This book explores important clinical problems in general nephrology, dialysis and transplantation, using a case-based approach. Together the 32 chapters form a comprehensive collection of clinical vignettes in renal medicine. Each chapter covers a separate clinical problem, posing multiple-choice questions and providing a detailed explanation for each. Clinical Pearls highlight the key issues. Each graded into three disctinct levels, to provide pertinent information tailored to the reader's knowledge level.
This document discusses acid-base homeostasis and disorders. It defines normal acid-base parameters and describes the body's response through buffering, lungs, and kidneys. It outlines the approach to evaluating acid-base disorders including initial assessment, acid-base diagnosis using arterial blood gases and electrolytes, identifying compensation, and formulating a diagnosis. Several examples are provided to demonstrate the systematic evaluation and diagnosis of mixed acid-base disorders.
Example 1 shows a metabolic acidosis with normal anion gap due to postoperative ulcerative colitis. Example 2 shows diabetic ketoacidosis with high anion gap metabolic acidosis and respiratory compensation. Example 3 shows a mixed picture of metabolic alkalosis from volume overload and respiratory acidosis. Example 4 shows mixed metabolic and respiratory acidosis in a patient with necrotizing fasciitis. Example 5 shows rhabdomyolysis with normal anion gap metabolic acidosis. Example 6 shows metabolic alkalosis from vomiting.
The document provides guidance on evaluating acid-base disorders by assessing whether there is a primary respiratory or metabolic component, determining if there is an anion gap and investigating compensatory responses. It outlines approaches for characterizing different types of acidosis and alkalosis based on pH, pCO2, HCO3 and anion gap measurements and urine anion gap.
Quantitative Acid Base Analysis Fencl Stewart Approachmcrohman
There are three main mechanisms by which the strong ion difference (SID) can change: 1) changing the water content of plasma through conditions like contraction alkalosis and dilutional acidosis, 2) changing the chloride level through hyperchloremic acidosis and hypochloremic alkalosis, and 3) increasing the concentration of unidentified anions through organic acidosis. The document then provides examples of how various fluid administrations can impact chloride levels and the SID, causing acid-base imbalances like hypchloremic alkalosis or acidosis. Treatment of elevated chloride and low SID would involve increasing the SID through sodium bicarbonate or sodium salts that contain a metabolizable anion like lact
This document provides an overview of acid-base disorders and their diagnosis and management. It discusses the regulation of acid-base balance and what arterial blood gases can reveal about a patient's condition. It then covers the diagnosis of acid-base disorders including sample handling and analysis. Key concepts around the Henderson-Hasselbalch equation and normal values are explained. The document breaks down simple and expected changes in various acid-base disorders. Case studies are presented and analyzed. Metabolic acidosis, alkalosis, respiratory compensation, and anion gaps are discussed in detail.
This document provides an overview of arterial blood gas interpretation, including the procedure for arterial blood gas sampling, the electrodes used to measure pH, PCO2, and PO2, and how to interpret arterial blood gas results based on acid-base homeostasis, buffers, respiratory regulation, and renal regulation. It describes how to systematically work through arterial blood gas reports to determine if there is acidemia or alkalemia, whether the primary disturbance is respiratory or metabolic, if compensation is adequate, and how to evaluate anion gap and identify mixed acid-base disorders.
This document discusses acid-base disturbances and the interpretation of arterial blood gases (ABGs). It covers various types of acid-base disorders including respiratory and metabolic acidosis and alkalosis. It provides guidance on evaluating an ABG report, including determining if there is acidosis or alkalosis based on pH, calculating anion gap, and using the Winter's formula to assess respiratory compensation. Examples of interpreting ABG results in patients with different clinical conditions are also provided.
This document discusses acid-base disturbances, including simple vs mixed disturbances, and how to approach and interpret acid-base abnormalities. It covers compensations for various metabolic and respiratory disturbances and how to determine the primary cause. Case examples are provided to demonstrate the approach and interpretation of acid-base status. The key steps are reviewing the history, ABG results including pH, pCO2, HCO3, and serum electrolytes. The appropriateness of compensation and causes such as respiratory, renal, gastrointestinal, or endocrine etiologies are considered.
This document discusses acid-base homeostasis and disorders. It defines normal acid-base parameters and describes the body's response through buffering, lungs, and kidneys. It outlines the approach to evaluating acid-base disorders including initial assessment, acid-base diagnosis using arterial blood gases and electrolytes, identifying compensation, and formulating a diagnosis. Several examples are provided to demonstrate the systematic evaluation and diagnosis of mixed acid-base disorders.
Example 1 shows a metabolic acidosis with normal anion gap due to postoperative ulcerative colitis. Example 2 shows diabetic ketoacidosis with high anion gap metabolic acidosis and respiratory compensation. Example 3 shows a mixed picture of metabolic alkalosis from volume overload and respiratory acidosis. Example 4 shows mixed metabolic and respiratory acidosis in a patient with necrotizing fasciitis. Example 5 shows rhabdomyolysis with normal anion gap metabolic acidosis. Example 6 shows metabolic alkalosis from vomiting.
The document provides guidance on evaluating acid-base disorders by assessing whether there is a primary respiratory or metabolic component, determining if there is an anion gap and investigating compensatory responses. It outlines approaches for characterizing different types of acidosis and alkalosis based on pH, pCO2, HCO3 and anion gap measurements and urine anion gap.
Quantitative Acid Base Analysis Fencl Stewart Approachmcrohman
There are three main mechanisms by which the strong ion difference (SID) can change: 1) changing the water content of plasma through conditions like contraction alkalosis and dilutional acidosis, 2) changing the chloride level through hyperchloremic acidosis and hypochloremic alkalosis, and 3) increasing the concentration of unidentified anions through organic acidosis. The document then provides examples of how various fluid administrations can impact chloride levels and the SID, causing acid-base imbalances like hypchloremic alkalosis or acidosis. Treatment of elevated chloride and low SID would involve increasing the SID through sodium bicarbonate or sodium salts that contain a metabolizable anion like lact
This document provides an overview of acid-base disorders and their diagnosis and management. It discusses the regulation of acid-base balance and what arterial blood gases can reveal about a patient's condition. It then covers the diagnosis of acid-base disorders including sample handling and analysis. Key concepts around the Henderson-Hasselbalch equation and normal values are explained. The document breaks down simple and expected changes in various acid-base disorders. Case studies are presented and analyzed. Metabolic acidosis, alkalosis, respiratory compensation, and anion gaps are discussed in detail.
This document provides an overview of arterial blood gas interpretation, including the procedure for arterial blood gas sampling, the electrodes used to measure pH, PCO2, and PO2, and how to interpret arterial blood gas results based on acid-base homeostasis, buffers, respiratory regulation, and renal regulation. It describes how to systematically work through arterial blood gas reports to determine if there is acidemia or alkalemia, whether the primary disturbance is respiratory or metabolic, if compensation is adequate, and how to evaluate anion gap and identify mixed acid-base disorders.
This document discusses acid-base disturbances and the interpretation of arterial blood gases (ABGs). It covers various types of acid-base disorders including respiratory and metabolic acidosis and alkalosis. It provides guidance on evaluating an ABG report, including determining if there is acidosis or alkalosis based on pH, calculating anion gap, and using the Winter's formula to assess respiratory compensation. Examples of interpreting ABG results in patients with different clinical conditions are also provided.
This document discusses acid-base disturbances, including simple vs mixed disturbances, and how to approach and interpret acid-base abnormalities. It covers compensations for various metabolic and respiratory disturbances and how to determine the primary cause. Case examples are provided to demonstrate the approach and interpretation of acid-base status. The key steps are reviewing the history, ABG results including pH, pCO2, HCO3, and serum electrolytes. The appropriateness of compensation and causes such as respiratory, renal, gastrointestinal, or endocrine etiologies are considered.
This document discusses acid-base disorders and presents three patient case studies. It provides the normal ranges for pH, pCO2, and HCO3 and outlines the six steps for acid-base analysis. The six steps are used to analyze each case study: a patient with metabolic acidosis and respiratory alkalosis, a patient with metabolic acidosis and metabolic alkalosis, and a patient with metabolic and respiratory acidosis. Causes are provided for different types of acid-base disturbances.
The document discusses acid-base regulation by the kidney. It does this through three main processes: 1) reabsorption of filtered bicarbonate in the proximal tubule, 2) secretion of hydrogen ions into the filtrate in the distal tubule, and 3) use of urinary buffers. It then provides detailed diagrams and explanations of the transport mechanisms involved in bicarbonate and hydrogen ion regulation throughout the renal tubular system. These include carbonic anhydrase, sodium-hydrogen antiporters, and the role of the collecting duct in final acid-base adjustments.
This document provides an overview of acid-base disorders. It defines different types of acid-base disorders based on pH, PCO2, and HCO3 levels. Primary acid-base disorders cause compensatory changes in PCO2 or HCO3 to maintain balance. Respiratory disorders involve changes in PCO2, while metabolic disorders involve changes in HCO3. Compensation occurs rapidly through breathing for metabolic disorders and slowly through the kidneys for respiratory disorders. Formulas are provided to assess acute vs chronic respiratory compensation and expected vs actual pH levels.
This document discusses the Stewart approach to acid-base disorders. It provides 3 key points:
1. The Stewart approach examines the independent variables that determine pH: the strong ion difference (SID), total weak acids (ATOT), and partial pressure of carbon dioxide (pCO2). Imbalances in these variables can lead to acid-base disorders.
2. Strong ions like sodium, chloride, and lactate influence pH through their effect on water dissociation. Increased sodium or lactate can increase SID and cause alkalosis, while increased chloride decreases SID and causes acidosis.
3. The presence of unmeasured anions can be detected using the Fencl-Stewart approach by
The document provides information on interpreting arterial blood gases (ABGs), including:
- A 6-step process for interpretation involving assessing pH, identifying the primary disorder as respiratory or metabolic, evaluating compensation, calculating anion gap, and considering differential diagnoses.
- Tables listing normal ranges for ABG components like pH, PaCO2, HCO3, and bases for common acid-base disorders.
- Explanations of key components like pH, partial pressure, base excess, bicarbonate, and their relationships in respiratory and metabolic acidosis/alkalosis.
- Causes and mechanisms of respiratory and metabolic acidosis and alkalosis are outlined.
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
This document discusses acid-base disorders and their physiology, evaluation, and treatment. It defines key terms like pH, acids, bases, and the four primary acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. For each disorder it describes the characteristics, pathophysiology, clinical features, and treatment approach. Primary investigations discussed include serum electrolytes, bicarbonate, PCO2, and anion gap to help evaluate the underlying cause and guide management.
This document discusses acid-base disorders and their physiology, regulation, and treatment. It begins by introducing acid-base balance and pH in the body. It then covers the chemical buffer systems that help regulate pH, as well as the roles of respiration and the kidneys. It discusses different types of acid-base disorders like metabolic acidosis and alkalosis, respiratory acidosis and alkalosis, and mixed disorders. Interpretation of blood gas analysis and various approaches for analyzing acid-base status are also outlined. Throughout, compensation mechanisms and typical treatment approaches for each disorder are described.
New models of acid-basebalance and their application to critical care nephro...Christos Argyropoulos
A short introduction to Stewart's model of acid-base disturbances. Modified from a talk I gave during a fellow's retreat back in 2006 in the beautiful Seven Spring's resort.
Will probably get excommunicated by the Nephrology Orthodoxy for endorsing Stewart's "heresy" :) but it is worth it!
Diagnosis and treatment of acid base disorders(1)aparna jayara
This document discusses the diagnosis and treatment of acid-base disorders. It begins by explaining the importance of precise pH regulation between 7.35-7.45 for cellular functions. Buffers help control free hydrogen ion concentration. Respiratory regulation controls PaCO2 through lung excretion of volatile acids, while renal regulation maintains plasma HCO3- concentration through kidney processes. Primary acid-base disorders are either metabolic, affecting HCO3-, or respiratory, affecting PaCO2. Expected compensatory responses occur but do not fully correct the primary disorder. Evaluation involves history, exam, basic labs, and arterial blood gas analysis to determine the primary disorder and characterize as acute or chronic.
This document discusses acid-base disorders and interpretation of arterial blood gases (ABGs). It defines acidosis and alkalosis, and describes respiratory and metabolic causes. Simple and mixed acid-base disorders are explained. Compensation by the lungs and kidneys in response to primary disorders is discussed. A stepwise approach to ABG interpretation is provided, including determining the primary disorder, checking for compensation, calculating the anion gap, and identifying specific etiologies. Characteristics of simple acid-base disturbances and combined disorders are summarized.
This document provides an overview of interpreting arterial blood gases (ABGs) and spirometry. It discusses the normal components of an ABG report and outlines a stepwise approach to solving acid-base disorders. The steps include assessing validity, determining if there is acidemia or alkalemia, identifying the primary disorder, assessing compensation, calculating the anion gap, and using the delta gap/ratio to diagnose combined disorders. Causes of metabolic acidosis, alkalosis, and normal anion gap acidosis are reviewed.
The document discusses metabolic acidosis, defining it as a primary decrease in bicarbonate with a compensatory decrease in PCO2. It notes the causes can include GI or renal bicarbonate loss, lactic acidosis, ketoacidosis from diabetes or alcohol, intoxication from ethylene glycol or methanol, and advanced renal failure. Metabolic acidosis is classified as having a normal or high anion gap, with high anion gap causes including ketoacidosis, lactic acidosis, and certain intoxications.
1. The patient has metabolic acidosis with a high anion gap and corrected anion gap, suggesting unmeasured anions like lactic acid.
2. Using the Stewart approach, the patient's strong ion difference (SID) is low, further indicating metabolic acidosis from unmeasured anions.
3. The base deficit gap is also high, quantifying the amount of unmeasured anions as lactate based on the blood level.
4. In summary, the patient has metabolic acidosis driven by lactic acidosis in the setting of septic shock and acute liver failure. Evaluation using different acid-base approaches consistently points to the same diagnosis.
Acid-base disorders occur when pH levels fall outside the normal range of 7.35-7.45. Precise pH regulation is vital for cellular functions and physiological processes. Buffers like bicarbonate help control hydrogen ion concentration. Disorders are classified as metabolic, affecting bicarbonate levels, or respiratory, affecting carbon dioxide levels. The kidneys and lungs work to compensate for changes and return pH to normal ranges through bicarbonate and carbon dioxide regulation. However, compensation cannot fully correct pH without also treating the underlying cause.
The document discusses acid-base balance and summarizes key concepts from traditional and modern physical-chemical approaches. It explains that the traditional view focused on hydrogen and bicarbonate ion concentrations, while the Stewart model emphasizes three independent variables: partial pressure of carbon dioxide, non-volatile weak acid concentration, and strong ion difference. The Stewart approach provides a more comprehensive understanding of factors influencing pH.
This document provides an overview of acid-base physiology, including:
- Definitions of acids, bases, and acid-base balance
- The three main systems that maintain pH balance: buffers, respiration, and renal
- The four basic types of acid-base imbalances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis
- Details on specific disorders like respiratory acidosis, metabolic acidosis, and mixed disorders
- Compensatory responses and interpretation of blood gas measurements
- Case studies on mixed disorders involving respiratory and metabolic components
In under 3 sentences, it summarizes key concepts in acid-base physiology and provides examples of interpreting acid-base imbalances.
El documento contiene varias preguntas y respuestas sobre funciones y fórmulas en Excel. Explica que Excel permite crear hojas de cálculo como parte de Microsoft Office y no es una característica independiente. También cubre que las filas y columnas se enumeran para facilitar el uso de hojas de cálculo, que las funciones comienzan con el signo "=", y que la función DIAS360() calcula el número de días entre dos fechas.
This document discusses acid-base disorders and presents three patient case studies. It provides the normal ranges for pH, pCO2, and HCO3 and outlines the six steps for acid-base analysis. The six steps are used to analyze each case study: a patient with metabolic acidosis and respiratory alkalosis, a patient with metabolic acidosis and metabolic alkalosis, and a patient with metabolic and respiratory acidosis. Causes are provided for different types of acid-base disturbances.
The document discusses acid-base regulation by the kidney. It does this through three main processes: 1) reabsorption of filtered bicarbonate in the proximal tubule, 2) secretion of hydrogen ions into the filtrate in the distal tubule, and 3) use of urinary buffers. It then provides detailed diagrams and explanations of the transport mechanisms involved in bicarbonate and hydrogen ion regulation throughout the renal tubular system. These include carbonic anhydrase, sodium-hydrogen antiporters, and the role of the collecting duct in final acid-base adjustments.
This document provides an overview of acid-base disorders. It defines different types of acid-base disorders based on pH, PCO2, and HCO3 levels. Primary acid-base disorders cause compensatory changes in PCO2 or HCO3 to maintain balance. Respiratory disorders involve changes in PCO2, while metabolic disorders involve changes in HCO3. Compensation occurs rapidly through breathing for metabolic disorders and slowly through the kidneys for respiratory disorders. Formulas are provided to assess acute vs chronic respiratory compensation and expected vs actual pH levels.
This document discusses the Stewart approach to acid-base disorders. It provides 3 key points:
1. The Stewart approach examines the independent variables that determine pH: the strong ion difference (SID), total weak acids (ATOT), and partial pressure of carbon dioxide (pCO2). Imbalances in these variables can lead to acid-base disorders.
2. Strong ions like sodium, chloride, and lactate influence pH through their effect on water dissociation. Increased sodium or lactate can increase SID and cause alkalosis, while increased chloride decreases SID and causes acidosis.
3. The presence of unmeasured anions can be detected using the Fencl-Stewart approach by
The document provides information on interpreting arterial blood gases (ABGs), including:
- A 6-step process for interpretation involving assessing pH, identifying the primary disorder as respiratory or metabolic, evaluating compensation, calculating anion gap, and considering differential diagnoses.
- Tables listing normal ranges for ABG components like pH, PaCO2, HCO3, and bases for common acid-base disorders.
- Explanations of key components like pH, partial pressure, base excess, bicarbonate, and their relationships in respiratory and metabolic acidosis/alkalosis.
- Causes and mechanisms of respiratory and metabolic acidosis and alkalosis are outlined.
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
This document discusses acid-base disorders and their physiology, evaluation, and treatment. It defines key terms like pH, acids, bases, and the four primary acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. For each disorder it describes the characteristics, pathophysiology, clinical features, and treatment approach. Primary investigations discussed include serum electrolytes, bicarbonate, PCO2, and anion gap to help evaluate the underlying cause and guide management.
This document discusses acid-base disorders and their physiology, regulation, and treatment. It begins by introducing acid-base balance and pH in the body. It then covers the chemical buffer systems that help regulate pH, as well as the roles of respiration and the kidneys. It discusses different types of acid-base disorders like metabolic acidosis and alkalosis, respiratory acidosis and alkalosis, and mixed disorders. Interpretation of blood gas analysis and various approaches for analyzing acid-base status are also outlined. Throughout, compensation mechanisms and typical treatment approaches for each disorder are described.
New models of acid-basebalance and their application to critical care nephro...Christos Argyropoulos
A short introduction to Stewart's model of acid-base disturbances. Modified from a talk I gave during a fellow's retreat back in 2006 in the beautiful Seven Spring's resort.
Will probably get excommunicated by the Nephrology Orthodoxy for endorsing Stewart's "heresy" :) but it is worth it!
Diagnosis and treatment of acid base disorders(1)aparna jayara
This document discusses the diagnosis and treatment of acid-base disorders. It begins by explaining the importance of precise pH regulation between 7.35-7.45 for cellular functions. Buffers help control free hydrogen ion concentration. Respiratory regulation controls PaCO2 through lung excretion of volatile acids, while renal regulation maintains plasma HCO3- concentration through kidney processes. Primary acid-base disorders are either metabolic, affecting HCO3-, or respiratory, affecting PaCO2. Expected compensatory responses occur but do not fully correct the primary disorder. Evaluation involves history, exam, basic labs, and arterial blood gas analysis to determine the primary disorder and characterize as acute or chronic.
This document discusses acid-base disorders and interpretation of arterial blood gases (ABGs). It defines acidosis and alkalosis, and describes respiratory and metabolic causes. Simple and mixed acid-base disorders are explained. Compensation by the lungs and kidneys in response to primary disorders is discussed. A stepwise approach to ABG interpretation is provided, including determining the primary disorder, checking for compensation, calculating the anion gap, and identifying specific etiologies. Characteristics of simple acid-base disturbances and combined disorders are summarized.
This document provides an overview of interpreting arterial blood gases (ABGs) and spirometry. It discusses the normal components of an ABG report and outlines a stepwise approach to solving acid-base disorders. The steps include assessing validity, determining if there is acidemia or alkalemia, identifying the primary disorder, assessing compensation, calculating the anion gap, and using the delta gap/ratio to diagnose combined disorders. Causes of metabolic acidosis, alkalosis, and normal anion gap acidosis are reviewed.
The document discusses metabolic acidosis, defining it as a primary decrease in bicarbonate with a compensatory decrease in PCO2. It notes the causes can include GI or renal bicarbonate loss, lactic acidosis, ketoacidosis from diabetes or alcohol, intoxication from ethylene glycol or methanol, and advanced renal failure. Metabolic acidosis is classified as having a normal or high anion gap, with high anion gap causes including ketoacidosis, lactic acidosis, and certain intoxications.
1. The patient has metabolic acidosis with a high anion gap and corrected anion gap, suggesting unmeasured anions like lactic acid.
2. Using the Stewart approach, the patient's strong ion difference (SID) is low, further indicating metabolic acidosis from unmeasured anions.
3. The base deficit gap is also high, quantifying the amount of unmeasured anions as lactate based on the blood level.
4. In summary, the patient has metabolic acidosis driven by lactic acidosis in the setting of septic shock and acute liver failure. Evaluation using different acid-base approaches consistently points to the same diagnosis.
Acid-base disorders occur when pH levels fall outside the normal range of 7.35-7.45. Precise pH regulation is vital for cellular functions and physiological processes. Buffers like bicarbonate help control hydrogen ion concentration. Disorders are classified as metabolic, affecting bicarbonate levels, or respiratory, affecting carbon dioxide levels. The kidneys and lungs work to compensate for changes and return pH to normal ranges through bicarbonate and carbon dioxide regulation. However, compensation cannot fully correct pH without also treating the underlying cause.
The document discusses acid-base balance and summarizes key concepts from traditional and modern physical-chemical approaches. It explains that the traditional view focused on hydrogen and bicarbonate ion concentrations, while the Stewart model emphasizes three independent variables: partial pressure of carbon dioxide, non-volatile weak acid concentration, and strong ion difference. The Stewart approach provides a more comprehensive understanding of factors influencing pH.
This document provides an overview of acid-base physiology, including:
- Definitions of acids, bases, and acid-base balance
- The three main systems that maintain pH balance: buffers, respiration, and renal
- The four basic types of acid-base imbalances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis
- Details on specific disorders like respiratory acidosis, metabolic acidosis, and mixed disorders
- Compensatory responses and interpretation of blood gas measurements
- Case studies on mixed disorders involving respiratory and metabolic components
In under 3 sentences, it summarizes key concepts in acid-base physiology and provides examples of interpreting acid-base imbalances.
El documento contiene varias preguntas y respuestas sobre funciones y fórmulas en Excel. Explica que Excel permite crear hojas de cálculo como parte de Microsoft Office y no es una característica independiente. También cubre que las filas y columnas se enumeran para facilitar el uso de hojas de cálculo, que las funciones comienzan con el signo "=", y que la función DIAS360() calcula el número de días entre dos fechas.
El olfato es uno de los cinco sentidos. Permite oler y distinguir diferentes aromas. El sentido del olfato es importante para actividades como la detección de alimentos, el reconocimiento social y la seguridad.
This document provides information about American food culture and popular tourist sites in the United States. It describes typical American breakfast, lunch, and dinner foods such as toast, cereal, eggs for breakfast and burgers, sandwiches, and soups for lunch and dinner. It also mentions mashed potatoes as a traditional American food. The document then discusses the World of Coca-Cola museum in Atlanta, describing its location, exhibits about the history and marketing of Coca-Cola over 100 years, and theaters that provide related experiences.
This document is a 3-page curriculum vitae for Hassan Nazmul Islam. It includes his personal details like name, address, contact information, nationality and date of birth. It outlines his relevant work experience including his current role as Secretary/Chief Executive Officer of Water&Essential and prior roles with Bangladesh National Women Lawyers Association and UNICEF Bangladesh. It also provides details of his education and training history as well as personal skills, languages, organizational experience, and technical skills.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
E-learning refers to the use of technology in learning and education. It includes various types of media like text, audio, video and interactive formats delivered through different technologies. E-learning can support traditional classroom subjects, act as a communication tool for knowledge exchange, be taught as its own subject, or be used for administrative purposes like education management systems. It can be self-paced and individualized using offline or online resources, or conducted synchronously or asynchronously in groups over intranets or the internet. While e-learning provides benefits like improved access and interactions, it also faces challenges like potential distractions, ease of cheating, and lack of direct feedback and social interaction.
La Directora de la Academia de Danzas Nacional e Internacional invita a la Profesora María Alejandra Urtado a una presentación de actos culturales de diferentes instituciones de varios municipios el 31 de octubre a las 3 pm en el Coliseo Atanasio Girardot. La presentación incluirá danzas tradicionales como Las Indias Caribes, Contradanza, El Bullerengue, Cumbias, El Mapale, El Fandango, El Garabato y El Cumbión representadas por municipios como El Peñol, Santa María, Argelia, Yarumal, San Ger
Magnetic tape and magnetic disks are common forms of secondary storage that allow data to be written and read from a storage medium. Magnetic tape provides sequential access to stored data while magnetic disks allow for direct and random access via disk drives and hard disks made up of spinning platters. Secondary storage interfaces with main memory and computers through peripherals like USB interfaces and modems that connect over telephone lines.
El documento describe un estudio que evaluó la utilidad de la procalcitonina y variables clínicas para diagnosticar neumonía en pacientes que acudieron a urgencias con falta de aire. El estudio incluyó 1641 pacientes de 15 centros internacionales y encontró que 155 (9.4%) tenían neumonía. Los niveles de procalcitonina pueden ofrecer información adicional para diagnosticar neumonía cuando hay incertidumbre clínica.
Este documento presenta un proyecto para crear una plataforma de aprendizaje y difusión de recursos educativos abiertos sobre matemáticas en la Escuela Secundaria 54 Mixta. El proyecto busca promover el intercambio de conocimientos entre docentes, alumnos y padres a través de redes sociales y herramientas digitales. La plataforma permitirá seleccionar, producir y compartir materiales sobre matemáticas y otras áreas con licencias abiertas.
This letter recommends Mr. Jad Abdo for graduate admission. The writer, who taught Mr. Abdo for three years, describes him as an insightful student who participated actively in class discussions and performed among the top 10% in his classes. A term paper Mr. Abdo wrote demonstrated his ability to independently analyze difficult problems and think creatively. The writer also attests that Mr. Abdo is well-liked, professional, and meets all deadlines. He concludes by strongly recommending Mr. Abdo as an excellent candidate who will contribute greatly to the admitting department's reputation.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
- The film writer Bob Gale revealed in an interview that the character Biff Tannen from Back to the Future Part II was based on Donald Trump.
- In the movie, Biff lives in a penthouse above a casino, similar to Trump's Plaza Hotel in New York.
- Both characters share similarities like their signature hairstyles and multiple marriages.
- The only thing the writers got wrong was not having Biff use Trump's signature insult of "loser" instead of calling people "buttheads".
Algunos avances tecnológicos importantes del año 2015 incluyen el Iphone6, Samsung Galaxy s6, Windows 10, Android 5.1.1 Lollipop y robots más avanzados. Otros hitos tecnológicos notables son el USB en 1996, Windows 8 en 2012 y las primeras tarjetas inteligentes en 1983.
La tuberculosis es una enfermedad infecciosa causada por el bacilo de Koch que afecta principalmente los pulmones y se transmite a través del aire cuando personas infectadas tosen o estornudan. Las personas con VIH/SIDA o con sistemas inmunitarios debilitados tienen un mayor riesgo de contraer la enfermedad. Los síntomas incluyen tos prolongada, dolor torácico, fiebre y pérdida de peso. Las medidas preventivas recomendadas son la vacunación BCG, el uso de mascarillas, la ventil
Avoid OSHA's Focus Four Fatal Workplace Hazards - an InfographicOsha .net
OSHA has identified the Focus Four fatal workplace hazards. Do you know what they are? And are you taking steps to avoid them? Find out all about them in our helpful infographic, and share it with coworkers to help raise awareness.
The document discusses the components of an arterial blood gas (ABG) test and how to interpret the results. An ABG measures pH, partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), bicarbonate (HCO3), and base excess (BE). The normal ranges for each component are provided. The effects of ABG collection errors on pH, PaCO2 and PaO2 values are outlined. A stepwise approach is described for interpreting ABG results which involves considering clinical clues, determining the primary acid-base disorder, checking the compensatory response, calculating anion and delta gaps, and identifying specific etiologies.
The document discusses various cases presenting with acid-base disturbances, analyzing each case to determine the underlying etiologies. Multiple cases involve combined metabolic and respiratory acid-base disorders, such as metabolic alkalosis from vomiting combined with respiratory alkalosis. The document examines diagnostic clues such as anion gaps, electrolyte levels, and clinical histories to deduce the specific causes in each complex case.
This document provides an overview of blood gas interpretation and acid-base physiology:
1) It discusses factors that can affect blood gas results like improper sampling technique and gives normal ranges for pH, PCO2, and HCO3.
2) Key concepts in acid-base physiology like the Henderson-Hasselbalch equation, bicarbonate buffering system, and renal regulation of bicarbonate are summarized.
3) The document outlines the pathophysiology and clinical effects of various acid-base disturbances like respiratory acidosis and metabolic alkalosis.
This document discusses acid-base balance and the anion gap. It contains the following key points:
1. The body strives for electrical neutrality by balancing cations and anions in the blood, and closely regulates hydrogen ion concentration.
2. The kidney plays an important role in regulating blood pH through reabsorption of bicarbonate and secretion of acids like ammonium and phosphate to balance the 4000 mmol of bicarbonate filtered daily.
3. Mixed acid-base disorders can be identified by calculating the bicarbonate gap, which should be zero for a single disorder but will vary if two disorders are present. This provides insight into the underlying condition(s).
This document defines and describes various acid-base disorders including metabolic and respiratory acidosis and alkalosis. It explains how the body normally buffers changes in blood pH and defines related terms like anion gap. Causes and treatments of different acid-base imbalances are outlined. Proper technique for obtaining arterial blood gas samples is also covered.
This document discusses arterial blood gas analysis and acid-base physiology. It provides indications for obtaining an ABG such as respiratory or metabolic disorders, hypoxia, shock, sepsis, and decreased cardiac output. It then defines the components of an ABG - pH, PaCO2, PaO2, HCO3, and base excess - and their normal ranges. It explains the Henderson-Hasselbalch equation and how the kidneys and respiratory system work to regulate pH levels and compensate for acid-base imbalances through bicarbonate and CO2 elimination. Various acid-base disorders like respiratory acidosis, metabolic acidosis, and mixed disorders are covered.
This document provides guidance on interpreting arterial blood gas (ABG) results through a 6-step process. It outlines normal ABG value ranges and defines acid-base disorders as respiratory or metabolic based on pH and PaCO2 relationship. Case studies are presented to demonstrate interpreting mixed or uncompensated disorders and determining appropriate interventions. The document is intended as an educational guide for healthcare professionals on systematically analyzing ABG results.
ABG interpret in critical care 16-1-2024Anwar Yusr
This document discusses arterial blood gas analysis and acid-base physiology. It provides indications for obtaining an ABG such as respiratory or metabolic disorders, hypoxia, shock, sepsis, and decreased cardiac output. It then defines the components of an ABG - pH, PaCO2, PaO2, HCO3, and base excess - and their normal ranges. It explains the Henderson-Hasselbalch equation and how the bicarbonate-carbonic acid buffer system regulates pH. Compensation by the respiratory and renal systems is described. Causes of metabolic acidosis and alkalosis are listed. The six step method for analyzing acid-base disorders is outlined.
The document provides an overview of arterial blood gas (ABG) analysis, including its objectives of assessing oxygenation and acid-base status, common sampling sites, factors that should be noted before performing an ABG, and how to properly analyze an ABG report to determine the primary acid-base disorder and any secondary responses or mixed disorders. It also discusses complications of heparin use, guidelines for interpreting ABG results using Henderson-Hasselbalch and other equations, and a stepwise approach to ABG analysis.
Acid base disorders, renal tubular acidosis &MoHa MmEd
This document discusses acid-base physiology and disorders. It begins by explaining how carbon dioxide and volatile and non-volatile acids are produced daily through metabolism. It then defines volatile and non-volatile acids. The document goes on to discuss various calculations used to interpret acid-base disorders, including anion gap, delta ratio, osmolal gap, and urine anion gap. It explains the causes and characteristics of metabolic acidosis and alkalosis, including mixed disorders. Throughout, it provides examples of how to approach and diagnose complex acid-base imbalances.
A pregnant woman presented with worsening nausea, vomiting and dehydration over 10 days. On examination, she was dehydrated with shallow breathing. Her arterial blood gas showed a pH of 7.45, PCO2 of 30 mmHg, HCO3 of 26 mEq/L, indicating a metabolic alkalosis due to vomiting and loss of hydrochloric acid leading to hypokalemia and hypochloremia. Compensation occurred through respiratory depression lowering PCO2.
This document provides information on interpreting arterial blood gas results to diagnose acid-base disorders. It discusses the four primary acid-base disorders: respiratory acidosis, metabolic acidosis, respiratory alkalosis, and metabolic alkalosis. Compensatory changes in response to these disorders are explained. The mechanisms by which the body controls acid-base balance through buffers, kidneys, and lungs are outlined. A stepwise approach to interpreting ABG results is provided to determine if there is acidemia/alkalemia, the primary disturbance, compensation, and high anion gap. Causes and characteristics of different acid-base disorders are described.
An arterial blood gas (ABG) test measures oxygen, carbon dioxide, acidity, oxygen saturation, and bicarbonate levels in arterial blood. It is used to identify acid-base disturbances, monitor respiratory and metabolic diseases, and assess responses to treatments. Contraindications include issues affecting the puncture site or coagulopathy. The test helps determine the primary acid-base disorder, presence of compensation, and if an anion gap exists.
This document discusses acid-base balance and acid-base disorders. It defines the anion gap and explains how to calculate it. It describes the causes and management of different types of acid-base disorders including metabolic acidosis, respiratory acidosis, metabolic alkalosis and respiratory alkalosis. Compensation mechanisms for each disorder are explained. Normal ranges for pH, HCO3, pCO2, pO2 and other electrolytes are provided. Multiple choice questions related to acid-base disorders are included at the end.
This document provides a 5-step approach to interpreting arterial blood gases (ABGs) and resolving acid-base imbalances:
1) Identify if the primary disorder is acidemia or alkalemia based on the pH.
2) Determine if the primary disorder is respiratory or metabolic based on pCO2 and HCO3 levels.
3) Assess the degree of compensation by the other system using formulas for different acid-base disturbances.
4) Calculate the anion gap to identify anion gap metabolic acidosis.
5) Use the "delta gap" to detect combined acid-base disorders or underlying alkalosis.
Work through examples of respiratory acidosis,
1. The document discusses acid-base imbalances and how to interpret arterial blood gases (ABGs).
2. It outlines the steps to analyze ABGs which include determining if there is acidemia or alkalemia, identifying if the disturbance is respiratory or metabolic, and assessing compensation.
3. Causes of different acid-base imbalances are provided such as respiratory acidosis resulting from airway obstruction or increased carbon dioxide production, and metabolic acidosis occurring in conditions like diabetic ketoacidosis or lactic acidosis.
Presentation by Dr. Mishal Saleem on Topic: Step wise approach to abgs interpretation.
Use of delta ratio and delta gap
Use of Anion Gap
Use of Urinary anion gap
1) The document discusses approaches to analyzing blood gases and acid-base disorders. It provides details on how the kidney regulates acid-base balance through bicarbonate reabsorption and secretion of hydrogen ions. Formulas for calculating compensation and identifying dominant acid-base disorders are presented.
2) Mechanisms of bicarbonate and hydrogen ion transport across renal tubular cells are illustrated through diagrams. Equations for calculating expected compensation in common acid-base imbalances are given to help identify the primary disorder.
3) Methods for evaluating systemic acid-base disorders are outlined, including using arterial blood gas results and serum electrolytes to identify
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Clinical Cases in Kidney Disease - sample chapter
1. 25
Case 2
Acid–base disturbance
DAVID HARRIS
LEVEL A
Case history
A 28-year-old woman is brought into the emergency department by her friends
who have noticed that for the past few days she has been confused, generally
weak and nauseated. She looks unwell. Her supine blood pressure is 90/60
mmHg. Her pulse is regular and rapid at >100 beats/min and she is afebrile.
She has moderate weakness affecting her upper and lower limbs and her
trunk. There are no focal neurological signs and examination of her abdomen,
chest and precordium is normal. The following arterial blood gas and serum
electrolyte results are obtained.
Laboratory data
Result Reference range
K+
1.9 mmol/L (3.2–5.5)
Na+
132 mmol/L (136–146)
Total CO2 8 mmol/L (24–31)
Cl–
113 mmol/L (94–107)
pH 7.10 (7.35–7.45)
PaO2 95 mmHg (95–100)
PaCO2 35 mmHg (35–45)
Question 1
Her arterial blood gas results can be explained by which of the following?
(a) Respiratory acidosis
(b) Severe metabolic acidosis with mild respiratory alkalosis
(c) Metabolic acidosis with adequate respiratory compensation
(d) Combined metabolic and respiratory acidosis
Answer
D
Harris Ch2.indd 25Harris Ch2.indd 25 13/11/07 11:48:52 AM13/11/07 11:48:52 AM
2. PART A FLUIDS AND ELECTROLYTES26A
Explanation
The patient is acidotic (pH 7.10). Partial pressure of both CO2 (PaCO2) and
serum bicarbonate (total CO2) are less than normal, indicating a metabolic
acidosis (answer A incorrect). With a pure respiratory acidosis, PaCO2 would
be elevated, as would serum bicarbonate in anything but an acute respiratory
acidosis (answer A incorrect). The respiratory compensation for a metabolic
acidosis is hyperventilation causing reduction in blood PaCO2. PaCO2 should fall
by 1 to 1.5 times the drop in serum bicarbonate which, with adequate respiratory
compensation in this case, would mean that PaCO2 should fall from the normal
value of 40 by 1 to 1.5 times (normal bicarbonate –8), or to between 16 and
24 mmHg. Another rule of thumb is that PaCO2 should fall to 100 times
(pH – 7.0) or in this case to 10 mmHg. Thus, her PaCO2 has not fallen sufficiently,
and so her respiratory compensation is inadequate (answer C incorrect). If she
had combined metabolic acidosis and respiratory alkalosis, her CO2 should have
been lower than predicted by the rules of thumb for metabolic acidosis with
adequate respiratory compensation (answer B incorrect). The alveolar–arterial
(A–a) gradient (FiO2 – PaO2 – PaCO2 × 1.2, which equals 13 in this case) is
normal, indicating that her alveolar gas exchange is normal and there is no
pulmonary disease. The hypoventilation in this case is probably due to muscle
weakness caused by hypokalaemia. Therefore, if this patient did not have any
metabolic acidosis, her respiratory acidosis would have been more obvious, and
her CO2 would have been higher than normal due to hypoventilation (despite a
near normal PaO2, which suggests her alveolar gas exchange is normal) (answer
D correct).
Clinical pearls
• In metabolic acidosis pH, PaCO2 and HCO3
–
(total CO2) should
all fall.
• The normal respiratory compensation for metabolic acidosis is
hyperventilation, causing a fall in PaCO2.
• PaCO2 should fall by 1 to 1.5 times the fall in serum bicarbonate.
• PaCO2 should approximate 100 times (pH – 7.0).
• A–a gradient will be normal (less than 15) with hypoventilation
and normal lungs.
• A–a gradient = FiO2 – PaO2 – PaCO2 ϫ 1.2.
Question 2
The plasma anion gap in this case is consistent with:
(a) addition of new anions to the body
(b) pre-pyloric gastrointestinal fluid loss
Harris Ch2.indd 26Harris Ch2.indd 26 13/11/07 11:48:53 AM13/11/07 11:48:53 AM
3. CASE 2 ACID–BASE DISTURBANCE 27 A
(c) impaired urinary acidification
(d) inhibition of carbonic anhydrase.
Answer
C and D
Explanation
The plasma anion gap is arbitrarily defined as the difference in plasma concen-
tration between the positive ions sodium and potassium and the negative ions
chloride and bicarbonate; most of the normal anion gap is comprised of the
negative charge on albumin (and so changes in albumin concentration will alter
the gap). The normal anion gap is less than 15. The anion gap in this case is 13.
(Note that some definitions of anion gap do not include potassium, in which
case the normal value would be lower.)
The most common causes of normal anion gap metabolic acidosis are loss of
bicarbonate from the gut (post-pyloric fluids which are alkaline, not pre-pyloric
which are acidic, so answer B is incorrect) and proximal (one example of many
is answer D) or distal (answer C correct) renal tubular acidosis.
Accumulation of new unmeasured anions in the plasma, giving rise to a
raised anion gap (e.g. with renal failure) occurs with addition of new acid from
exogenous sources (e.g. toxic alcohols, salicylate) or endogenously (e.g. lactic
acid, ketoacid) or failure of renal excretion of the anions of new acids (e.g. with
renal failure) (answer A incorrect). This is shown in Figure 2.1.
Figure 2.1 The anion gap in patients with normal acid–base balance, and those
with metabolic acidosis
Na+
ϩ
K+
Cl–
Na+
ϩ
K+
Cl–
Na+
ϩ
K+
Cl–
Na+
ϩ
K+
Cl–
UC
Normal High AG
metabolic adidosis
Normal AG
(hyperchloraemic)
UA UC UA UC UA
UC UA
HCO3
– HCO3
–
HCO3
–
HCO3
–
UC ϭ unmeasured cations
UA ϭ unmeasured anions
ϭ anion gap (AG) ϭ increased Cl concentration
Harris Ch2.indd 27Harris Ch2.indd 27 13/11/07 11:48:53 AM13/11/07 11:48:53 AM
4. PART A FLUIDS AND ELECTROLYTES28A
Clinical pearls
• Plasma anion gap = Na+
+ K+
– Cl–
– HCO3
–
, and is normally <15.
• Normal anion gap metabolic acidosis commonly arises due to
gastrointestinal bicarbonate loss or renal tubular acidosis.
• Hypokalaemia with metabolic alkalosis can occur in many
conditions, but when hypokalaemia coexists with metabolic acidosis,
the cause is usually either diarrhoea or renal tubular acidosis.
• Raised anion gap (>15) metabolic acidosis occurs due to addition
of new acid (with a non-chloride anion) or renal failure.
Question 3
The body’s defences against this acidosis include:
(a) buffering by intracellular proteins
(b) respiratory hypoventilation
(c) increased renal titratable acid production
(d) increased renal ammonium excretion.
Answer
A and D
Explanation
Intracellular and extracellular buffering occurs immediately. Extracellular buff-
ering is effected predominantly by HCO3
–
/CO2. While intracellular buffering
likewise involves HCO3
–
/CO2, it also involves proteins and phosphates (answer
A correct).
Asdiscussedpreviously,therespiratorycompensationisthatofhyperventilation,
not hypoventilation, to blow off acid in the form of CO2 (answer B incorrect).
The kidneys do not produce titratable acids (answer C incorrect); rather, they
filter certain ions (mainly phosphates) which titrate H+
in the tubular lumen, to
excrete a total of about 30 mmol per day.
Normalammoniaproductionandammoniumexcretionbythekidneyisabout
40 mmol per day, and in the case of acidosis this can increase to 200 mmol per day
or more (answer D correct). Ammonia is produced from glutamine enzymatically,
mainlyintheproximaltubularcell;becauseoftheneedtomakemoreenzyme,there
is a delay of several days before maximum ammoniagenesis can occur.
Clinical pearl
• Body defence against metabolic acidosis includes buffering,
hyperventilation and increased renal ammonia production.
Harris Ch2.indd 28Harris Ch2.indd 28 13/11/07 11:48:54 AM13/11/07 11:48:54 AM
5. CASE 2 ACID–BASE DISTURBANCE 29 A
Question 4
At this stage, treatment for this patient should include:
(a) artificial ventilation
(b) potassium replacement
(c) dialysis
(d) bicarbonate administration
(e) rehydration with normal saline.
Answer
B and E
Explanation
The patient’s potassium needs to be corrected to restore muscle power and
normal ventilation (answer B correct). The patient is relatively hypotensive; for
adequate intracellular buffering, normal tissue perfusion is required to remove
CO2 from the periphery to the lungs for exhalation. In the case of poor tissue
perfusion, CO2 accumulates within the cells, and so buffering instead involves
proteins (‘bad’ buffering) thereby possibly altering their structure and function.
Restoration of tissue perfusion with normal saline permits optimal intracellular
buffering (answer E correct).
Acidosis per se, of this severity, is not life-threatening and so there is no need
for immediate correction with bicarbonate; moreover, bicarbonate administration
may worsen hypokalaemia by driving potassium into cells (answer D incorrect).
Bicarbonate therapy could be used after potassium replacement, especially when
acidosis is severe. Artificial ventilation is not required at this stage because the
patient is not in frank respiratory failure (answer A incorrect). Dialysis would
correct the electrolyte abnormalities quickly, but so too would the simpler
measures of potassium replacement (to improve ventilation) and volume resto-
ration (to improve tissue buffering by delivering CO2 to the lungs). Moreover,
the normal plasma anion gap indicates that there are no new potentially toxic
unmeasured anions (of, for example, a toxic alcohol) to be removed by dialysis
(answer C incorrect).
Clinical pearl
• Emergencies in metabolic acidosis relate to associated derangement
of potassium, toxic alcohols and severity of acidosis.
Harris Ch2.indd 29Harris Ch2.indd 29 13/11/07 11:48:54 AM13/11/07 11:48:54 AM
6. PART A FLUIDS AND ELECTROLYTES30B
LEVEL B
Case history (continued)
Additional results are obtained on the patient. These include the following.
Plasma creatinine 110 μmol/L (60–125)
Plasma urea 15 mmol/L (2.5–6.5)
Plasma osmolality 295 mosm/kg (275–295)
Plasma glucose 6 mmol/L (3.6–7.7)
Urinary pH 6.0
Question 5
Based on these additional results, which of the following is/are likely to explain the
pathophysiology of the acidosis?
(a) Ingestion of toxic alcohol
(b) Diabetic ketoacidosis
(c) Rapid metabolism of a toxic alcohol with rapid excretion of its metabolites
(d) Rapid metabolism of a toxic alcohol without excretion of its metabolites
(e) Treatment with ethanol to inhibit metabolism of toxic alcohol
Answer
C
Explanation
Toxic alcohols such as methanol and ethylene glycol are osmotically active and
raise the serum osmolar gap. The osmolar gap is the difference between measured
and calculated osmolality. The main osmotically active substances in normal
serum are electrolytes, urea and glucose. Calculated osmolality is thus the sum
of Na+
+ K+
multiplied by two (to account for the accompanying negative ions)
plus glucose plus urea. Osmolar gap is normally <15 mosm/kg. The osmolar gap
in this case is 6 mosm/kg and so there is nothing to suggest additional osmotically
active agents (such as toxic alcohols) in the plasma (answer A incorrect). Toxic
alcohols are not acidic but are metabolised by alcohol and aldehyde dehydroge-
nase to form acidic metabolites that cause the acidosis and can be toxic. If the
toxic alcohol were rapidly metabolised, then the osmolar gap might be normal
but the anion gap should be raised due to the accumulation of metabolites (new
anions); the anion gap is normal in this case (answer D incorrect). However, if the
metabolites are rapidly excreted then both the osmolar and the anion gaps could
be normal as in this case (answer C correct). Diabetic ketoacidosis is most usually
associated with a raised anion gap, though occasionally the plasma anion gap in
Harris Ch2.indd 30Harris Ch2.indd 30 13/11/07 11:48:54 AM13/11/07 11:48:54 AM
7. CASE 2 ACID–BASE DISTURBANCE 31 B
diabetic ketoacidosis can be normal (answer B unlikely). During the recovery
phase of diabetic ketoacidosis, patients can develop a normal anion gap metabolic
acidosis by an intriguing mechanism. In the early phase of ketoacidosis, some
of the hydrogen of ketoacid is buffered by intracellular buffers and some of the
ketoanions are lost in urine. Treatment with saline and insulin converts available
ketoanions back to bicarbonate. Some of the newly generated bicarbonate is used
to replenish the intracellular buffer so that plasma bicarbonate does not return
to normal. Since ketoanions have already been lost in urine, a normal anion gap
acidosis results. Treatment with ethanol prevents the metabolism of the alcohol
to acidic metabolites and so the osmolar gap should be raised but the anion gap
should be normal (answer E incorrect).
Clinical pearls
• Plasma osmolar gap is the difference between measured and
calculated osmolality. Calculated osmolality is 2(Na+
+ K+
) +
glucose + urea (all in mmol/L).
• The normal plasma osmolar gap is <15, as is the normal anion gap
and A–a gradient. (The magic gap number is 15!)
• Raised osmolar gap suggests toxic alcohols as the cause of
metabolic acidosis.
Question 6
In this case the urinary pH is 6.0. This can be explained by:
(a) bicarbonate wastage
(b) impaired secretion of hydrogen ions into the distal tubular lumen
(c) impaired sodium reabsorption in the distal nephron
(d) impaired potassium secretion in the distal nephron
(e) impaired ammoniagenesis
(f) superimposed metabolic alkalosis.
Answer
B and C
Explanation
The urinary pH is inappropriately high in this case. In proximal renal tubular
acidosis due to failure to reabsorb HCO3
–
appropriately in the proximal tubule (see
Fig. 2.2), urinary pH varies depending on the amount of HCO3
–
reaching the distal
tubule. If its concentration in plasma and therefore glomerular filtrate is low, then
despite the defect sufficient HCO3
–
may be reabsorbed in the proximal tubule to
preventthelessimportantunimpaireddistaltubularHCO3
–
reabsorption(normally
Harris Ch2.indd 31Harris Ch2.indd 31 13/11/07 11:48:54 AM13/11/07 11:48:54 AM
8. PART A FLUIDS AND ELECTROLYTES32B
15% of total HCO3
–
reabsorption) being overwhelmed, thus resulting in no urinary
bicarbonate wastage and a low urinary pH. However, if sufficient HCO3
–
leaves the
proximal tubule (if the filtered HCO3
–
is high) then urinary HCO3
–
wastage will
occur, to buffer H+
secreted into the distal tubule lumen and raise urinary pH. In
this case, plasma HCO3
–
is low and so there should be no HCO3
–
wastage, even in
the case of proximal renal tubular acidosis (answer A incorrect).
Impaired Na+
reabsorption by the principal cells of the distal tubule causes type
4 (distal) renal tubular acidosis because the resultant increased Na+
concentration
in the distal tubule lumen raises luminal positive charge, thus impairing secretion
of positively charged ions (H+
and K+
) into the distal tubular lumen (answer C cor-
rect), as seen in Figure 2.3 (a). The impaired secretion of K+
is thus a consequence
of impaired Na+
reabsorption (answer D incorrect) and results in hyperkalaemia
which is typical of type 4 (but not type 1) renal tubular acidosis. Type 1 (distal)
renal tubular acidosis occurs due to a defect in the H+
secretion by intercalated cells
(answer B correct), as shown in Figure 2.3 (b). The low luminal H+
concentration
in distal renal tubular acidosis reduces formation of ammonium (NH4
+
) from
ammonia (NH3) and therefore NH4
+
excretion. In normal kidneys during the acute
phase of acidosis, urinary pH would be expected to be 5. However, during chronic
acidosis there is time for increased ammoniagenesis and (after buffering of NH3 by
Lumen Blood
Na+
H+ ATPase
AQP-1
NHE3
H+
CA IV CA II
Filtered
HCO3 + H+ 3 HCO3
-
NBCe1-A
Sensors
Proximal tubule
AQP = aquaporin channel
CA = carbonic anhydrase (isotopes II and IV)
NBCe1-A = electrogenic sodium bicarbonate
co-transporter
NHE3 = sodium hydrogen exchanger (isotope 3)
HCO3
CO2
Na+
H2CO3H2CO3
H2O + CO2 CO2 + H2O
Figure 2.2 Disturbances in H+
secretion and/or HCO3
–
reclamation by the proximal
tubule cell lead to proximal renal tubular acidosis
Harris Ch2.indd 32Harris Ch2.indd 32 14/11/07 3:15:16 PM14/11/07 3:15:16 PM
9. CASE 2 ACID–BASE DISTURBANCE 33 B
H+
to form NH4
+
) increased luminal NH4
+
and reduced H+
concentration, and so
urinary pH may rise. Therefore, impaired ammoniagenesis is unlikely to increase
urinary pH (answer E incorrect). In summary, urinary pH is somewhat difficult
to interpret and depends not only on H+
secretion but also the amount of buffer
(bicarbonate, ammonia) reaching the distal tubule.
ATP
ATP
Lumen
Cortical collecting duct
Na+
3Na+
2K
+
K
+
Cl-
H
+
Cl-
HCO3
-
Blood
principal cell
site of defect
in RTA type 1
intercalated cell
–
**
ATP
ATP
Lumen
(a)
(b)
Cortical collecting duct
Na+
3Na+
2K
+
K
+
Cl-
H
+
Cl-
HCO3
-
Blood
principal cell
site of defect
in RTA type 4
intercalated cell
–
**
Figure 2.3 (a) Type 4 (distal) renal tubular acidosis occurs due to a defect in Na+
reabsorption by principal cells. (b) Type 1 (distal) renal tubular acidosis
occurs due to a defect in H+
secretion by intercalated cells
Harris Ch2.indd 33Harris Ch2.indd 33 13/11/07 11:48:56 AM13/11/07 11:48:56 AM
10. PART A FLUIDS AND ELECTROLYTES34C
Mixed acid–base disturbances can be difficult to appreciate. One hint that
there might be a superimposed metabolic alkalosis is when the level of serum
bicarbonate is not as low as might be expected for the accumulated new anions
(whose concentration is equivalent to calculated minus normal anion gap). Here,
anion gap is normal and so there is no accumulation of new anions (answer F
incorrect).
Clinical pearls
• Urinary pH 5 excludes distal renal tubular acidosis; higher urinary
pHs are not diagnostically useful.
• Urinary tract infections with urea splitting organisms can produce
a high urine pH and should be excluded prior to attributing the
high urine pH to renal tubular acidosis.
• Distal renal tubular acidosis can arise due to a primary defect in
H+
secretion or to increased permeability of luminal cell membrane
allowing back-diffusion of H+
, or can be secondary to reduced
distal tubular Na+
reabsorption causing a high luminal positive
charge which opposes H+
secretion.
• Impaired distal sodium delivery due to volume depletion leads
to distal acidification defect; therefore urine pH >5 should not
be considered suggestive of renal tubular acidosis when urinary
sodium is <25 mmol/L.
LEVEL C
Case history continued ...
The patient has a normal anion gap and normal osmolar gap metabolic acidosis.
The diagnosis is still uncertain. Additional urinary results are received:
Na+
40 mmol/L
K+
35 mmol/L
Cl–
5 mmol/L
Creatinine 5000 μmol/L
Urea 80 mmol/L
Osmolality 510 mosm/kg
Glucose 0 mmol/L
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11. CASE 2 ACID–BASE DISTURBANCE 35 C
Question 7
True statements about urinary ammonium excretion include which of the
following?
(a) It can be measured directly.
(b) It can be easily calculated from the urinary anion gap.
(c) It can be best calculated from the urinary osmolar gap.
(d) If reduced, it is diagnostic of distal renal tubular acidosis.
Answer
A and C
Explanation
Urinary ammonia can be measured directly, but may be falsely elevated in the
presence of urea-splitting micro-organisms (answer A correct).
Under some circumstances, urinary ammonium can be calculated from
the urinary anion gap. The concept of using urinary anion gap to estimate
urinary ammonium excretion assumes that most of the ammonium is excreted
as ammonium chloride. The sum of the main urinary cations (Na+
, K+
, NH4
+
)
should equal the sum of the main anions (Cl–
, HCO3
–
, sulphate, phosphate) in the
absence of new ‘unmeasured’ anions. Except under conditions of HCO3
–
wastage,
urinary HCO3
–
should be very low. Normal sulphate and phosphate excretion
totals about 80 mEq/per day. Thus, in the absence of unmeasured anion, NH4
+
=
Cl–
+ 80 – Na+
– K+
(assuming one litre of urine output per day). However, in the
presence of unmeasured anions this equation will underestimate the concentra-
tion of ammonium (answer B incorrect). A negative urinary anion gap suggests
intact ammonia excretion, whereas a positive urinary anion gap may either be
because of deficient urinary ammonium excretion or because ammonium is
being excreted bound to an anion other than chloride. Therefore, the urinary
osmolar gap gives a more reliable estimation (answer C correct).
The equation for calculated urinary osmolality is the same as that for plasma,
with the addition of ammonium; that is, calculated Uosm = 2(Na+
+ K+
+ NH4
+
) +
glucose + urea. Rearranging this equation NH4
+
= 0.5 × (calculated Uosm – glucose
– urea – 2[Na+
+ K+
]). In the absence of uncharged osmotically active species in the
urine, calculated urinary osmolality should approximate measured urinary osmo-
lality. (An unmeasured anion would not alter the difference between measured and
calculated urinary osmolality, because anions are accounted for in the equation
by doubling the concentration of cations.) Using the calculated urinary osmolal-
ity equation, urinary NH4
+
in this case is 140 mmol/L, suggesting that adequate
urinary ammoniagenesis and ammonium excretion (which requires titration of
NH3 by secreted H+
) has occurred and excluding distal renal tubular acidosis.
Low ammonium excretion may occur not only due to reduced H+
secretion
(as with distal renal tubular acidosis) but also due to reduced ammoniagenesis, for
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12. PART A FLUIDS AND ELECTROLYTES36C
example with renal failure, and is therefore not diagnostic of the former (answer
D incorrect).
Clinical pearls
• When negative, urine anion gap is a good indicator of urinary
ammonium excretion but when positive, it can indicate either
reduced ammonium excretion or an unmeasured anion in urine.
• Urinary ammonium excretion can be calculated using the equation
for calculating urinary osmolality.
• Normal urinary ammonium excretion requires intact proximal
ammoniagenesis and distal H+
secretion.
Question 8
True statements about unmeasured urinary anion include which of the following?
In this patient, unmeasured urinary anion is:
(a) low due to poor renal excretion
(b) filtered but almost entirely reabsorbed
(c) filtered and secreted
(d) most likely lactate or ketoacid.
Answer
C
Explanation
Calculating ammonium from the urinary anion gap equation suggests a urinary
NH4
+
concentration of 10 mmol/L, but from the calculated osmolality equa-
tion it is 140 mmol/L. Either by solving these two equations simultaneously or
by simply looking at the difference, there must be 130 mmol/L (140 – 10) of
unmeasured anions in the urine. The plasma anion gap is normal and so there are
no unmeasured anions retained in the plasma as they are rapidly cleared by the
kidney (answer A incorrect). Renal handling of the anion is best determined by
its fractional excretion; or its clearance compared to that of creatinine. Clearance
is defined as UV/P, where U and P are the concentrations of the species in urine
and plasma respectively and V is the urine volume. Thus, fractional excretion of
an anion = (urinary anion/plasma anion) ϫ (plasma creatinine/urine creatinine)
ϫ 100. In this case, if one assumes plasma unmeasured anion is 1 mmol/L,
then fractional excretion of the anion is 286%. If the fractional excretion is
100% then the substance is filtered only with no net flux across the tubule, if
it is less than 100% there is impaired filtration or significant reabsorption or
if it is greater than 100% it is filtered and secreted. Thus, in this case the anion
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13. CASE 2 ACID–BASE DISTURBANCE 37 C
is filtered and secreted (answer B incorrect, answer C correct). L-lactate is
largely reabsorbed and fractional excretion is usually less than 5%; fractional
excretion of ketoacids and D-lactate is usually 20 to 80% (answer D incorrect).
Hippuric acid, which is a product of the metabolism of toluene, is filtered and
secreted and is most likely the unmeasured anion in this case. In other words,
the patient is a glue sniffer.
Clinical pearls
• Fractional excretion of unmeasured anions is useful in determining
their net handling by the kidney.
• Fractional excretion of 100% suggests filtration without
reabsorption or secretion; of less than 100% suggests reduced
filtration (e.g. large size or protein bound) or significant
reabsorption; of greater than 100% suggests filtration and
secretion.
Question 9
Which of the following can occur with metabolic acidosis of glue sniffing?
(a) Raised plasma anion gap
(b) Raised plasma osmolar gap
(c) Distal renal tubular acidosis
(d) Proximal renal tubular acidosis
(e) Endogenous acid production
Answer
A, C and E
Explanation
Toluene is metabolised in the liver to benzyl alcohol by the cytochrome P450
system, benzyl alcohol by alcohol dehydrogenase to benzidine, and benzidine
is oxidised to benzoic acid and conjugated with glycine to form hippuric acid.
This occurs rapidly within the liver and so plasma alcohol levels should not be
elevated and osmolar gap should be normal (answer B incorrect). The negatively
charged hippurate is excreted rapidly and drags with it Na+
and K+
, leading to
volume depletion and hypokalaemia. This can cause renal impairment (prerenal
azotaemia) which can cause a raised anion gap metabolic acidosis (as has been
reported in 10 to 20% of cases) (answer A correct). Distal renal tubular acidosis
probably only occurs in the minority of patients (answer C correct). The acidosis
is mainly due to the metabolism of toluene and the production of benzoic and
in particular hippuric acid (answer E correct).
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14. PART A FLUIDS AND ELECTROLYTES38C
Other hallmarks of toluene exposure include neuropsychiatric abnormali-
ties, gastrointestinal symptoms, muscle weakness and rhabdomyolysis (due to
hypokalaemia), hypophosphataemia and central hypothyroidism.
Bibliography
Level A
1. Field, M.J., Pollock, C.A. & Harris, D.C.H. (eds). (2001) Acid-base balance and
regulation of pH. The Renal System. Sydney: Church-Livingstone.
Level C
2. Carlisle. E.J.P., Donnelly, S.M., Vasuvattakul, S., Kamel, K.S., Tobe, S. & Halperin,
M.L. (1991) Glue sniffing and distal renal tubular acidosis: sticking to the facts.
J Am Soc Nephrol 1, pp. 1019–27.
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