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.
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.
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 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.
Respiratory acidosis and alkalosis are acid-base disorders caused by problems with ventilation.
Respiratory acidosis occurs when Paco2 is elevated due to conditions that decrease ventilation like lung disease or muscle fatigue. It causes a decrease in pH but HCO3 rises in compensation. Chronic respiratory acidosis is treated by gradually lowering Paco2.
Respiratory alkalosis is caused by excessive ventilation lowering Paco2, seen in anxiety, pain, or drug effects. It increases pH but HCO3 falls as the kidneys compensate. Severe acute respiratory alkalosis can reduce blood flow and cause arrhythmias.
Diabetes and various types have been discussed in detail as regard for Pg entrance and with various images, tables .....
Topics discussed: 1) introduction
2) types of diabetes
3) comp0lication of diabetes
4) DKA
5) NKHOC
6) Diabetic nephropathy
7) skin diseases in diabetes
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.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
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.
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.
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 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.
Respiratory acidosis and alkalosis are acid-base disorders caused by problems with ventilation.
Respiratory acidosis occurs when Paco2 is elevated due to conditions that decrease ventilation like lung disease or muscle fatigue. It causes a decrease in pH but HCO3 rises in compensation. Chronic respiratory acidosis is treated by gradually lowering Paco2.
Respiratory alkalosis is caused by excessive ventilation lowering Paco2, seen in anxiety, pain, or drug effects. It increases pH but HCO3 falls as the kidneys compensate. Severe acute respiratory alkalosis can reduce blood flow and cause arrhythmias.
Diabetes and various types have been discussed in detail as regard for Pg entrance and with various images, tables .....
Topics discussed: 1) introduction
2) types of diabetes
3) comp0lication of diabetes
4) DKA
5) NKHOC
6) Diabetic nephropathy
7) skin diseases in diabetes
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.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
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.
This document provides information on metabolic acidosis, including:
- Metabolic acidosis occurs when there is an excess of fixed or exogenous acids in the blood, accompanied by a drop in plasma bicarbonate concentration.
- It is classified based on calculations of anion gap, delta ratio, and osmolar gap. An increased anion gap suggests retained fixed acids while a normal anion gap acidosis involves bicarbonate loss.
- Causes include lactic acidosis, ketoacidosis, and renal tubular acidosis. Treatment involves identifying and treating the underlying cause while monitoring the patient and correcting fluid, electrolyte and pH imbalances.
Renal Tubular Acidosis is a condition characterized by a normal anion gap metabolic acidosis due to impaired kidney function. There are different types of RTA defined by the location of the defect in the kidney tubules. Type 1 RTA involves a defect in distal tubules resulting in decreased secretion of hydrogen ions and inability to maximally acidify urine. Patients experience metabolic acidosis, hypokalemia, nephrocalcinosis, and in some cases hearing loss or growth issues. Treatment focuses on correcting electrolyte abnormalities and metabolic acidosis with alkali solutions.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
Metabolic alkalosis is a condition where the pH of the blood is elevated beyond the normal range due to a higher than normal bicarbonate level. This can be caused by loss of hydrochloric acid through vomiting or diarrhea, or by excessive intake of bicarbonate. The kidneys compensate by retaining bicarbonate, leading to hypokalemia and hypocalcemia. Symptoms include confusion, seizures, and muscle cramps or weakness. The condition is diagnosed based on arterial blood gas values showing elevated pH and bicarbonate levels. Treatment focuses on replacing fluid and electrolyte losses and identifying the underlying cause.
The document discusses different types of metabolic acidosis, including non-anion gap metabolic acidosis (NAGMA) and renal tubular acidosis (RTA). It provides details on evaluating acid-base imbalances and determining if a metabolic acidosis is respiratory or metabolic. Causes of NAGMA include loss of bicarbonate from the GI tract or kidneys. Proximal and distal RTA can result from different defects in renal bicarbonate reabsorption and new bicarbonate production.
This document discusses metabolic acidosis and provides a systematic approach to diagnosis and treatment. Key points include:
1. Metabolic acidosis is defined by a primary reduction in serum bicarbonate and low blood pH. Common causes seen in practice include lactic acidosis, diabetic ketoacidosis, and acute kidney injury.
2. Evaluation involves assessing the anion gap, bicarbonate levels, electrolytes, and clinical context to determine the underlying etiology. Mixed disorders can occur.
3. Treatment focuses on correcting the primary cause. Bicarbonate therapy may be used in severe cases to raise the pH, but adverse effects are possible and the underlying condition still needs treatment.
Respiratory acidosis and alkalosis as well as metabolic acidosis and alkalosis are discussed.
The key points are:
- Respiratory acidosis is defined as increased PaCO2 and decreased pH due to inadequate alveolar ventilation. Metabolic acidosis is defined as decreased HCO3 and pH.
- Causes, clinical manifestations, and management strategies are outlined for each condition.
- Mixed acid-base disorders can occur, and compensatory mechanisms aim to return pH to normal levels through respiratory and renal responses.
- A structured approach is recommended to diagnose acid-base disorders based on blood gas results, including evaluating pH, PaCO2, HCO3, and anion
1. Chronic Kidney Disease (CKD) is defined as kidney damage or reduced kidney function lasting over 3 months as measured by GFR <60 mL/min/1.73m2 and/or albuminuria.
2. CKD is a major public health problem and leading cause of ESRD. Diabetes and hypertension are the leading causes of CKD.
3. The kidneys maintain homeostasis through filtration, reabsorption, secretion and other functions. Progressive loss of nephrons in CKD disrupts this balance and leads to physiological changes and clinical manifestations.
Acute Kidney Injury (AKI) is a common complication, affecting 5-7% of hospital admissions and 30% of intensive care unit patients. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Biomarkers like cystatin C and kidney injury molecule 1 can help detect AKI earlier than creatinine. Treatment involves fluid resuscitation, eliminating nephrotoxins, and renal replacement therapy for complications like electrolyte imbalances or uremia. Outcomes depend on the underlying cause, with pre-renal and post-renal AKI having a better prognosis than intrinsic renal injury.
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.
differences & indications of ringers (solution/buffered with lactate & acetate) Vs Normal saline in different medical conditions
Presented as lecture at 25th.July 2022
This document discusses various calculations used to diagnose and distinguish between different types of acid-base disorders, including anion gap, delta gap, urine anion gap, and osmolar gap. It provides detailed explanations of how to calculate each value and what they indicate. The anion gap is useful for determining the cause of metabolic acidosis. The delta gap can identify mixed acid-base disorders. A negative urine anion gap suggests GI bicarbonate loss while a positive value suggests renal tubular acidosis. An increased osmolar gap may indicate ethylene glycol or methanol poisoning in the setting of an unexplained metabolic acidosis.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and oxygen saturation. It outlines a 4 step method for ABG interpretation including identifying the primary disturbance, determining if it is respiratory or metabolic, and assessing for compensation. Several case examples are provided to demonstrate application of this analytical approach.
This document provides an overview of arterial blood gas analysis. It discusses the physiology of acid-base status including the basics of pH, acids, bases and buffers. The key buffers that help regulate acid-base balance are the bicarbonate buffer system and protein buffers. Respiratory regulation is also important as carbon dioxide production is a major factor influencing hydrogen ion concentration and pH. The kidneys play an important role in excretion of acids and bases to help maintain homeostasis.
Metabolic acidosis is a condition caused by a decrease in bicarbonate levels in the blood, resulting in an acidic pH. It can be divided into high anion gap metabolic acidosis, caused by an accumulation of organic acids in the blood, or normal anion gap metabolic acidosis, caused by loss of bicarbonate through diarrhea or kidney problems. The body has mechanisms to balance pH, such as moving hydrogen ions into cells or increasing respiration to exhale more carbon dioxide.
Acute Kidney Injury (AKI), also known as Acute Renal Failure, can be defined as an abrupt loss of kidney function over hours to days resulting in retention of waste products and electrolyte dysregulation. The document discusses the definition, epidemiology, classification, evaluation, and management of AKI. It provides details on the RIFLE and AKI Network classification systems. Common causes of AKI include acute tubular necrosis (ATN) due to ischemia, nephrotoxins, or endogenous factors. ATN is characterized by patchy necrosis of tubular epithelial cells and higher mortality is associated with more severe AKI and underlying comorbidities.
This document discusses acid-base disorders and ABG analysis. It defines acids and bases, describes the mechanisms that regulate acid-base balance, and classifies different types of acid-base imbalances including respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Causes, compensatory mechanisms, and treatments are provided for each type of imbalance. The document also covers ABG analysis, normal values, interpretation of results, and provides two sample problems to identify acid-base disturbances.
Dr. Samaresh Das provides an overview of arterial blood gas analysis including:
1. Alveolar ventilation and oxygenation are important gas exchange processes measured by arterial blood gases. High alveolar ventilation brings in fresh oxygen while low ventilation results in carbon dioxide retention.
2. An arterial blood gas analysis aids in diagnosis, treatment planning, and monitoring patients on ventilators. It provides important information about a patient's acid-base and electrolyte status.
3. A stepwise approach is used to analyze primary versus secondary acid-base disorders and determine if additional disorders are present based on relationships between pH, PCO2, and HCO3 levels.
This document provides information about hepatopulmonary syndrome (HPS). It defines HPS as the presence of liver disease, impaired oxygenation, and intrapulmonary vascular abnormalities. The pathophysiology involves widespread pulmonary vasodilatation leading to ventilation-perfusion mismatching and right-to-left shunting, causing hypoxemia. Clinical features include signs of liver disease in most patients and dyspnea in some. Diagnosis requires confirming the three criteria through tests like contrast echocardiography to detect intrapulmonary shunting.
Dr. Y. Krishna presented on arterial blood gas analysis. Key points include:
- ABG analysis provides pH, PaCO2, PaO2, HCO3, SaO2 and other values to assess acid-base status and ventilation.
- Primary acid-base disorders involve changes in PaCO2 or HCO3, while secondary involve compensatory changes. Acute vs chronic compensation affects HCO3 changes.
- Anion gap is used to determine if metabolic acidosis is due to organic acids or HCO3 loss. Delta gap identifies additional hidden processes.
- Common causes of acid-base imbalances include respiratory disorders like hypoventilation; and metabolic disorders like ketoacidosis
Here are the key points about assessing ventilation from an ABG:
- PaCO2 is used to assess ventilation. The normal range is 35-45 mmHg.
- A PaCO2 higher than 45 mmHg indicates respiratory acidosis from hypoventilation or obstruction.
- A PaCO2 lower than 35 mmHg indicates respiratory alkalosis from hyperventilation.
- The pH and HCO3- will be affected by changes in PaCO2 based on the type of respiratory problem (acidosis vs alkalosis). They move in opposite directions for respiratory issues.
- Compensation by the kidneys will cause the HCO3- to rise or fall in the same direction as PaCO
This document provides information on metabolic acidosis, including:
- Metabolic acidosis occurs when there is an excess of fixed or exogenous acids in the blood, accompanied by a drop in plasma bicarbonate concentration.
- It is classified based on calculations of anion gap, delta ratio, and osmolar gap. An increased anion gap suggests retained fixed acids while a normal anion gap acidosis involves bicarbonate loss.
- Causes include lactic acidosis, ketoacidosis, and renal tubular acidosis. Treatment involves identifying and treating the underlying cause while monitoring the patient and correcting fluid, electrolyte and pH imbalances.
Renal Tubular Acidosis is a condition characterized by a normal anion gap metabolic acidosis due to impaired kidney function. There are different types of RTA defined by the location of the defect in the kidney tubules. Type 1 RTA involves a defect in distal tubules resulting in decreased secretion of hydrogen ions and inability to maximally acidify urine. Patients experience metabolic acidosis, hypokalemia, nephrocalcinosis, and in some cases hearing loss or growth issues. Treatment focuses on correcting electrolyte abnormalities and metabolic acidosis with alkali solutions.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
Metabolic alkalosis is a condition where the pH of the blood is elevated beyond the normal range due to a higher than normal bicarbonate level. This can be caused by loss of hydrochloric acid through vomiting or diarrhea, or by excessive intake of bicarbonate. The kidneys compensate by retaining bicarbonate, leading to hypokalemia and hypocalcemia. Symptoms include confusion, seizures, and muscle cramps or weakness. The condition is diagnosed based on arterial blood gas values showing elevated pH and bicarbonate levels. Treatment focuses on replacing fluid and electrolyte losses and identifying the underlying cause.
The document discusses different types of metabolic acidosis, including non-anion gap metabolic acidosis (NAGMA) and renal tubular acidosis (RTA). It provides details on evaluating acid-base imbalances and determining if a metabolic acidosis is respiratory or metabolic. Causes of NAGMA include loss of bicarbonate from the GI tract or kidneys. Proximal and distal RTA can result from different defects in renal bicarbonate reabsorption and new bicarbonate production.
This document discusses metabolic acidosis and provides a systematic approach to diagnosis and treatment. Key points include:
1. Metabolic acidosis is defined by a primary reduction in serum bicarbonate and low blood pH. Common causes seen in practice include lactic acidosis, diabetic ketoacidosis, and acute kidney injury.
2. Evaluation involves assessing the anion gap, bicarbonate levels, electrolytes, and clinical context to determine the underlying etiology. Mixed disorders can occur.
3. Treatment focuses on correcting the primary cause. Bicarbonate therapy may be used in severe cases to raise the pH, but adverse effects are possible and the underlying condition still needs treatment.
Respiratory acidosis and alkalosis as well as metabolic acidosis and alkalosis are discussed.
The key points are:
- Respiratory acidosis is defined as increased PaCO2 and decreased pH due to inadequate alveolar ventilation. Metabolic acidosis is defined as decreased HCO3 and pH.
- Causes, clinical manifestations, and management strategies are outlined for each condition.
- Mixed acid-base disorders can occur, and compensatory mechanisms aim to return pH to normal levels through respiratory and renal responses.
- A structured approach is recommended to diagnose acid-base disorders based on blood gas results, including evaluating pH, PaCO2, HCO3, and anion
1. Chronic Kidney Disease (CKD) is defined as kidney damage or reduced kidney function lasting over 3 months as measured by GFR <60 mL/min/1.73m2 and/or albuminuria.
2. CKD is a major public health problem and leading cause of ESRD. Diabetes and hypertension are the leading causes of CKD.
3. The kidneys maintain homeostasis through filtration, reabsorption, secretion and other functions. Progressive loss of nephrons in CKD disrupts this balance and leads to physiological changes and clinical manifestations.
Acute Kidney Injury (AKI) is a common complication, affecting 5-7% of hospital admissions and 30% of intensive care unit patients. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Biomarkers like cystatin C and kidney injury molecule 1 can help detect AKI earlier than creatinine. Treatment involves fluid resuscitation, eliminating nephrotoxins, and renal replacement therapy for complications like electrolyte imbalances or uremia. Outcomes depend on the underlying cause, with pre-renal and post-renal AKI having a better prognosis than intrinsic renal injury.
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.
differences & indications of ringers (solution/buffered with lactate & acetate) Vs Normal saline in different medical conditions
Presented as lecture at 25th.July 2022
This document discusses various calculations used to diagnose and distinguish between different types of acid-base disorders, including anion gap, delta gap, urine anion gap, and osmolar gap. It provides detailed explanations of how to calculate each value and what they indicate. The anion gap is useful for determining the cause of metabolic acidosis. The delta gap can identify mixed acid-base disorders. A negative urine anion gap suggests GI bicarbonate loss while a positive value suggests renal tubular acidosis. An increased osmolar gap may indicate ethylene glycol or methanol poisoning in the setting of an unexplained metabolic acidosis.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and oxygen saturation. It outlines a 4 step method for ABG interpretation including identifying the primary disturbance, determining if it is respiratory or metabolic, and assessing for compensation. Several case examples are provided to demonstrate application of this analytical approach.
This document provides an overview of arterial blood gas analysis. It discusses the physiology of acid-base status including the basics of pH, acids, bases and buffers. The key buffers that help regulate acid-base balance are the bicarbonate buffer system and protein buffers. Respiratory regulation is also important as carbon dioxide production is a major factor influencing hydrogen ion concentration and pH. The kidneys play an important role in excretion of acids and bases to help maintain homeostasis.
Metabolic acidosis is a condition caused by a decrease in bicarbonate levels in the blood, resulting in an acidic pH. It can be divided into high anion gap metabolic acidosis, caused by an accumulation of organic acids in the blood, or normal anion gap metabolic acidosis, caused by loss of bicarbonate through diarrhea or kidney problems. The body has mechanisms to balance pH, such as moving hydrogen ions into cells or increasing respiration to exhale more carbon dioxide.
Acute Kidney Injury (AKI), also known as Acute Renal Failure, can be defined as an abrupt loss of kidney function over hours to days resulting in retention of waste products and electrolyte dysregulation. The document discusses the definition, epidemiology, classification, evaluation, and management of AKI. It provides details on the RIFLE and AKI Network classification systems. Common causes of AKI include acute tubular necrosis (ATN) due to ischemia, nephrotoxins, or endogenous factors. ATN is characterized by patchy necrosis of tubular epithelial cells and higher mortality is associated with more severe AKI and underlying comorbidities.
This document discusses acid-base disorders and ABG analysis. It defines acids and bases, describes the mechanisms that regulate acid-base balance, and classifies different types of acid-base imbalances including respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Causes, compensatory mechanisms, and treatments are provided for each type of imbalance. The document also covers ABG analysis, normal values, interpretation of results, and provides two sample problems to identify acid-base disturbances.
Dr. Samaresh Das provides an overview of arterial blood gas analysis including:
1. Alveolar ventilation and oxygenation are important gas exchange processes measured by arterial blood gases. High alveolar ventilation brings in fresh oxygen while low ventilation results in carbon dioxide retention.
2. An arterial blood gas analysis aids in diagnosis, treatment planning, and monitoring patients on ventilators. It provides important information about a patient's acid-base and electrolyte status.
3. A stepwise approach is used to analyze primary versus secondary acid-base disorders and determine if additional disorders are present based on relationships between pH, PCO2, and HCO3 levels.
This document provides information about hepatopulmonary syndrome (HPS). It defines HPS as the presence of liver disease, impaired oxygenation, and intrapulmonary vascular abnormalities. The pathophysiology involves widespread pulmonary vasodilatation leading to ventilation-perfusion mismatching and right-to-left shunting, causing hypoxemia. Clinical features include signs of liver disease in most patients and dyspnea in some. Diagnosis requires confirming the three criteria through tests like contrast echocardiography to detect intrapulmonary shunting.
Dr. Y. Krishna presented on arterial blood gas analysis. Key points include:
- ABG analysis provides pH, PaCO2, PaO2, HCO3, SaO2 and other values to assess acid-base status and ventilation.
- Primary acid-base disorders involve changes in PaCO2 or HCO3, while secondary involve compensatory changes. Acute vs chronic compensation affects HCO3 changes.
- Anion gap is used to determine if metabolic acidosis is due to organic acids or HCO3 loss. Delta gap identifies additional hidden processes.
- Common causes of acid-base imbalances include respiratory disorders like hypoventilation; and metabolic disorders like ketoacidosis
Here are the key points about assessing ventilation from an ABG:
- PaCO2 is used to assess ventilation. The normal range is 35-45 mmHg.
- A PaCO2 higher than 45 mmHg indicates respiratory acidosis from hypoventilation or obstruction.
- A PaCO2 lower than 35 mmHg indicates respiratory alkalosis from hyperventilation.
- The pH and HCO3- will be affected by changes in PaCO2 based on the type of respiratory problem (acidosis vs alkalosis). They move in opposite directions for respiratory issues.
- Compensation by the kidneys will cause the HCO3- to rise or fall in the same direction as PaCO
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 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.
This document provides an overview of acid-base balance and disorders. It discusses the major buffer system involving carbonic acid and bicarbonate, and how the lungs and kidneys work to maintain acid-base balance. Various acid-base disorders are described including their primary events, compensatory responses, and interpretations based on blood parameters such as bicarbonate, PCO2, and anion gap.
The document provides an overview of acid-base physiology and disorders, covering topics such as the carbonic acid buffer system, primary acid-base disorders including their causes and compensatory responses, and approaches for evaluating mixed acid-base disorders. It also reviews instrumentation and practical exercises for analyzing acid-base imbalances.
This document provides an overview of acid-base homeostasis and acid-base disorders. It discusses the key roles of the lungs, kidneys, and buffers in maintaining acid-base balance. The lungs regulate carbon dioxide levels through respiration. The kidneys regulate bicarbonate levels through reabsorption and new generation. Buffers function instantly to regulate pH. Acid-base disorders are classified as respiratory or metabolic based on underlying causes. Compensation mechanisms aim to restore pH. Clinical assessment involves analyzing blood gases, electrolytes, and calculating the anion gap. Case examples demonstrate applying this analysis to diagnose the acid-base disorder.
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.
acid base balance (5 steps in diagnosis)Zahoor Khan
The document discusses acid-base balance and how to determine if an abnormality is respiratory or metabolic based on pH, CO2, and HCO3 levels. It provides normal ranges for pH, CO2, and HCO3 and defines acidosis and alkalosis. It explains that if pH and CO2 match, the primary abnormality is respiratory, and if pH and HCO3 match, it is metabolic. Various scenarios are presented and determined to be respiratory or metabolic acidosis/alkalosis, or a primary problem with compensation. Complete compensation returns pH to normal.
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 respiratory and metabolic acidosis and alkalosis. It covers:
- The definitions and mechanisms of respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis.
- The causes, signs and symptoms, and compensation mechanisms for each condition.
- Specific types like acute vs chronic respiratory acidosis, and chloride responsive vs chloride resistant metabolic alkalosis.
- How the kidneys, lungs, and buffering systems work to regulate pH and compensate for acid-base imbalances.
This document provides a summary of acid-base physiology, including:
1) Homeostatic mechanisms that regulate acid-base balance, including chemical buffers, respiratory regulation, and renal regulation.
2) Definitions of acids, bases, and the pH scale. Acidosis and alkalosis can arise from excess or deficits of volatile or fixed acids.
3) Key concepts in acid-base regulation including the Henderson-Hasselbalch equation and analyzing arterial blood gases.
The document discusses acid-base balance and acid-base disorders. It describes three main systems that help maintain pH balance - buffers, the respiratory system, and the renal system. It explains how to interpret arterial blood gases by evaluating the pH, pCO2, HCO3, and other values to determine if a patient has respiratory or metabolic acidosis or alkalosis. Compensation by other systems is discussed when one system is imbalanced. Interpreting values and identifying primary vs compensated disorders is key to proper nursing care.
This document discusses acid-base balance and disorders. It begins by defining acids and bases, and describing the normal physiology of acid-base balance. It then discusses the four main types of acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. For each disorder it describes the primary disturbance (pH or HCO3-) and the secondary compensatory response. The document goes on to provide details on the causes, mechanisms, and clinical assessments of different metabolic and respiratory acid-base disorders.
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
This document provides information on arterial blood gas analysis, including contraindications for arterial puncture, reasons to order an ABG, normal values, equations, and approaches to interpreting ABG results. It discusses how to determine if a patient has acidosis or alkalosis, whether it is respiratory or metabolic, and if the compensation is adequate. It provides steps to classify the acid-base disorder, consider anion and osmolal gaps, and evaluate for mixed disorders. Causes and treatments of different acid-base imbalances are outlined.
This document discusses metabolic acidosis, a condition caused by excessive acid production or inadequate removal of acid from the body. It causes a low blood pH (below 7.35). Symptoms are non-specific but can include altered mental status and respiratory changes. Diagnosis involves blood gas analysis showing low bicarbonate and pH. The anion gap is used to classify types of metabolic acidosis as high, normal, or low. Treatment focuses on resolving the underlying cause while supporting organ function through respiratory and renal compensation mechanisms.
This document provides information about arterial blood gas (ABG) analysis, including what it is, its purpose, interpretation, and conditions it can assess like diabetic ketoacidosis (DKA). ABG measures oxygen, carbon dioxide, pH in blood and helps evaluate lung and kidney function in acid-base balance. It determines pH levels and the partial pressures of carbon dioxide and oxygen. The 6 steps to interpret ABGs are analyzing pH, pCO2, HCO3, matching acid-base disturbances, checking for compensation, and analyzing pO2 and oxygen saturation. DKA is a life-threatening complication of diabetes where lack of insulin causes ketone production from fat breakdown.
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.
This document provides an overview of acid-base balance and discusses the buffer systems, acid-base disorders, and how to analyze arterial blood gases (ABGs). It notes that the pH of blood is maintained between 7.35-7.45 through various buffer systems, including bicarbonate, proteins, phosphates, and bones. The main types of acid-base disorders - metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis - are explained. The document provides steps for ABG analysis, including determining the primary disturbance, expected compensation, calculating the anion gap and delta gap, and considering differential diagnoses. Common causes of each disorder are also listed.
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.
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.
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.
ABGs or VBGs interpretation made simple straight forward easy to remember and easy to apply. The presentation is designed to help the residents and junior ER physicians. The second part will discuss the oxygenation and the third part will review the "Stewart Approach" while fourth and last part is meant for the Experts.
This document outlines the steps for analyzing arterial blood gases (ABG) and diagnosing acid-base disorders. It discusses evaluating the pH, identifying the primary disorder as respiratory or metabolic based on pCO2 and bicarbonate levels, assessing compensation, calculating anion and delta gaps to identify hidden disorders, and providing examples of respiratory and metabolic acidosis/alkalosis causes. Five patient cases are presented and analyzed using these ABG analysis steps to diagnose complex, multi-component acid-base disorders.
This document provides information on blood gas analysis and acid-base disorders. It discusses the respiratory and renal compensatory mechanisms for regulating pH, defines different types of acid-base disorders, and outlines six steps for systematically evaluating acid-base status. Rules for assessing the compensatory responses in respiratory and metabolic acid-base disorders are presented. Mixed acid-base disorders and case examples are also covered.
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 provides information about arterial blood gas (ABG) analysis, including defining ABG, listing its components and normal values, discussing indications for the test, and interpreting abnormal values. It describes how ABG analysis can be used to evaluate respiratory and acid-base conditions and effectiveness of oxygen therapy. The document also outlines acid-base imbalances like respiratory acidosis and alkalosis and metabolic acidosis and alkalosis, and how the body compensates for these imbalances through respiratory and renal systems.
1. The pH is normal but HCO3 is high and PaCO2 is high, indicating a mixed picture.
2. The high PaCO2 suggests respiratory acidosis as the primary process (from COPD).
3. The high HCO3 indicates metabolic alkalosis as the secondary process (from vomiting losing hydrochloric acid).
3. This patient has a mixed acid-base disorder of respiratory acidosis combined with metabolic alkalosis.
1. The pH is normal but HCO3 is high and PaCO2 is high, indicating a mixed picture.
2. The high PaCO2 suggests respiratory acidosis as the primary process (from COPD).
3. The high HCO3 indicates metabolic alkalosis as the secondary process (from vomiting).
3. This patient has a mixed acid-base disorder of respiratory acidosis combined with metabolic alkalosis.
Dr. Dene W. Daugherty aims to decrease postoperative complications by accurately identifying risk factors for infection through wound classification. Wound classification predicts infection risk based on bacterial load at surgery, assisting surgeons in postoperative care. It categorizes wounds as clean (class I), clean-contaminated (class II), contaminated (class III), or dirty (class IV) based on degree of contamination, with infection risks of 2%, 5-15%, >15%, and >30% respectively. The classification should be documented after surgery to account for any events influencing wound status.
This document provides an overview of pulmonary function testing (PFT), including the components measured, indications for testing, interpretation of results, and clinical applications. It describes common PFT measurements like spirometry, lung volumes, diffusing capacity, and bronchoprovocation testing. Obstructive and restrictive patterns are discussed. The document also reviews indications for PFTs in diagnosis and prognosis of lung diseases and provides examples of PFT patterns in conditions like asthma, COPD, and interstitial lung disease.
The document summarizes venous disease, including the anatomy and physiology of the venous system, chronic venous insufficiency, varicose veins, superficial thrombophlebitis, deep vein thrombosis, inferior vena cava interruption, and pulmonary thromboembolism. Key points include:
1) The venous system returns blood to the heart against gravity using valves, the calf muscle pump, and other factors. Veins have thin walls and valves to allow changes in caliber.
2) Chronic venous insufficiency is caused by valve incompetence leading to increased venous pressure, edema, skin changes, and ulceration. Treatment includes compression, elevation, and surgery.
3) Deep vein thrombosis occurs
- A 60 year old smoker presented for a routine physical and was found to have an abnormality on chest x-ray
- The next appropriate test would be a CT scan of the chest with IV contrast to further characterize any lung lesions found on CXR
- A CT-guided biopsy would not be the next test, as further imaging is needed first to identify and stage any potential lung cancer before invasive testing
The best answer is A) CT chest with IV contrast to further evaluate and characterize any lung abnormalities found on CXR before considering an invasive biopsy.
This document provides information about hiatal hernias, including their types and causes. It discusses the clinical presentation of hiatal hernias and methods for diagnosis. Treatment options are medical management or surgical repair, with the surgical approach depending on the hernia type but generally aiming to reduce hernia contents and repair the diaphragmatic defect. Laparoscopic surgery is gaining popularity but may have a higher recurrence rate than open surgery. Outcomes are generally good, with relief of symptoms in most patients after surgical repair.
This document summarizes information about gastric neoplasms, including gastric adenocarcinoma and lymphoma. Some key points:
- Gastric adenocarcinoma incidence is highest in Japan and other Asian countries. Infection with H. pylori is a major risk factor. Premalignant lesions include hyperplastic and adenomatous polyps.
- Adenomatous polyps carry a 10-20% risk of developing carcinoma. Hyperplastic polyps have no neoplastic potential. Gastritis and pernicious anemia increase cancer risk.
- H. pylori infection increases cancer risk threefold. Cancer is staged based on tumor invasion and metastasis. Intestinal and
The document describes the anatomy and physiology of the esophagus. It details the different segments of the esophagus from the pharyngoesophageal junction to the gastroesophageal junction. Key structures like the lower esophageal sphincter are described. Motility disorders, diseases, cancers and treatments related to the esophagus are summarized. Evaluation methods for esophageal conditions are also outlined.
This document provides information on chest tube management including indications, contraindications, supplies needed for insertion, sizing, positioning, insertion technique, complications, nursing role, documentation, drainage system components, safety, exercise, pain management, dressing changes, and signs to monitor and report. The goal of chest tube placement is to drain fluid or air from the pleural space and re-expand the lung. Nursing plays a key role in monitoring the patient and drainage system.
This document discusses abdominal compartment syndrome, which occurs when intra-abdominal pressure increases due to fluid accumulation in the abdominal space from trauma, surgery, edema, or tumor growth. As pressure rises, blood flow to organs is compromised, which can lead to organ dysfunction or failure and death if left untreated. Early detection and treatment are important to prevent multiple organ failure. The document defines grades of intra-abdominal hypertension and abdominal compartment syndrome and discusses causes, pathophysiology, measurement, and impact on organ systems.
This document discusses bullet physics and traumatic injuries from gunshot wounds. It begins with an introduction to gunshot wound statistics and the different types of firearms. It then covers the physics of bullet trajectory, explaining the permanent and temporary cavities created. Various anatomical regions are discussed in terms of evaluation and management of gunshot wounds, including the head, neck, thorax, abdomen, genitals and extremities. Key points emphasized are the need for thorough examination, imaging, fluid resuscitation, antibiotics and surgery as appropriate for each region.
This document provides an overview of suturing techniques and knot tying. It discusses the history of suturing dating back to ancient Egypt, different suture materials and needles, wound healing processes, and various suturing techniques like simple interrupted, vertical mattress, and subcuticular stitches. It emphasizes the importance of mastering suturing skills like tying secure square knots using proper two-handed techniques to aid in wound healing and produce good cosmetic results.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
1. Acid and Base DisturbancesAcid and Base Disturbances
D. W. Daugherty, DOD. W. Daugherty, DO
SURGICAL CRITICAL CARESURGICAL CRITICAL CARE
2. Simple vs. MixedSimple vs. Mixed
• SimpleSimple
When compensation is appropriateWhen compensation is appropriate
• MixedMixed
When compensation is inappropriateWhen compensation is inappropriate
4. Stepwise ApproachesStepwise Approaches
History & physical examinationHistory & physical examination
Arterial blood gas for pH, pCOArterial blood gas for pH, pCO22, (HCO, (HCO33))
Use the HCOUse the HCO33 from ABG to determine compensationfrom ABG to determine compensation
Serum Na, K, Cl, COSerum Na, K, Cl, CO22 contentcontent
Use COUse CO22 content to calculate anion gapcontent to calculate anion gap
Calculate anion gapCalculate anion gap
Anion gap = {Na - (Cl + COAnion gap = {Na - (Cl + CO22 content)}content)}
Determine appropriate compensationDetermine appropriate compensation
Determine the primary causeDetermine the primary cause
8. CO2 content
Low Normal High
Metabolic acidosis Normal Metabolic
alkalosis
Resp alkalosis Mixed Resp acidosis
A normal CO2 content + high anion gap = metabolic acidosis +
Metabolic alkalosis or metabolic ac + compensatory respiratory ac.
9. Stepwise ApproachesStepwise Approaches
History & physical examinationHistory & physical examination
Arterial blood gas for pH, pCOArterial blood gas for pH, pCO22, (HCO, (HCO33))
Use the HCOUse the HCO33 from ABG to determine compensationfrom ABG to determine compensation
Serum Na, K, Cl, COSerum Na, K, Cl, CO22 contentcontent
Use COUse CO22 content to calculate anion gapcontent to calculate anion gap
Calculate anion gapCalculate anion gap
Anion gap = {Na - (Cl + COAnion gap = {Na - (Cl + CO22 content)}content)}
Determine appropriate compensationDetermine appropriate compensation
Determine the primary causeDetermine the primary cause
10. Stepwise ApproachesStepwise Approaches
History & physical examinationHistory & physical examination
Arterial blood gas for pH, pCOArterial blood gas for pH, pCO22, (HCO, (HCO33))
Use the HCOUse the HCO33 from ABG to determine compensationfrom ABG to determine compensation
Serum Na, K, Cl, COSerum Na, K, Cl, CO22 contentcontent
Use COUse CO22 content to calculate anion gapcontent to calculate anion gap
Calculate anion gapCalculate anion gap
Anion gap = {Na - (Cl + COAnion gap = {Na - (Cl + CO22 content)} (normal = 8-12)content)} (normal = 8-12)
Determine appropriate compensationDetermine appropriate compensation
Determine the primary causeDetermine the primary cause
11. Compensations for Metabolic DisturbancesCompensations for Metabolic Disturbances
• Metabolic acidosisMetabolic acidosis
pCOpCO22 = 1.5 x HCO= 1.5 x HCO33 + 8 (+ 8 ( ±± 2)2)
• Metabolic alkalosisMetabolic alkalosis
pCOpCO22 increases by 7 for every 10 mEq increaseincreases by 7 for every 10 mEq increase
in HCOin HCO33
12. How does the kidneyHow does the kidney
compensate for metaboliccompensate for metabolic
acidosis?acidosis?
13. How does the kidney compensate forHow does the kidney compensate for
metabolic acidosis?metabolic acidosis?
• By reabsorbing all filtered HCOBy reabsorbing all filtered HCO33
• By excreting HBy excreting H++
as NHas NH44
++
(and H(and H22POPO44
--
))
Urine pHUrine pH < 5.5< 5.5
Urine anion gap NegativeUrine anion gap Negative
14. Compensations for Respiratory AcidosisCompensations for Respiratory Acidosis
• Acute respiratory acidosisAcute respiratory acidosis
HCOHCO33 increases by 1 for every 10 increase inincreases by 1 for every 10 increase in
pCOpCO22
• Chronic respiratory acidosisChronic respiratory acidosis
HCOHCO33 increases by 3 for every 10 increase inincreases by 3 for every 10 increase in
pCOpCO22
15. Compensations for Respiratory AlkalosisCompensations for Respiratory Alkalosis
• Acute respiratory alkalosisAcute respiratory alkalosis
HCOHCO33 decreases by 2 for every 10 decrease indecreases by 2 for every 10 decrease in
pCOpCO22
• Chronic respiratory alkalosisChronic respiratory alkalosis
HCOHCO33 decreases by 4 for every 10 decrease indecreases by 4 for every 10 decrease in
pCOpCO22
16. Mixed Acid-Base DisordersMixed Acid-Base Disorders
• Mixed respiratory alkalosis & metabolicMixed respiratory alkalosis & metabolic
acidosisacidosis
ASA overdoseASA overdose
SepsisSepsis
Liver failureLiver failure
• Mixed respiratory acidosis & metabolicMixed respiratory acidosis & metabolic
alkalosisalkalosis
COPD with excessive use of diureticsCOPD with excessive use of diuretics
17. Mixed Acid-Base DisordersMixed Acid-Base Disorders
• Mixed respiratory acidosis & metabolicMixed respiratory acidosis & metabolic
acidosisacidosis
Cardiopulmonary arrestCardiopulmonary arrest
Severe pulmonary edemaSevere pulmonary edema
• Mixed high gap metabolic acidosis &Mixed high gap metabolic acidosis &
metabolic alkalosismetabolic alkalosis
Renal failure with vomitingRenal failure with vomiting
DKA with severe vomitingDKA with severe vomiting
18. Generation of Metabolic AcidosisGeneration of Metabolic Acidosis
H+
HCO
3
-
Exogenous acids
ASA
Toxic alcohol
Endogenous acids
ketoacids
DKA
starvation
alcoholic
Lactic acid
L-lactic
D-lactate
Administration of
HCl, NH4
+
Cl, CaCl2, lysine HCl
Loss of HCO3
diarrhea
Compensations
Buffers
Lungs
Kidneys
High gap Normal gap If kidney function is normal, urine anion gap Neg
19. H
HCO3
Loss of H+
from GI
Vomiting, NG suction
Congenital Cl diarrhea
Loss of H+
from kidney
1st
& 2nd
aldosterone
ACTH
Diuretics
Bartter’s, Gitelman’s, Liddle’s
Inhibition of β – OH steroid deh
Gain of HCO3
Administered HCO3,
Acetate, citrate, lactate
Plasma protein products
Compensations
Buffer
Respiratory
Forget the kidney
20. CASE 1CASE 1
A 24 year old diabetic was admitted for
weakness.
Na 140
K 1.8
Cl 125
CO2 6
Gap 9
pH 6.84 (H+
144)
pCO2 30
HCO3 5
21. Interpretation of Case 1Interpretation of Case 1
Patient has normal gapPatient has normal gap
metabolic acidosismetabolic acidosis
22. Interpretation of Case 1Interpretation of Case 1
• Next determine the appropriateness of respiratoryNext determine the appropriateness of respiratory
compensationcompensation
pCOpCO22 = 1.5 x HCO= 1.5 x HCO33 + 8 (+ 8 ( ±± 2)2)
pCOpCO22 = 1.5 x 5 + 8 + 2 = 17.5= 1.5 x 5 + 8 + 2 = 17.5
The patientThe patient’s pCO’s pCO22 is 30is 30
• The respiratory compensation is inappropriateThe respiratory compensation is inappropriate
23. Interpretation of Case 1Interpretation of Case 1
This patient has normal anion gap metabolicThis patient has normal anion gap metabolic
acidosis with inappropriate respiratoryacidosis with inappropriate respiratory
compensationcompensation
The finding does not fit DKA but isThe finding does not fit DKA but is
consistent with HCOconsistent with HCO33 loss from the GI tractloss from the GI tract
or kidneyor kidney
24. How do you differentiate aHow do you differentiate a
normal gap acidosis resultingnormal gap acidosis resulting
from GI HCOfrom GI HCO33 loss (diarrhea)loss (diarrhea)
vs RTA?vs RTA?
26. Case 2Case 2
A 26 year old woman, complains of weakness.
She denies vomiting or taking medications.
P.E. A thin woman with contracted ECF.
Na 133
K 3.1
Cl 90
CO2 32
Gap 11
pH 7.48 (H+
32) / pCO2 43 / HCO3 32.
UNa 52 / UK 50 / UCl 0 / UpH 8
27. Interpretation of Case 2Interpretation of Case 2
• Determine the appropriateness of respiratoryDetermine the appropriateness of respiratory
compensationcompensation
For every increase of HCOFor every increase of HCO33 by 1, pCOby 1, pCO22 shouldshould
increase by 0.7increase by 0.7
pCOpCO22 = 40 + (32-25) x 0.7 = 44.9= 40 + (32-25) x 0.7 = 44.9
The patientThe patient’’s pCOs pCO22 = 43= 43
28. Interpretation of Case 2Interpretation of Case 2
This patient has metabolic alkalosis withThis patient has metabolic alkalosis with
appropriate respiratory compensationappropriate respiratory compensation
29. Interpretation of Case 2Interpretation of Case 2
Urine NaUrine Na++
52, UK52, UK++
50, Cl50, Cl--
0, pH 80, pH 8
Urine pH = 8 suggests presence of large amountUrine pH = 8 suggests presence of large amount
of HCOof HCO33. The increased UNa and UK are to. The increased UNa and UK are to
accompany HCOaccompany HCO33 excretion. The kidneyexcretion. The kidney
conserves Clconserves Cl
The findings are consistent with loss of HClThe findings are consistent with loss of HCl
from the GI tractfrom the GI tract
Final diagnosis = Self-induced vomitingFinal diagnosis = Self-induced vomiting
30. Vomiting vs DiureticVomiting vs Diuretic
• Active vomitingActive vomiting
ECF depletionECF depletion
Metabolic alkalosisMetabolic alkalosis
High UNa, UK, low UClHigh UNa, UK, low UCl
Urine pH > 6.5Urine pH > 6.5
• Remote vomitingRemote vomiting
ECF depletionECF depletion
Metabolic alkalosisMetabolic alkalosis
Low UNa, high UK, lowLow UNa, high UK, low
ClCl
Urine pH 6Urine pH 6
• Active diureticActive diuretic
ECF depletionECF depletion
Metabolic alkalosisMetabolic alkalosis
High UNa, UK and ClHigh UNa, UK and Cl
Urine pH 5-5.5Urine pH 5-5.5
• Remote diureticRemote diuretic
ECF depletionECF depletion
Metabolic alkalosisMetabolic alkalosis
Low UNa, high UK, lowLow UNa, high UK, low
ClCl
Urine pH 5-6Urine pH 5-6
31. Case 3Case 3
A 40 year old man developed pleuritic chestA 40 year old man developed pleuritic chest
pain and hemoptysis. His BP 80/50.pain and hemoptysis. His BP 80/50.
pH 7.4pH 7.4
pCOpCO22 2525
HCOHCO33 1515
pOpO22 5050
32. Interpretation of Case 3Interpretation of Case 3
A normal pH suggests mixed disturbancesA normal pH suggests mixed disturbances
33. Interpretation of Case 3Interpretation of Case 3
His pCOHis pCO22 is 25, his HCOis 25, his HCO33 1515
If this is acute respiratory alkalosis his HCOIf this is acute respiratory alkalosis his HCO33
should have been 25-{(40-25) x 2/10}= 22should have been 25-{(40-25) x 2/10}= 22
If this is chronic respiratory alkalosis, his HCOIf this is chronic respiratory alkalosis, his HCO33
should have been 25 – {(40-25) x 4/10} = 19should have been 25 – {(40-25) x 4/10} = 19
If this is metabolic acidosis, his pCOIf this is metabolic acidosis, his pCO22 should haveshould have
been 1.5 x 15 + 8 = 30-31been 1.5 x 15 + 8 = 30-31
34. Interpretation of Case 3Interpretation of Case 3
He has combined respiratory alkalosis andHe has combined respiratory alkalosis and
metabolic acidosismetabolic acidosis
The likely diagnosis is pulmonary embolism withThe likely diagnosis is pulmonary embolism with
hypotension and lactic acidosis or pneumoniahypotension and lactic acidosis or pneumonia
with sepsis and lactic acidosiswith sepsis and lactic acidosis
Other conditions are ASA overdose, sepsis, liverOther conditions are ASA overdose, sepsis, liver
failurefailure
35. Case 4Case 4
A patient with COPD developed CHF. Prior toA patient with COPD developed CHF. Prior to
treatmenttreatment
pH 7.35pH 7.35
pCOpCO22 6060
HCOHCO33 3232
During treatment with diuretics he vomited a fewDuring treatment with diuretics he vomited a few
times. His pH after treatment wastimes. His pH after treatment was
pH7.42 / pCOpH7.42 / pCO22 80 / HCO80 / HCO33 4848
36. Interpretation of Case 4Interpretation of Case 4
PtPt’’s data pH 7.35, pCOs data pH 7.35, pCO22 60 and HCO60 and HCO33 3232
For acute respiratory acidosisFor acute respiratory acidosis
For every 10 mm elevation of pCOFor every 10 mm elevation of pCO22, HCO, HCO33 increases byincreases by
1, his HCO3 should have been 25 + (60-40) x 1/10 =1, his HCO3 should have been 25 + (60-40) x 1/10 =
2727
He did not have acute respiratory acidosisHe did not have acute respiratory acidosis
37. Interpretation of Case 4Interpretation of Case 4
PtPt’’s data pH 7.35, pCOs data pH 7.35, pCO22 60 and HCO60 and HCO33 3232
For chronic respiratory acidosisFor chronic respiratory acidosis
For every 10mm elevation of pCOFor every 10mm elevation of pCO22, HCO, HCO33 increases by 3increases by 3
His HCOHis HCO33 should have been 25 + (60-40) x 3/10 = 31should have been 25 + (60-40) x 3/10 = 31
His HCOHis HCO33 is 32is 32
He had well compensated chronic respiratoryHe had well compensated chronic respiratory
acidosisacidosis
38. Interpretation of Case 4Interpretation of Case 4
His pH is now 7.42, pCOHis pH is now 7.42, pCO22 80, HCO80, HCO33 4848
If pCOIf pCO22 of 80 is due to chronic respiratoryof 80 is due to chronic respiratory
acidosis, HCOacidosis, HCO33 should only be 32 +(80-60) xshould only be 32 +(80-60) x
3/10=38 and not 483/10=38 and not 48
He had combined metabolic alkalosis andHe had combined metabolic alkalosis and
respiratory acidosis after treatment of CHFrespiratory acidosis after treatment of CHF
39. Case 5Case 5
A cirrhotic patient was found to be confusedA cirrhotic patient was found to be confused..
Na 133Na 133
K 3.3K 3.3
Cl 115Cl 115
COCO22 1414
Gap 4Gap 4
pH 7.44 (HpH 7.44 (H++
36)36)
pCOpCO22 2020
HCOHCO33 1313
40. Interpretation of Case 5Interpretation of Case 5
Determine the respiratory compensationDetermine the respiratory compensation
For chronic respiratory alkalosis, every 10 reduction in pCOFor chronic respiratory alkalosis, every 10 reduction in pCO22,,
HCOHCO33 should decrease by 4should decrease by 4
HCOHCO33 should be 25 - (40-20) x 4/10=17should be 25 - (40-20) x 4/10=17
For acute respiratory alkalosis, HCOFor acute respiratory alkalosis, HCO33 = 21= 21
PatientPatient’’s HCO3 is 13, suggesting a metabolic acidotics HCO3 is 13, suggesting a metabolic acidotic
component is presentcomponent is present
Anion gap is 4, even corrected for low albumin, is still lowAnion gap is 4, even corrected for low albumin, is still low
suggesting a normal gap metabolic acidosissuggesting a normal gap metabolic acidosis
Patient had combined metabolic acidosis and respiratory alkalosisPatient had combined metabolic acidosis and respiratory alkalosis