Hypercapnia does not shorten emergence time from propofol anesthesia: a pilot randomized clinical study / 대한마취과학회지

BACKGROUND: The elimination of anesthetic agents is a decisive factor in the emergence from general anesthesia. In this pilot study, we hypothesized that hypercapnia would decrease the emergence time from propofol anesthesia by increasing cardiac output and cerebral blood flow. METHODS: A total of 32 patients were randomly divided into two groups based on the end-tidal carbon dioxide values: 30 mmHg (the hypocapnia group) and 50 mmHg (the hypercapnia group). Propofol and remifentanil were infused to maintain a bispectral index of 40–50. Remifentanil infusion was stopped 10 min before the discontinuation of propofol. After cessation of propofol infusion, ventilation settings in the hypocapnia group were maintained constant; a rebreathing tube was connected to the respiratory circuit in the hypercapnia group. The time to spontaneous respiration, eye opening (primary endpoint), mouth opening, and tracheal extubation was recorded and analyzed. RESULTS: Time to eye opening was 9.7 (1.3) min in the hypocapnia group and 9.0 (1.0) min in the hypercapnia group. The difference in the mean times to eye opening between groups was −0.7 min (95% CI, −4.0 to 2.7, P = 0.688). On multiple regression analysis, there was a significant difference in the mean time to eye opening between males and females. Females recovered about 3.6 min faster than males (95% CI, −6.1 to −1.1, P = 0.009). CONCLUSIONS: We could not detect a beneficial effect of hypercapnia on propofol emergence time. Irrespective of hypercapnia, females seemed to recover faster than males.

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.

Laryngeal Spasm Mimicking Asthma and Vitamin D Deficiency

We present a woman with heterozygous carnitine palmitoyl transferase 2 (CPT-2) deficiency who in the last 6 months suffered from episodic dyspnea and choking. Symptoms could not be attributed to her muscular energy defect, since heterozygous CPT-2 deficiency is usually asymptomatic or causes only mild muscle fatigability. Myopathy is usually triggered by concurrent factors, either genetic (additional muscle enzymes defects) or acquired (metabolic stress). The patient was referred to our respiratory clinic for suspect bronchial asthma. Spirometry showed mild decrease in inspiratory flows. Methacholine challenge was negative. Dyspnea was triggered by hyperventilation-induced hypocapnia, which produced marked decrease in airflow rates, particularly in inspiratory flows, consistent with laryngospasm. Nutritional assessment of the patient showed low serum level of calcium and vitamin D, attributable to avoidance of milk and dairy products for lactose intolerance and to insufficient sunlight exposure. After calcium and vitamin D supplementation episodic laryngospasm disappeared and hypocapnic hyperventilation test induced very mild change in airflow rates. Calcium and vitamin D deficiency may favour laryngeal spasm mimicking asthma, particularly in subjects with underlying myopathy.

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.

A Case of Seizure in a Patient Following Percutaneous Endoscopic Lumbar Discectomy

Seizure following percutaneous endoscopic lumbar discectomy (PELD) is extremely rare. We report that generalized seizure occurred in a patient with radiating right leg pain after PELD under sevoflurane anesthesia. Cerebrospinal fluid (CSF) was detected from a dura tear in the operative field. On emergence from anesthesia, generalized tonic-clonic activity continued for approximately 2 minutes and the level of consciousness was decreased to a stuporous state. Under sedation, a pneumocephalus which was thought to be caused by the dura tear was evaluated with a brain computed tomography (CT) and a continuous slow wave was found on electroencephalography (EEG) without any epileptiform discharges. Eight hours postoperatively, the decreased level of consciousness recovered, and after 2 weeks, the patient was discharged without any neurologic sequealae. Clinicians should recognize the epileptogenic potential of sevoflurane and limit the maximum dose with avoidance of hypocapnia by hyperventilation. If an intracerebral lesion is accompanied, it may increase the possibility of the occurrence of seizure.

Intraoperative acute brain swelling when performing indirect anastomosis in a patient with moyamoya disease: A case report / 대한마취과학회지

A 6-year-old male patient who was suffering from a cold and a transient ischemic attack was scheduled to undergo encephalo-duro-arterio-synangiosis for treating his moyamoya disease. Acute brain edema occurred just after opening the dura mater. Head elevation, reduction of the head rotation and hyperventilation were done. The inhalational agents were discontinued and total intravenous anesthesia was started. The swelling was reduced after intravenously infusing mannitol. An abrupt return from hypocapnia to normocapnea during the induction of general anesthesia was thought to be the cause of the acute brain swelling. In conclusion, correction of hypocapnea needs to be performed gradually during the induction of anesthesia and when performing an operation for treating a patient with moyamoya disease.

Hypocapnia Attenuates, and Nitrous Oxide Disturbs the Cerebral Oximetric Response to the Rapid Introduction of Desflurane

The aim of this study was to develop a nonlinear mixed-effects model for the increase in cerebral oximetry (rSO2) during the rapid introduction of desflurane, and to determine the effect of hypocapnia and N2O on the model. Twelve American Society of Anesthesiologist physical status class 1 and 2 subjects were allocated randomly into an Air and N2O group. After inducing anesthesia, desflurane was then increased abruptly from 4.0 to 12.0%. The PET(CO2), PET(DESF) and rSO2 were recorded at 12 predetermined periods for the following 10 min. The maximum increase in rSO2 reached +24-25% during normocapnia. The increase in rSO2 could be fitted to a four parameter logistic equation as a function of the logarithm of PET(DESF). Hypocapnia reduced the maximum response of rSO2, shifted the EC50 to the right, and increased the slope in the Air group. N2O shifted the EC50 to the right, and reduced the slope leaving the maximum rSO2 unchanged. The N2O-effects disappeared during hypocapnia. The cerebrovascular reactivity of rSO2 to CO2 is still preserved during the rapid introduction of desflurane. N2O slows the response of rSO2. Hypocapnia overwhelms all the effects of N2O.

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.

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...

Retinopathy of prematurity among 1000-2000 gram birth weight newborn infants

The goal of this study was to identify the risk factors of retinopathy of prematurity [ROP] in neonatal intensive care unit in preterm infants born with birth weight 1000-2000g or at gestational age less than 34 weeks. From August 2000 to December 2001, 50 preterm newborn infants with birth weights less than 2000 g or gestational age less than 34 weeks admitted to the NICU were studied. Newborn infants with birth weight between 1200-2000g who received more than 6 hours oxygen and newborn infants with birth weight 1000-1200 g regardless of oxygen therapy, who survived until 4 weeks postnatal, were enrolled and followed. Patients underwent indirect ophthalmologic examination by two ophthalmologists between 4-8 weeks post partum. The newborn infants who had ROP were assigned to case group and those without ROP to control group, both groups were reexamined every 2-4 weeks or according to international classification of retinopathy of prematurity [ICROP] advice Fifty newborn infants, 36 [72%] in control group, 14 [28%] in case group, were studied. Gestational age and birth weight of the patients with ROP were significantly lower than those of control group. Duration of oxygen therapy, hyperoxia, acidosis, hypercarbia, hypocarbia and phototherapy are suggested as risk factors contributing to ROP. The results of this study demonstrate that the ROP frequency remains elevated among premature and very low birth weight infants. Infants at risk for ROP should have screening eye examinations and proper treatment

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.

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.

Development of Brain Infarction after Extracranial-Intracranial Bypass Surgery in a Patient with Moyamoya Disease: A case report / 대한마취과학회지

Moyamoya disease is characterized by a narrowing or occlusion of both internal carotid arteries in the presence of an abnormal hemangiomatosis vascular network at the base of the brain. These patients increasingly present for surgical management to improve the cerebral circulation. However, surgery may be complicated by cerebral ischemia, and thus patients require particular care during the perioperative period. The risk factors of perioperative ischemic complications include the presence of a preoperative low density area by computed tomography, the occurrence of frequent preoperative transient ischemic attacks, or hypocapnia or hypotension. We describe one case of general anesthesia for superficial temporal artery to middle cerebral artery anastomosis (STA-MCA) with encephalomyosynangiosis (EMS) in a moyamoya disease patient. The patient expired because of a developing cerebral infarction on the fifth postoperative day.

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.

Effect of controlled hyperventilation on the pressor response to laryngoscopy and tracheal intubation

Pressor response to laryngoscopy and tracheal intubation includes rises in blood pressure and heart rate. This response may be harmful in the presence of cerebral or myocardial diseases. Although different preventive measures have been developed the choice of the agent or method has not been defined clearly. Hypocapnia is commonly used in anesthesia practice for different indications. It depresses the cardiovascular system and lowers the cardiac output. This study investigated the effect of controlled hyperventilation on the pressor response to laryngoscopy and tracheal intubation in three groups of healthy adult patients with different levels of end tidal CO2. The blood pressure and heart rate were recorded during induction of general anesthesia before and after laryngoscopy and tracheal intubation. The pressor responses to laryngoscopy and tracheal intubation in hypocapnic and normocapnic groups were comparable. Moderate degrees of controlled hyperventilation caused relatively more fluctuation in blood pressure during induction of anesthesia. It can be concluded that controlled hyperventilation has no beneficial effect upon the pressor response to laryngoscopy and tracheal intubation

Reliability of rSO2 to Measure CO2 Reactivity of Cerebral Vasculatures during Desflurane-N2O Anesthesia / 대한마취과학회지

BACKGROUND: Near infrared spectroscopy (NIRS) to monitor regional cerebral oxygen saturation (rSO2) is a noninvasive and simple modal ity in clinical use. The ability of rSO2 as an index of cerebral oxygenation has been well demonstrated. However, the reliability of rSO2 to reflect the changes of cerebral vascular reactivity in the changes of arterial partial pressure of CO2 (PaCO2) has not been established. The aim of this study was to verify the reliability of rSO2 to measure the CO2 reactivity of cerebral vasculatures. METHODS: Twenty healthy adult patients undergoing general anesthesia were enrolled in this study. Anesthesia was induced with propofol and maintained with desflurane/N2O. Respiration was mechanically controlled. The radial artery and jugular bulb were cannulated. The sensor of the NIRS was attached to the ipsilateral forehead. During normocapnia (PaCO2 40 +/- 1.3 mmHg) and hypocapnia (PaCO2 30 +/- 2.4 mmHg), blood was obtained from the radial artery and jugular bulb and analyzed. rSO2 was compared with fSO2 (estimated field oxygen satuation), and the gold standard of tissue oxygen saturation. fSO2 was calculated from the following equation: fSO2 = 0.75 SjO2 + 0.25 SaO2. RESULTS: rSO2 significantly correlated with fSO2 (P = 0.000, r2 = 0.56). A bias of - 5.8% with a precision 12.94% was found. CONCLUSIONS: We concluded that rSO2 can be a reliable predictor to measure CO2 reactivity of cerebral vasculatures during normocapnia and hypocapnia.

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.