RESUMO
Metabolic alkalosis is a unique acid-base disorder because it can be induced and sustained by functional alterations in renal ion transport. This review summarizes more than 50 years of research into the pathophysiologic processes causing this disorder. The evidence reviewed supports the hypothesis that virtually all forms of metabolic alkalosis are sustained by enhanced collecting duct hydrogen ion secretion, induced by stimulation of sodium uptake through the epithelial sodium channel (ENaC). Enhanced collecting duct hydrogen ion secretion in metabolic alkalosis occurs most commonly secondary to changes in ion transport earlier along the nephron, but also can occur as the result of primary stimulation of ENaC. In both these settings, potassium secretion is stimulated, and abnormal potassium losses cause depletion of body potassium stores. Potassium depletion has a key role in sustaining metabolic alkalosis by stimulating renal hydrogen ion secretion, enhancing renal ammonium production and excretion, and downregulating sodium reabsorption in the loop of Henle and early distal tubule. A new classification of the causes of metabolic alkalosis is proposed based on these pathophysiologic events rather than response to treatment.
Assuntos
Alcalose/fisiopatologia , Canais Epiteliais de Sódio/metabolismo , Transporte de Íons , Túbulos Renais Coletores/metabolismo , Aldosterona/fisiologia , Alcalose/classificação , Alcalose/etiologia , Cloretos/metabolismo , Diuréticos/farmacologia , Doenças Genéticas Inatas/metabolismo , ATPase Trocadora de Hidrogênio-Potássio/metabolismo , Humanos , Hidrogênio/metabolismo , Transporte de Íons/efeitos dos fármacos , Túbulos Renais Proximais/metabolismo , Proteínas de Membrana Transportadoras/metabolismo , Modelos Biológicos , Potássio/metabolismo , ATPases Translocadoras de Prótons/metabolismo , Sódio/metabolismo , Simportadores de Cloreto de Sódio/metabolismo , Trocadores de Sódio-Hidrogênio/metabolismo , Simportadores de Cloreto de Sódio-Potássio/metabolismo , Transportadores de SulfatoAssuntos
Acidose/diagnóstico , Alcalose/diagnóstico , Bicarbonatos/sangue , Equilíbrio Ácido-Base , Acidose/classificação , Acidose/etiologia , Alcalose/classificação , Alcalose/etiologia , Biomarcadores/sangue , Gasometria , Complicações do Diabetes , Diarreia/complicações , Humanos , Concentração de Íons de Hidrogênio , Hiperventilação/complicações , Doença Pulmonar Obstrutiva Crônica/complicações , Fibrose Pulmonar/complicações , Insuficiência Respiratória/complicações , Síndromes da Apneia do Sono/complicações , Uremia/complicações , Vômito/complicaçõesRESUMO
Inherited hypokalemic metabolic alkalosis, or Bartter syndrome, comprises several closely related disorders of renal tubular electrolyte transport. Recent advances in the field of molecular genetics have demonstrated that there are four genetically distinct abnormalities, which result from mutations in renal electrolyte transporters and channels. Neonatal Bartter syndrome affects neonates and is characterized by polyhydramnios, premature delivery, severe electrolyte derangements, growth retardation, and hypercalciuria leading to nephrocalcinosis. It may be caused by a mutation in the gene encoding the Na-K-2Cl cotransporter (NKCC2) or the outwardly rectifying potassium channel (ROMK), a regulator of NKCC2. Classic Bartter syndrome is due to a mutation in the gene encoding the chloride channel (CLCNKB), also a regulator of NKCC2, and typically presents in infancy or early childhood with failure to thrive. Nephrocalcinosis is typically absent despite hypercalciuria. The hypocalciuric, hypomagnesemic variant of Bartter syndrome (Gitelman syndrome), presents in early adulthood with predominantly musculoskeletal symptoms and is due to mutations in the gene encoding the Na-Cl cotransporter (NCCT). Even though our understanding of these disorders has been greatly advanced by these discoveries, the pathophysiology remains to be completely defined. Genotype-phenotype correlations among the four disorders are quite variable and continue to be studied. A comprehensive review of Bartter and Gitelman syndromes will be provided here.
Assuntos
Alcalose/genética , Síndrome de Bartter/genética , Hipopotassemia/genética , Canais de Potássio Corretores do Fluxo de Internalização , Receptores de Droga , Erros Inatos do Transporte Tubular Renal/genética , Simportadores , Alcalose/classificação , Alcalose/etiologia , Síndrome de Bartter/classificação , Síndrome de Bartter/etiologia , Proteínas de Transporte , Humanos , Hipopotassemia/classificação , Hipopotassemia/etiologia , Lactente , Recém-Nascido , Canais de Potássio/genética , Erros Inatos do Transporte Tubular Renal/classificação , Erros Inatos do Transporte Tubular Renal/etiologia , Simportadores de Cloreto de Sódio , Simportadores de Cloreto de Sódio-Potássio/genética , Membro 1 da Família 12 de Carreador de Soluto , Membro 3 da Família 12 de Carreador de Soluto , SíndromeRESUMO
The arterial blood gas (ABG) analysis, one of the most common tests ordered, provides clinicians with valuable information on a patient's oxygenation and acid-base balance. Interpreting ABG analysis results can be challenging, even for the most experienced practitioners, because it requires knowledge of the physiology and cause-and-effect relationship of the disturbances. Applying the principles and the ABG algorithm described in this article will provide nurses with a systematic way to interpret uncomplicated arterial blood gas results, including primary, mixed, and compensated acidbase disturbances.
Assuntos
Acidose/enfermagem , Algoritmos , Alcalose/enfermagem , Gasometria/enfermagem , Árvores de Decisões , Avaliação em Enfermagem/métodos , Acidose/sangue , Acidose/classificação , Acidose/etiologia , Alcalose/sangue , Alcalose/classificação , Alcalose/etiologia , Cuidados Críticos/métodos , Homeostase , HumanosAssuntos
Acidose , Alcalose , Complicações na Gravidez , Equilíbrio Ácido-Base , Acidose/sangue , Acidose/classificação , Acidose/etiologia , Acidose/fisiopatologia , Acidose/terapia , Alcalose/sangue , Alcalose/classificação , Alcalose/etiologia , Alcalose/fisiopatologia , Alcalose/terapia , Gasometria , Feminino , Humanos , Gravidez , Complicações na Gravidez/sangue , Complicações na Gravidez/classificação , Complicações na Gravidez/etiologia , Complicações na Gravidez/fisiopatologia , Complicações na Gravidez/terapiaRESUMO
The pathogenesis, classification, diagnosis and treatment of alkalosis are described. Alkalemia is defined as an elevation in the blood pH and alkalosis refers to processes that tend to raise the pH, and divided into two types; metabolic alkalosis (a primary increase in plasma HCO3- concentration) and respiratory alkalosis (a primary decrease in PCO2). These disorders are most frequently observed in the hospitalized patients. As the critically ill-patients with severe alkalemia are often associated with high mortality, treatment should be directed to the underlying diseases and severe alkalemia should be corrected promptly.
Assuntos
Alcalose/etiologia , Alcalose/classificação , Alcalose/diagnóstico , HumanosRESUMO
An ability to rapidly and effectively diagnose and treat acid-base disorders is essential to the management of seriously ill patients. In this paper an approach to the diagnosis of pure and mixed acid-base disorders is presented that is based upon an understanding of the bicarbonate buffer system and a knowledge of the well defined and predictable compensatory responses that occur in association with each of the primary acid-base disorders. With this approach a number of acid-base problems are presented and solved.