted and adjusted analyses examining minimum PCO(2) and cumulative exposure to PCO(2) <35 mm Hg. The relationship between cumulative PCO(2) <35 mm Hg (calculated as the difference between 35 mm Hg and the sampled PCO(2) multiplied by the duration of time spent <35 mm Hg) and outcome was evaluated by level of exposure (none-high) using a multiple logistic regression analysis with adjustments for pH, level of encephalopathy, treatment group (± hypothermia), and time to spontaneous respiration and ventilator days; results were expressed as odds ratios and 95% confidence intervals. Alternative models of CO(2) concentration were explored to account for fluctuations in CO(2). RESULTS: Both minimum PCO(2) and cumulative PCO(2) <35 mm Hg were associated with poor outcome (P < .05). Moreover, death/disability increased with greater cumulative exposure to PCO(2) <35 mm Hg. CONCLUSIONS: Hypocarbia is associated with poor outcome after hypoxic-ischemic encephalopathy.

[Effect of hypocapnia/alkalosis on the fluid filtration rate in isolated and perfused rabbit lungs]. / Efecto de la hipocapnia/alcalosis sobre la tasa de filtración de liquidos en pulmones aislados y perfundidos de conejos.

Hypocapnia/alkalosis is a consequence of several lung and metabolic pathologies. The aim of this study was to determine whether the increase of fluid filtration rate (FFR) that occurs during Hypocapnia/alkalosis circumstances is determined by hypocapnia, alkalosis or both. 7 groups were formed (N=36) using isolated rabbit lungs. Group 1: Control (PCO2 6%, pH: 7.35-7.45); Group 2 (n=6): Hypocapnia/Alkalosis (CO2 1%, pH: 7.9); Group 3 (n=6): Hypocapnia/Normo-pH (CO2 1% pH 7.35-7.45), Group 4 (n=6) Normocapnia/Alcalosis (CO2 6%, pH: 7.9). Fenoterol, papaverine and hydrocortisone were added to Groups 5, 6 and 7 (n=4) respectively, all under Normocapnia/Alkalosis. FFR and Pulmonary Arterial Pressure (Pap) were considerably higher in group 2 than in control (FFR: 1.92g/min +/- 0.6 vs 0.0 g/min +/- 0.006). A strong influence exerted by pH was observed when Group 3 and group 4 were compared (FFR: 0.02 g/min +/- 0.009 vs 2.3 g/min +/- 0.9) and (Pap: 13.5 cmH2O +/- 1.4 vs 90 cmH2O +/- 15). A reduced effect was observed in groups 5 and 6 (papaverine and hydrocorisone) and a totally abolished effect was observed in group 7 (fenoterol) (FFR: 0.001 +/- 0.0003 mL/min and Pap: 14 +/- 0.8 cmH2O). Pulmonary edema induced by Hypocapnia/alkalosis is a consequence of alkalosis and not of hypocapnia. This effect could be due to inflammatory damage in the lung parenchyma and alkalosis-mediated vasoconstriction.

Efecto de la hipocapnia/alcalosis sobre la tasa de filtración de líquidos en pulmones aislados y perfundidos de conejos / Effect of hypocapnia/alkalosis on the fluid filtration rate in isolated and perfused rabbit lungs

La hipocapnia/alcalosis es una situación que se presenta como consecuencia de diversas patologías pulmonares o metabólicas. El objetivo de este estudio fue determinar si el aumento de la tasa de filtración de liquido (TFL) que ocurre bajo estas circunstancias, está determinado por la hipocapnia, la alcalosis o la suma de ambas. Se realizaron 7 grupos (n=36), utilizando pulmones aislados de conejos. Grupo 1: Control (PCO2 6 por ciento, pH: 7,35-7,45); Grupo 2 (n=6): Hipocapnia/Alcalosis (CO2 1 por ciento, pH: 7,9); Grupo 3 (n=6): Hipocapnia/Normo-pH (CO2 1 por ciento pH 7,35-7,45), Grupo 4 (n=6) Normocapnia/Alcalosis (CO2 6 por ciento, pH: 7,9). En los grupos 5, 6 y 7 (n=4), todos bajo condición de Normocapnia/Alcalosis se añadió fenoterol, papaverina, e hidrocortisona respectivamente. La TFL y la presión de arteria pulmonar (Pap) fueron considerablemente mayores en el grupo 2 que en el control (TFL:1,92g/min ± 0,6 vs 0,0g/min ± 0,006), observándose una marcada influencia del pH, al comparar el grupo 3 y el grupo 4 (TFL: 0,02g/min ± 0,009 vs 2,3g/min ± 0,9) y (Pap: 13,5 cmH2O ± 1,4 vs 90 cmH2O ± 15). Se observó una disminución del efecto en los grupos 5 y 6 (papaverina e hidrocortisona) y su abolición total con fenoterol (grupo 7) (TFL: 0,001 ± 0,0003 g/min y Pap: 14 ± 0,8 cmH2O). El edema pulmonar inducido por Hipocapnia/Alcalosis es consecuencia principalmente de la alcalosis y no de la hipocapnia. Dicho efecto podría ser debido a un daño inflamatorio a nivel del parénquima y a la vasoconstricción causada por la alcalosis.

Ventilação periódica durante vigília prediz a respiração de Cheyne-Stokes durante o sono em pacientes com insuficiência cardíaca / Awake periodic breathing predicts Cheyne-Stokes respiration during sleep in patients with heart failure

Introdução: Os distúrbios respiratórios do sono na forma de apnéia central associada à respiração de Cheyne-Stokes (RCS) e apnéia obstrutiva do sono (AOS), são comuns nos pacientes com insuficiência cardíaca (IC) e podem contribuir para morbimortalidade. A RCS é uma forma exagerada de ventilação periódica (VP) na qual apnéias centrais alternam com períodos de hiperventilação. Em contraste, a AOS resulta em um colapso completo ou parcial da via aérea superior recorrente durante o sono. Objetivo: Fizemos à hipótese que VP durante vigília prediz a RCS durante o sono em pacientes com IC. Métodos: Estudamos pacientes do ambulatório de Cardiopatia Geral, do Instituto do Coração (InCor), recrutados no período de 2001 a 2003, submetidos a avaliação clínica e ecocardiográfica. Os pacientes foram submetidos à monitoração do padrão respiratório em posição supina, com luz acesa por 10 minutos, imediatamente antes do início de registro do sono por polissonografia noturna. Na manhã seguinte, o padrão respiratório foi monitorado por 10 minutos em repouso, os pacientes permaneciam sentados, seguido por teste de exercício cardiopulmonar em bicicleta ergométrica, com medida de fração expirada de CO2 e relação ventilação/CO2 (VE/VCO2). A presença dos distúrbios respiratórios do sono foi determinada através de polissonografia (índice de apnéia-hipopnéia 15 eventos/hora), os pacientes foram divididos nos grupos sem Distúrbio Respiratório do Sono (sem DRS), RCS e AOS. Os resultados estão apresentados como média ± desvio padrão. Resultados: Foram incluídos no estudo 47 pacientes, 5 foram excluídos por falta de coordenação motora e incapacidade de realizar o teste de exercício em bicicleta. O grupo final se constituiu de 42 pacientes (67% masculino, idade = 62±9 anos, fração de ejeção ventricular esquerda = 35±6%), sendo 22 do grupo sem DRS, 11 do grupo RCS e 9 do grupo AOS. Não houve diferenças significativas nos grupos nos parâmetros antropométricos e fração de ejeção...

Introduction: Sleep disordered breathing in the form of central sleep apnea and Cheyne-Stokes respiration (CSR) and obstructive sleep apnea (OSA) are common among heart failure (HF) patients and can independently contribute to morbimortality. CSR is an exaggerated form of periodic breathing (PB) in which central apneas alternate with periods of hyperventilation. In contrast, OSA results from recurrent collapse of upper airway during sleep. Objective: We hypothesize that PB while awake predicts CSR during sleep in patients with HF. Methods: Patients were recruited from one outpatient heart failure clinic (Instituto do Coração, InCor) in the period 2001 until 2003. All patients were submitted respiratory monitoring, for 10 minutes while awake in supine position immediately before overnight polysomnography. In the next morning, the patients were monitored for 10 minutes while sitting in a comfortable chair at rest, followed by cardiopulmonary exercise tests (electromagnetic-braked cycle). The presence of sleep disordered breathing was determined through polysomnography (apnea-hypopnea index 15 events/hour). The patients were divided according to the respiratory pattern during sleep in no-Sleep Disordered Breathing (no-SDB), CSR and OSA. Results: Forty seven patients were included in the study, 5 were excluded because of inability to perform exercise. The final group consisted of 42 patients (67% males, age: 62±9 yr, left ventricular ejection fraction: 35±6%). There were 22 in the no-SDB group, 11 in the CSR group and 9 in the OSA group. There were no significant differences among groups regarding anthropometric measurements and left ventricular ejection fraction. The CSR group presented a significantly increased proportion of NYHA functional class III-IV (p=0.03), lower PETCO2 (p=0.01) and increased VE/VCO2 slope (p=0.03) than no-SDB and OSA groups. PB while awake was present 19%, 31% e 36% before and during exercise and before sleep, respectively...

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.

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.

Hiperóxia e risco aumentado de displasia broncopulmonar em prematuros / Hyperoxia and greater risk for bronchopulmonary dysplasia in preterm infants

Objetivo: estudar a associação entre hiperóxia e hipocapnia precoces e displasia broncopulmonar )DBP) em recém-nascidos pré-termo (RNPT) de muito baixo peso. Métodos: estudo retrospectivo com 181 RNPT admitidos na Unidade de Terapia Intensiva Neonatal (Unineo) da Maternidade de Santa Fé, em Belo Horizonte (MG), entre agosto de 1995 a agosto de 2004. Foram incluídos neonatos com idade gestacional <37 semanas e peso ao nascer <1.500g, submetidos à ventilação mecânica nas primeiras 72 horas de vida. Analisou-se, por meio de análise multivariada, a presença de associação entre DBP e as variáveis: hiperóxia (PaO2>80 mmHg) e hipocapnia (PaCO2<30 mmHg) entre seis e 72 horas de vida, idade gestacional, relação peso/IG, Apgar no primeiro e quinto minutos, uso de surfactante, uso de corticosteróides no período pré-natal e antibioticoterapia após o quinto dia de vida. Resultados: na população estudada, a idade gestacional foi <=30 semanas em 138(76 por cento) neonatos, 59(33 por cento) eram pequenos para a idade gestacional, 85(47 por cento) do sexo masculino; 122(67 por cento) receberam surfactante e 105(58 por cento) receberam antibioticoterapia após o quinto dia de vida. A média e a mediana foram respectivamente, para a PaO2, 87,4 e 80 mmHg e, para a PaCO2, 34,6 e 33 mmHg, entre seis e 72 horas de vida. A DBP ocorreu em 38(21 por cento) dos 181 RNPT e em 28(42 por cento) dos 67 RNPT com peso ao nascer <1.000 g. A análise multivariada confirmou a associação entre DBP e hiperóxia (p=0,011), peso ao nascer<1.000 g(p<0,001) e antibioticoterapia após o quinto dia (p<0,001). Conclusões: A DBP se associou à hiperóxia, no período neonatal precoce, ao peso mais baixo ao nascer e aos fatores inflamatórios.

Parámetros fisiológicos en caninos pre y post competencia de Agility en Bogotá, Colombia / Canine physiological parameters pre and post agility competition at Bogotá, Colombia

El estudio se llevó a cabo en la ciudad de Bogotá, ubicada a una altura media 2600 msnm, con temperatura promedio de 14°C. Se realizó un muestreo en el Polideportivo el Salitre y otro en el parque central de Modelia. El objetivo principal fue monitorear y estandarizar los cambios fisiológicos que se presentan en caninos atletas, como respuesta al ejercicio realizado en pruebas de Agility. Se muestrearon 15 caninos hembras de diferentes razas practicantes del Agility, de las escuelas Atalanta y X-treme Dog. El control se obtuvo de individuos en reposo, previo al ejercicio, inmediatamente a su llegada al área de investigación, donde se situaron las pistas para el entrenamiento, que incluía la toma de temperatura rectal, frecuencia de pulso, frecuencia respiratoria y de sangre arterial (arteria femoral). La muestra arterial se procesó con analizador sanguíneo portátil, obteniendo de hematocrito, hemoglobina, sodio, potasio, cloruro, nitrógeno uréico (BUN), glucosa, lactato, pH sanguíneo, presión de dióxido de carbono (PCO2), presión de oxígeno (PO2), bicarbonato, tensión de dióxido de carbono(TCO2), saturación de oxígeno (SO2), exceso de base (BE), anion gap y osmolalidad. Luego se inició el entrenamiento, simulando una competencia real, donde cada canino pasó cuatro veces por pista, y al final se monitorearon, siguiendo el procedimiento descrito para el control. Se compararon los resultados pre y post ejercicio, presentándose: aumento para temperatura, frecuencia respiratoria, pulso, pH, hematocrito, hemoglobina, sodio, cloro y osmolalidad (p<0,001); incremento en los valores de potasio, lactato y glucosa (p<0,01); ascenso para PO2, SO2 y BUN (p<0,05); descenso para PCO2, TCO2, BE y Anión Gap (p<0,001). Se concluye que los caninos deportistas en Bogotá presentan hipertermia, taquicardia, hipocapnia, alcalosis respiratoria acompañada de una acidosis metabólica compensatoria y hemoconcentración por una deshidratación clasificada como hiperosmótica, luego de una competencia de Agility.

Cambios postoperatorios de la función pulmonar / Pulmonary postoperative changes

La anestesia y la cirugía producen cambios en la fisiología pulmonar desde el inicio del acto operatorio. Dichos cambios -reducción de la capacidad residual funcional, de la capacidad de cierre, producción de microatelectasias, alteración del intercambio gaseoso, alteraciones del V/Q, etc. -pueden verse agravados por la presencia de alteraciones mórbidas de los pacientes (hábito de fumar, obesidad, edad) o por causas inherentes al tipo de cirugía (tórax, abdomen superior). Diferentes aspectos del manejo anestésico pueden agravar las condiciones que favorecerán la aparición de complicaciones postoperatorias, si no se tienen en cuenta justamente las características del paciente y de la cirugía por realizarse. El control de la correcta oxigenación, de los valores del CO2, del estado ácidobase, de la administración de líquidos, de la transfusión de sangre, de los volúmenes de gas que ingresan y egresan del árbol broncopulmonar, la elección de modos ventilatorios no habituales, la prevención de broncoespasmos, tromboembolismo, el control del dolor, etc.; en suma, el conocimiento de la fisiología del intraoperatorio y la aplicación de dichos conocimientos en el postoperatorio permiten al anestesiólogo evitar o hacer menos probable la aparición de complicaciones. Las alteraciones pulmonares son más comunes en pacientes y cirugías que reúnen ciertas características: fumadores, obesos, mayores de setenta años, cirugía torácica o del abdomen superior o de larga duración, con antecedentes tromboembólicos, pacientes con enfermedad pulmonar obstructiva crónica o con enfermedad espástica bronquial. Muchas maniobras han sido descriptas en el postoperatorio para evitar las complicaciones pulmonares; las más efectivas incluyen fisioterapia respiratoria, posición semisentada precoz, soporte de O2 para mantener saturaciones periféricas por encima del 93 por ciento o, por lo menos, para alcanzar los valores preoperatorios con una FIO2 del 21 por ciento.

Cambios postoperatorios de la función pulmonar / Pulmonary postoperative changes

La anestesia y la cirugía producen cambios en la fisiología pulmonar desde el inicio del acto operatorio. Dichos cambios -reducción de la capacidad residual funcional, de la capacidad de cierre, producción de microatelectasias, alteración del intercambio gaseoso, alteraciones del V/Q, etc. -pueden verse agravados por la presencia de alteraciones mórbidas de los pacientes (hábito de fumar, obesidad, edad) o por causas inherentes al tipo de cirugía (tórax, abdomen superior). Diferentes aspectos del manejo anestésico pueden agravar las condiciones que favorecerán la aparición de complicaciones postoperatorias, si no se tienen en cuenta justamente las características del paciente y de la cirugía por realizarse. El control de la correcta oxigenación, de los valores del CO2, del estado ácidobase, de la administración de líquidos, de la transfusión de sangre, de los volúmenes de gas que ingresan y egresan del árbol broncopulmonar, la elección de modos ventilatorios no habituales, la prevención de broncoespasmos, tromboembolismo, el control del dolor, etc.; en suma, el conocimiento de la fisiología del intraoperatorio y la aplicación de dichos conocimientos en el postoperatorio permiten al anestesiólogo evitar o hacer menos probable la aparición de complicaciones. Las alteraciones pulmonares son más comunes en pacientes y cirugías que reúnen ciertas características: fumadores, obesos, mayores de setenta años, cirugía torácica o del abdomen superior o de larga duración, con antecedentes tromboembólicos, pacientes con enfermedad pulmonar obstructiva crónica o con enfermedad espástica bronquial. Muchas maniobras han sido descriptas en el postoperatorio para evitar las complicaciones pulmonares; las más efectivas incluyen fisioterapia respiratoria, posición semisentada precoz, soporte de O2 para mantener saturaciones periféricas por encima del 93 por ciento o, por lo menos, para alcanzar los valores preoperatorios con una FIO2 del 21 por ciento. (AU)