Comparación del efecto de omeprazol como monoterapia y su combinación con bicarbonato de sodio en el tratamiento de la pirosis moderada a severa: ensayo clínico controlado, aleatorizado y doble ciego / Comparison of the effect of omeprazole monotherapy and its combination with sodium bicarbonate in the treatment of moderate to severe heartburn: a double-blind, randomized controlled clinical trial

Heartburn occurs in 75% of patients with digestive discomfort of any origin and is one of the main symptoms of gastroesophageal reflux disease. Treatment focuses on lifestyle modification and symptomatology management with various drugs; when heartburn is moderate to severe, a proton pump inhibitor is more suitable. Omeprazole (OMZ) combined with sodium bicarbonate (BC) has demonstrated significant and sustained suppression of acid secretion. The objective was to compare the effect of sequential OMZ/BC therapy compared to OMZ monotherapy for the improvement of heartburn in Mexican individuals. The study was a double-blind, randomized, controlled, multicenter clinical study including 277 subjects with moderate to severe heartburn. Patients received 7 days of OMZ/BC and 7 days of OMZ (OMZ/BC7) or 14 days of OMZ (OMZ14). The primary endpoint was defined as the change in the number of days a week that the patient has heartburn, it was evaluated at 14 days. Both treatments reduced time (days) with heartburn by less than 4 days (OMZ14 3.9 vs. 4.2 days OMZ/BC7), as well as duration, number of events and intensity of heartburn. The treatments improved the quality of life, and the control of the symptoms. The proportion of adverse events was lower with OMZ/BC. The non-inferiority of OMZ/BC7 with respect to OMZ14 was verified.

La pirosis se presenta en el 75% de los pacientes con molestias digestivas de cualquier origen y es uno de los principales síntomas de la enfermedad por reflujo gastroesofágico. El tratamiento se enfoca en la modificación del estilo de vida y el manejo de la sintomatología con diversos fármacos; cuando la pirosis es moderada a severa, un inhibidor de la bomba de protones es más adecuado. El omeprazol (OMZ) combinado con bicarbonato de sodio (BC) ha demostrado supresión significativa y sostenida de la secreción ácida. El objetivo fue comparar el efecto de la terapia secuencial de OMZ/BC en comparación con el tratamiento continuo de OMZ para la mejoría de la pirosis en individuos mexicanos. Estudio clínico multicéntrico, doble ciego, controlado, aleatorizado que incluyó 277 sujetos con pirosis moderada a severa. Los pacientes recibieron 7 días de OMZ/BC y 7 días de OMZ (OMZ/BC7) o 14 días de OMZ (OMZ14). La variable primaria fue definida como el cambio del número de días a la semana que el paciente presenta pirosis, se evaluó a los 14 días. Ambos tratamientos redujeron los días con pirosis en menos 4 días (OMZ14 3,9 vs. 4,2 días OMZ/BC7), así como la duración, el número de eventos e intensidad de la pirosis. Los tratamientos mejoraron los indicadores de calidad de vida, y el control del padecimiento. La proporción de eventos adversos fue menor con OMZ/BC. Se comprobó la no-inferioridad de OMZ/BC7 respecto OMZ14.

Bicarbonato de sodio intravenoso ¿Cuándo, cómo y por qué utilizarlo? / Intravenous sodium bicarbonate. When, how and why to use it?

Severe metabolic acidosis is defined by a pH < 7.2 with HCO3− < 8 mE- q/L in plasma. Its best treatment is to correct the underlying cause. However, acidemia produces multiple complications such as resistance to the action of catecholamines, pulmonary vasoconstriction, impaired cardiovascular function, hyperkalemia, immunological dysregulation, respiratory muscle fatigue, neurological impairment, cellular dysfunction, and finally, it contributes to multisystemic failure. Intravenous NaHCO3 buffers severe acidemia, preventing the associated damage and gains time while the causal disease is corrected. Its indication requires a risk-benefit assessment, considering its complications. These are hypernatremia, hypokalemia, ionic hypocalcemia, rebound alkalosis, and intracellular acidosis. For this reason, therapy must be "adapted" and administered judiciously. The patient will require monitoring with serial evaluation of the internal environment, especially arterial blood gases, plasma electrolytes, and ionized calcium. Isotonic solutions should be preferred instead of hypertonic bicarbonate. The development of hypernatremia must be prevented, calcium must be provided for hypocalcemia to improve cardiovascular function. Furthermore, in mechanically ventilated patients, a respiratory response similar to the one that would develop physiologically, must be established to be able to extract excess CO2 and thus avoid intracellular acidosis. It is possible to estimate the bicarbonate deficit, speed, and volume of its infusion. However, the calculations are only for reference. More important is to start intravenous NaHCO3 when needed, administer it judiciously, manage its side effects, and continue it to a safe goal. In this review we address all the necessary elements to consider in the administration of intravenous NaHCO3, highlighting why it is the best buffer for the management of severe metabolic acidosis.

[Intravenous sodium bicarbonate. When, how and why to use it?] / Bicarbonato de sodio intravenoso ¿Cuándo, cómo y por qué utilizarlo?

Severe metabolic acidosis is defined by a pH < 7.2 with HCO3- < 8 mE- q/L in plasma. Its best treatment is to correct the underlying cause. However, acidemia produces multiple complications such as resistance to the action of catecholamines, pulmonary vasoconstriction, impaired cardiovascular function, hyperkalemia, immunological dysregulation, respiratory muscle fatigue, neurological impairment, cellular dysfunction, and finally, it contributes to multisystemic failure. Intravenous NaHCO3 buffers severe acidemia, preventing the associated damage and gains time while the causal disease is corrected. Its indication requires a risk-benefit assessment, considering its complications. These are hypernatremia, hypokalemia, ionic hypocalcemia, rebound alkalosis, and intracellular acidosis. For this reason, therapy must be "adapted" and administered judiciously. The patient will require monitoring with serial evaluation of the internal environment, especially arterial blood gases, plasma electrolytes, and ionized calcium. Isotonic solutions should be preferred instead of hypertonic bicarbonate. The development of hypernatremia must be prevented, calcium must be provided for hypocalcemia to improve cardiovascular function. Furthermore, in mechanically ventilated patients, a respiratory response similar to the one that would develop physiologically, must be established to be able to extract excess CO2 and thus avoid intracellular acidosis. It is possible to estimate the bicarbonate deficit, speed, and volume of its infusion. However, the calculations are only for reference. More important is to start intravenous NaHCO3 when needed, administer it judiciously, manage its side effects, and continue it to a safe goal. In this review we address all the necessary elements to consider in the administration of intravenous NaHCO3, highlighting why it is the best buffer for the management of severe metabolic acidosis.

Safety, Tolerability, and Effects of Sodium Bicarbonate Inhalation in Cystic Fibrosis.

BACKGROUND: Among the many consequences of loss of CFTR protein function, a significant reduction of the secretion of bicarbonate (HCO3-) in cystic fibrosis (CF) is a major pathogenic feature. Loss of HCO3- leads to abnormally low pH and impaired mucus clearance in airways and other exocrine organs, which suggests that NaHCO3 inhalation may be a low-cost, easily accessible therapy for CF. OBJECTIVE: To evaluate the safety, tolerability, and effects of inhaled aerosols of NaHCO3 solutions (4.2% and 8.4%). METHODS: An experimental, prospective, open-label, pilot, clinical study was conducted with 12 CF volunteer participants over 18 years of age with bronchiectasis and pulmonary functions classified as mildly to severely depressed. Sputum rheology, pH, and microbiology were examined as well as spirometry, exercise performance, quality-of-life assessments, dyspnea, blood count, and venous blood gas levels. RESULTS: Sputum pH increased immediately after inhalation of NaHCO3 at each clinical visit and was inversely correlated with rheology when all parameters were evaluated: [G' (elasticity of the mucus) = - 0.241; G″ (viscosity of the mucus) = - 0.287; G* (viscoelasticity of the mucus) = - 0.275]. G* and G' were slightly correlated with peak flow, forced expiratory volume in 1 s (FEV1), and quality of life; G″ was correlated with quality of life; sputum pH was correlated with oxygen consumption (VO2) and vitality score in quality of life. No changes were observed in blood count, venous blood gas, respiratory rate, heart rate, peripheral oxygen saturation of hemoglobin (SpO2), body temperature, or incidence of dyspnea. No adverse events associated with the study were observed. CONCLUSION: Nebulized NaHCO3 inhalation appears to be a safe and well tolerated potential therapeutic agent in the management of CF. Nebulized NaHCO3 inhalation temporarily elevates airway liquid pH and reduces sputum viscosity and viscoelasticity.

Intranasal instillation of distilled water, hypertonic saline and sodium bicarbonate promotes redox imbalance and acute lung inflammation in adult mice.

Bronchial obstruction, caused by retained secretions, is often treated by the administration of mucoactive agents including distilled water, saline, hypertonic saline, and sodium bicarbonate. However, the inflammatory effect of these solutions on the lungs remains unclear. This study evaluated the instillation effects of different solutions on oxidative stress and lung inflammatory response in C57BL/6 mice. Fifty C57BL/6 mice were divided into 5 groups: control (CG); distilled water (DWG), hypertonic saline (HSG), saline (SG) and sodium bicarbonate (SBG). CG was exposed to ambient air while DWG, HSG, SG and SBG had 50 µl of respective solutions administered intranasally for 5 consecutive days. Twenty-four hours after the last intranasal instillation, all animals were euthanized for subsequent analysis. All solutions promoted increased recruitment of inflammatory cells to the lung compared to controls. Superoxide dismutase activity was lower in HSG compared to all other groups; catalase activity was reduced in SG, while it increased in SBG and DWG compared to CG. Finally, there was an increase in the inflammatory markers TNF-α, CCL2 and IFN-γ in DWG compared to CG, SG and HSG. In conclusions, the intranasal instillation of different solutions promotes redox imbalance and inflammation on lungs of adult mice.

Nutritional Strategies to Modulate Intracellular and Extracellular Buffering Capacity During High-Intensity Exercise.

Intramuscular acidosis is a contributing factor to fatigue during high-intensity exercise. Many nutritional strategies aiming to increase intra- and extracellular buffering capacity have been investigated. Among these, supplementation of beta-alanine (~3-6.4 g/day for 4 weeks or longer), the rate-limiting factor to the intramuscular synthesis of carnosine (i.e. an intracellular buffer), has been shown to result in positive effects on exercise performance in which acidosis is a contributing factor to fatigue. Furthermore, sodium bicarbonate, sodium citrate and sodium/calcium lactate supplementation have been employed in an attempt to increase the extracellular buffering capacity. Although all attempts have increased blood bicarbonate concentrations, evidence indicates that sodium bicarbonate (0.3 g/kg body mass) is the most effective in improving high-intensity exercise performance. The evidence supporting the ergogenic effects of sodium citrate and lactate remain weak. These nutritional strategies are not without side effects, as gastrointestinal distress is often associated with the effective doses of sodium bicarbonate, sodium citrate and calcium lactate. Similarly, paresthesia (i.e. tingling sensation of the skin) is currently the only known side effect associated with beta-alanine supplementation, and it is caused by the acute elevation in plasma beta-alanine concentration after a single dose of beta-alanine. Finally, the co-supplementation of beta-alanine and sodium bicarbonate may result in additive ergogenic gains during high-intensity exercise, although studies are required to investigate this combination in a wide range of sports.

[Correlation between the use of sodium bicarbonate and intraventricular hemorrhage in preterms]. / Relación entre bicarbonato de sodio y hemorragia intraventricular en prematuros.

BACKGROUND: Being born preterm implies comorbidities, among them the risk of intraventricular hemorrhage (IVH). The use of sodium bicarbonate has been linked to the presence of IVH. The main purpose of this study was to determine if the infusion of sodium bicarbonate during the first 24 hours increases the risk of IVH in preterm infants. METHODS: Our study is a cohort; we analyzed the files of 160 patients and divided them into two groups: one in which sodium bicarbonate was not used and another in which it was; this latter group was subdivided into two considering if the use was therapeutic of prophylactic. RESULTS: In our total group of patients 10 % presented IVH; had a mean weight of 1500 g and 31 weeks of gestational age. The incidence of IVH was identical between both groups, although patients in which bicarbonate was used were more premature, unstable, and in worse clinical conditions. CONCLUSIONS: Our data indicate the need of large scale studies to determine if the clinical benefits of the use of sodium bicarbonate outweigh the risk of IVH.

Introducción: nacer prematuro conlleva riesgos, como la posibilidad de sufrir hemorragia intraventricular. El 90 % de los casos se presenta dentro de los primeros 4 a 7 días; Se ha relacionado el uso de bicarbonato de sodio con su aparición. El propósito de este estudio fue determinar si el uso de bicarbonato en infusión continua, en las primeras 24 horas, aumenta el riesgo de hemorragia intraventricular. Métodos: cohorte retrospectiva, se revisaron 160 expedientes formándose 2 grupos: uno sin y otro con uso de bicarbonato. Posteriormente, el grupo con uso se dividió en dos: uso terapéutico y profiláctico. Resultados: Del total de los prematuros, 10 % presentaron hemorragia intraventricular, tenían un peso promedio de 1,500 g y una edad gestacional promedio de 31 semanas. La incidencia fue idéntica entre los grupos, aunque en el grupo con bicarbonato había pacientes más prematuros, y clínicamente más inestables. Se realizó una regresión logística donde se observó asociación entre la incidencia de hemorragia intraventricular y el peso al nacimiento (OR de 0.99); así como en el caso del uso de bicarbonato de sodio con una OR 1.22. Conclusiones: Nuestros datos indican la necesidad de evaluación sistemática del uso de bicarbonato, con el fin de determinar si los beneficios sobrepasan el riesgo de hemorragia intraventricular.

Effectiveness of intra-articular injections of sodium bicarbonate and calcium gluconate in the treatment of osteoarthritis of the knee: a randomized double-blind clinical trial.

BACKGROUND: A novel therapeutic management of osteoarthritis (OA) of the knee was assessed. The study aimed to evaluate the effect of monthly sodium bicarbonate with a single (SBCG1) or double dose (SBCG2) of calcium gluconate injections on OA of the knee; as well as the efficacy and safety of both SBCG interventions in the long term. METHODS: A double-blind parallel-group clinical trial with 74 knee OA patients was performed during 12 months, both SBCG interventions were followed-up for another 6mo after intervention. The outcome variables were the Western Ontario-McMaster University Osteoarthritis Index (WOMAC), the Lequesne's functional index and joint-space width changes from serial radiographs. RESULTS: After 12 months, group SBCG1 decreased -14.8 (95% CI:-14.2, -17.0) and group SBCG2 decreased -14.6 (-16.9, -12.4) in the global WOMAC score, the mean changes represent 80% and 82% lessened pain, respectively. In the Lequesne Functional Index scale, SBCG1 decreased -11.9 (-10.4, -14.2) and SBCG2 decreased -11.9 (-13.8, -10.0), representing 66 and 69% of improvement. Both mean scores were maintained after intervention discontinued. SBCG2 improved the knees' joint space width more than SBCG1 at 3 and 18 months. Both SBCG interventions were well tolerated after 12 months of treatment CONCLUSION: A solution of sodium bicarbonate and calcium gluconate is effective on reducing the symptoms associated with OA. Its beneficial effect is maintained for one year of continuous monthly administration and at least for 6 months after the administration is discontinued. When the dose of calcium gluconate is increased, it prevents further narrowing of joint-space. TRIAL REGISTRATION: Clinicaltrials.gov NCT00977444 September 11, 2009.

Additive effects of beta-alanine and sodium bicarbonate on upper-body intermittent performance.

We examined the isolated and combined effects of beta-alanine (BA) and sodium bicarbonate (SB) on high-intensity intermittent upper-body performance in judo and jiu-jitsu competitors. 37 athletes were assigned to one of four groups: (1) placebo (PL)+PL; (2) BA+PL; (3) PL+SB or (4) BA+SB. BA or dextrose (placebo) (6.4 g day⁻¹) was ingested for 4 weeks and 500 mg kg⁻¹ BM of SB or calcium carbonate (placebo) was ingested for 7 days during the 4th week. Before and after 4 weeks of supplementation, the athletes completed four 30-s upper-body Wingate tests, separated by 3 min. Blood lactate was determined at rest, immediately after and 5 min after the 4th exercise bout, with perceived exertion reported immediately after the 4th bout. BA and SB alone increased the total work done in +7 and 8 %, respectively. The co-ingestion resulted in an additive effect (+14 %, p < 0.05 vs. BA and SB alone). BA alone significantly improved mean power in the 2nd and 3rd bouts and tended to improve the 4th bout. SB alone significantly improved mean power in the 4th bout and tended to improve in the 2nd and 3rd bouts. BA+SB enhanced mean power in all four bouts. PL+PL did not elicit any alteration on mean and peak power. Post-exercise blood lactate increased with all treatments except with PL+PL. Only BA+SB resulted in lower ratings of perceived exertion (p = 0.05). Chronic BA and SB supplementation alone equally enhanced high-intensity intermittent upper-body performance in well-trained athletes. Combined BA and SB promoted a clear additive ergogenic effect.

Metabolic acidosis in childhood: why, when and how to treat.

OBJECTIVES: To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. SOURCES: Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. SUMMARY OF THE FINDINGS: There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies. CONCLUSIONS: Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease and the mechanisms generating metabolic acidemia. Other promising treatment alternatives have been proposed; however, the side effects and absence of controlled studies with pediatric populations translate into lack of evidence to support the routine use of such treatments.

Acidose metabólica na infância: por que, quando e como tratá-la? / Metabolic acidosis in childhood: why, when and how to treat

OBJETIVO: Apresentar uma revisão atualizada e crítica sobre os mecanismos das principais patologias associadas e o tratamento da acidose metabólica, discutindo aspectos controversos quanto aos benefícios e riscos da utilização do bicarbonato de sódio e outras formas de terapia. FONTES DOS DADOS: Revisão da literatura publicada, obtida através de busca eletrônica com as palavras-chave acidose metabólica, acidose láctica, cetoacidose diabética, ressuscitação cardiopulmonar, bicarbonato de sódio e terapêutica nas bases de dados PubMed/MEDLINE, LILACS e Cochrane Library, entre 1996 e 2006, além de publicações clássicas referentes ao tema, sendo selecionadas as mais atuais e representativas, buscando-se consensos e diretrizes. SíNTESE DOS DADOS: A utilização de bicarbonato de sódio não demonstra benefícios no quadro hemodinâmico, evolução clínica, morbidade e mortalidade nos quadros de acidose metabólica de anion gap elevado, relacionados à acidose láctica, cetoacidose diabética e ressuscitação cardiorrespiratória. Assim, a sua utilização rotineira não é indicada. Devem ser considerados os potenciais efeitos colaterais. O tratamento da doença de base é fundamental para reversão do processo. Outras terapias alternativas não demonstram efetividade comprovada em grande escala. CONCLUSÕES: Apesar dos efeitos conhecidos da acidemia em situações críticas no organismo, discute-se o papel protetor da acidemia nas células sob hipoxemia e os riscos da alcalemia secundária à intervenção medicamentosa. Existe consenso na reposição de álcalis e bicarbonato de sódio nos casos de acidose de anion gap normal; entretanto, nos casos de acidose de anion gap elevado, particularmente na acidose láctica, cetoacidose diabética e na ressuscitação cardiorrespiratória, o uso de bicarbonato de sódio não demonstra benefícios, além dos potenciais efeitos adversos, o que torna restrita sua indicação. Apesar da controvérsia, o único ponto concordante refere-se à abordagem...

OBJECTIVES: To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. SOURCES: Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. SUMMARY OF THE FINDINGS: There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies. CONCLUSIONS: Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease...

Paro circulatorio por fibrilación ventricular (2¬ parte): ¿Es posible la reanimación y la protección cerebral? / Circulatory arrest due to ventricular fibrillation (Part II): are brain reanimation and protection possible?

El manejo clínico del daño cerebral posterior a un paro circulatorio y reanimación cardiopulmonar puede dividirse en 2 etapas terapéuticas: la 1¬ etapa es la isquémica y corresponde a la suma del tiempo transcurrido hasta diagnosticar el paro circulatorio y el correspondiente a la reanimación cardíaca propiamente dicha, hasta la recuperación de la circulación espontánea; la 2¬ etapa es el período postisquémico que comienza una vez restaurada la perfusión cerebral espontánea. Ambas etapas son de fundamental importancia para la recuperación ad integrum del SNC. Pero mientras que en la etapa isquémica propiamente dicha, la eficacia del proceso de reanimación depende de los cuidados inmediatos brindados por los profesionales que atienden la emergencia, los procesos fisiopatológicos de la 2¬ etapa terapéutica son tan complejos y variados, como lo son las terapéuticas propuestas para tratar de resolver el intricado problema de la "reanimación" y de la "protección cerebral". En este resumen podemos afirmar sin temor a equivocarnos que, si bien se ha avanzado mucho en el conocimiento de los factores que llevan a la muerte cerebral, no se puede decir lo mismo respecto de las terapéuticas propuestas para evitarla o, por lo menos, para reducir la incidencia de las lesiones neurológicas residuales e irreversibles relacionadas con el proceso de reanimación cerebral. Mediante una lectura de la bibliografía especializada, el énfasis terapéutico aún está puesto en las medidas generales de preservación del metabolismo cerebral dentro de las precarias condiciones funcionales en las que se encuentra. El esquema básico propuesto por Grupta y Matta es el que está más al alcance de nuestra posibilidad de incidir en forma positiva sobre el pronóstico del paciente que ha sufrido una isquemia cerebral global como consecuencia de un paro circulatorio. (AU)

Paro circulatorio por fibrilación ventricular (1¬ parte) / Circulatory arrest due to ventricular fibrillation (Part I)

La velocidad y la amplitud de las ondas fibrilatorias son una expresión, en cierta manera, de las condiciones funcionales del miocardio y de su grado de oxigenación. Se reconocen tres tipos de ondas fibrilatorias. A) Fibrilación convulsiva o gruesa: con ondas fibrilatorias de alta frecuencia (>150/minuto y entre 0,5 y 1 mV de amplitud). Observando directamente al corazón, el órgano se sacude violentamente como si convulsivara. B) Fibrilación trémula o fina: la frecuencia sigue siendo alta (>100/minuto) pero de menor amplitud y las ondas recorren en forma anárquica la superficie de la pared ventricular. Esta fase es consecuencia del gran consumo de oxígeno de la fase anterior. Dura de 3 a 5 minutos. C) Fibrilación hipotónica o lenta: las ondas fibrilatorias son anchas, de baja amplitud y baja frecuencia. (>100/minuto), el corazón luce cianótico, dilatado e hipotónico. Puede durar entre 5 y 15 minutos hasta que el corazón para totalmente en asistolia. Un corazón globalmente hipóxico difícilmente se fibrile en forma espontánea. El corazón debe ser desfibrilado durante las fases de fibrilación rápida. La desfibrilación es un intento de despolarizar globalmente a todo el corazón mediante una descarga eléctrica, y con ello producir una asistolia de breve duración durante la cual el corazón tiene la oportunidad de reanudar su actividad normal a partir de la activación espontánea del marcapaso natural, es decir, el nodo sinusal, y arrancar con ritmo sinusal. Estudios anteriores con descargas de baja energía (175-200 joules para un adulto) no lograron demostrar beneficio alguno de choques iniciales inferiores a 2 j/kg y choques en rápida sucesión de 3 a 4 j/kg (apróximadamente 200 a 400 joules de energía). Según el protocolo de la American Heart Association, el paciente debe ser desfibrilado con dos primeros choques de 2 a 3 j/kg. en rápida sucesión. Y si éstos fracasan deberá recibir un tercero de 4 j/kg. Los tres choques deben hacerse en rápida sucesión (no todos los autores concuerdan con este criterio), sin intervención medicamentosa intermedia y sin levantar las paletas del lugar, para evitar modificaciones en la impedancia transtorácica y lesiones de la piel (eritema, edema) en otras regiones del tórax. En el texto se analiza también el efecto de los medicamentos habitualmente utilizados en la reanimación cardíaca, sus indicaciones e inconvenientes. (AU)

Paro circulatorio por fibrilación ventricular (1ª parte) / Circulatory arrest due to ventricular fibrillation (Part I)

La velocidad y la amplitud de las ondas fibrilatorias son una expresión, en cierta manera, de las condiciones funcionales del miocardio y de su grado de oxigenación. Se reconocen tres tipos de ondas fibrilatorias. A) Fibrilación convulsiva o gruesa: con ondas fibrilatorias de alta frecuencia (>150/minuto y entre 0,5 y 1 mV de amplitud). Observando directamente al corazón, el órgano se sacude violentamente como si convulsivara. B) Fibrilación trémula o fina: la frecuencia sigue siendo alta (>100/minuto) pero de menor amplitud y las ondas recorren en forma anárquica la superficie de la pared ventricular. Esta fase es consecuencia del gran consumo de oxígeno de la fase anterior. Dura de 3 a 5 minutos. C) Fibrilación hipotónica o lenta: las ondas fibrilatorias son anchas, de baja amplitud y baja frecuencia. (>100/minuto), el corazón luce cianótico, dilatado e hipotónico. Puede durar entre 5 y 15 minutos hasta que el corazón para totalmente en asistolia. Un corazón globalmente hipóxico difícilmente se fibrile en forma espontánea. El corazón debe ser desfibrilado durante las fases de fibrilación rápida. La desfibrilación es un intento de despolarizar globalmente a todo el corazón mediante una descarga eléctrica, y con ello producir una asistolia de breve duración durante la cual el corazón tiene la oportunidad de reanudar su actividad normal a partir de la activación espontánea del marcapaso natural, es decir, el nodo sinusal, y arrancar con ritmo sinusal. Estudios anteriores con descargas de baja energía (175-200 joules para un adulto) no lograron demostrar beneficio alguno de choques iniciales inferiores a 2 j/kg y choques en rápida sucesión de 3 a 4 j/kg (apróximadamente 200 a 400 joules de energía). Según el protocolo de la American Heart Association, el paciente debe ser desfibrilado con dos primeros choques de 2 a 3 j/kg. en rápida sucesión. Y si éstos fracasan deberá recibir un tercero de 4 j/kg. Los tres choques deben hacerse en rápida sucesión (no todos los autores concuerdan con este criterio), sin intervención medicamentosa intermedia y sin levantar las paletas del lugar, para evitar modificaciones en la impedancia transtorácica y lesiones de la piel (eritema, edema) en otras regiones del tórax. En el texto se analiza también el efecto de los medicamentos habitualmente utilizados en la reanimación cardíaca, sus indicaciones e inconvenientes.

Superfície radicular - instrumentaçäo manual, aplicaçäo do jato de bicarbonato de sódio e polimento. Análise em microscopia eletrônica de varredura / Root surface - manual instrumentation, use of air powder abrasive system and polishing. A scanning ellectron microscopy study

Este estudo teve como objetivo avaliar através da microscopia eletrônica de varredura o efeito do polimento com pastas de diferentes abrasividades, sobre superfície radiculares após instrumentaçäo manual associada a aplicaçäo do jato de bicarbonato de sódio. Utilizou-se 39 superfícies radiculares que foram divididas em 5 grupos: I controle (somente raspagem), II raspagem e aplicaçäo de jato de bicarbonato de sódio, III raspagem, aplicaçäo de jato de bicarbonato de sódio e polimento compasta de granulaçäo fina, IV raspagem, aplicaçäo de jato de bicarbonato de sódio e polimento com pasta de granulaçäo grossa e V raspagem, aplicaçäo de jato de bicarbonato de sódio e polimento com pasta de granulaçäo grossa seguida com pasta de granulaçäo fina. A raspagem foi realizada com curetas de Gracey n§ 5-6, com 40 movimentos de traçäo no sentido ápico-cervical e tanto o jato de bicarbonato de sódio como as pastas foram aplicadas por 10 segundos. Os grupos I, IV e V apresentaram graus intermediários de irregularidade de superfície, enquanto que o grupo II - maiores graus e o grupo III - menores graus...