The document provides information on arterial blood gases (ABG), including the basics and interpretation of ABG results. It discusses key points such as the regulation of pH and factors involved in acid-base balance. Causes of acid-base disturbances like respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis are summarized. Technical aspects of ABG sampling and a stepwise approach to interpreting ABG results are also outlined in the document.
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 discusses metabolic alkalosis and presents a case of a 3-year-old female with recurrent episodes of quadriparesis. Laboratory investigations found hypokalemic metabolic alkalosis with increased urine chloride. This pattern is characteristic of Bartter syndrome, an autosomal recessive renal tubular disorder characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal blood pressure. The document further details the pathophysiology, classification, clinical features, biochemical markers, and treatment of Bartter syndrome. It emphasizes that hypokalemic metabolic alkalosis should not be overlooked in cases of unexplained paralysis or paresis in children.
This document discusses acid-base balance and disorders. It defines the anion gap and explains how it is calculated. Causes of increased or decreased anion gap are explained. Acid-base disorders are classified as simple or complex based on whether HCO3- or PCO2 is affected alone or together. The document outlines the primary event, compensation, and correction stages of acid-base disorders. Specific types of disorders discussed include respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Key lab findings and treatments are provided for each disorder type.
metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.
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.
Basics In Arterial Blood Gas Interpretationgueste36950a
This document provides guidelines for interpreting arterial blood gas results, including:
1. It describes how to summarize the acid-base and oxygenation status based on pH, PCO2, HCO3, PO2, and other values.
2. It outlines the steps to determine if a disturbance is respiratory or metabolic in nature, and whether it is acute or chronic.
3. Causes and compensation mechanisms for various acid-base imbalances like respiratory acidosis/alkalosis and metabolic acidosis/alkalosis are reviewed.
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.
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 discusses metabolic alkalosis and presents a case of a 3-year-old female with recurrent episodes of quadriparesis. Laboratory investigations found hypokalemic metabolic alkalosis with increased urine chloride. This pattern is characteristic of Bartter syndrome, an autosomal recessive renal tubular disorder characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal blood pressure. The document further details the pathophysiology, classification, clinical features, biochemical markers, and treatment of Bartter syndrome. It emphasizes that hypokalemic metabolic alkalosis should not be overlooked in cases of unexplained paralysis or paresis in children.
This document discusses acid-base balance and disorders. It defines the anion gap and explains how it is calculated. Causes of increased or decreased anion gap are explained. Acid-base disorders are classified as simple or complex based on whether HCO3- or PCO2 is affected alone or together. The document outlines the primary event, compensation, and correction stages of acid-base disorders. Specific types of disorders discussed include respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Key lab findings and treatments are provided for each disorder type.
metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.
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.
Basics In Arterial Blood Gas Interpretationgueste36950a
This document provides guidelines for interpreting arterial blood gas results, including:
1. It describes how to summarize the acid-base and oxygenation status based on pH, PCO2, HCO3, PO2, and other values.
2. It outlines the steps to determine if a disturbance is respiratory or metabolic in nature, and whether it is acute or chronic.
3. Causes and compensation mechanisms for various acid-base imbalances like respiratory acidosis/alkalosis and metabolic acidosis/alkalosis are reviewed.
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.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
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.
1. The document discusses acid-base balance and interpretation of arterial blood gases (ABGs). It covers definitions of pH, PCO2, and PO2 and their normal ranges.
2. Procedures for obtaining ABGs are outlined along with potential errors and complications.
3. A stepwise approach is provided for interpreting ABGs, identifying respiratory or metabolic acidosis or alkalosis and their underlying causes. Compensatory mechanisms are also addressed.
Metabolic alkalosis is a primary acid-base disturbance characterized by elevated serum bicarbonate and pH levels, along with increased PaCO2 levels. It can be caused by loss of stomach acid from vomiting or diarrhea, or by excessive intake of bicarbonate. The kidneys compensate by retaining bicarbonate, sodium, and chloride. Symptoms may include confusion, seizures, muscle cramps or weakness due to accompanying hypokalemia or hypocalcemia. Respiratory compensation occurs via hypoventilation and increased PaCO2 levels.
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.
Abg.2 Arterial blood gas analysis and example interpretationsamirelansary
This document provides an overview of different approaches to analyzing arterial blood gases (ABG), including the Copenhagen, Boston, and Stewart approaches. It discusses key parameters measured in an ABG such as pH, PaCO2, PaO2, HCO3, and oxygen saturation. The document also summarizes the steps involved in interpreting an ABG, including classifying acid-base disturbances as respiratory or metabolic, assessing compensation, and considering the anion gap in cases of metabolic acidosis.
Acid base abnormalities (causes and treatment)Vernon Pashi
This document provides an overview of acid-base abnormalities and their management. It defines key terms, outlines regulatory mechanisms like buffers and respiration, and describes different acid-base disorders including their causes and treatments. An example case is presented of a patient with metabolic and respiratory acidosis on admission, resolving to metabolic acidosis and respiratory alkalosis after treatment. Overall it reviews acid-base physiology and the approach to diagnosing and managing common acid-base imbalances.
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.
Short Review regarding Metabolic Acidosis
The Causes, anion gap,urine osmolal gap, Renal Tubular Acidosis, approach to Metabolic Acidosis in Final Slide
Lactic acidosis is defined as a serum lactate level greater than 5mmol/L accompanied by acidosis and a low serum pH. It occurs when lactate production exceeds utilization, commonly due to tissue hypoxia or impaired liver/kidney function. Management involves treating the underlying cause to restore oxygen delivery and lactate clearance. Bicarbonate therapy can raise the pH but risks hypercapnia and is not recommended in some cases. New therapies like dichloroacetate aim to increase lactate utilization but have not reduced mortality in clinical trials.
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.
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 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.
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
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 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 provides information on interpreting blood gas analysis (ABG). It discusses common errors in ABG sampling and outlines steps to analyze ABG results. Key points include checking if the pH indicates acidosis or alkalosis, identifying the primary disorder, assessing compensation, and calculating the anion and delta gaps to detect mixed disorders. Non-gap causes of acidosis are distinguished using urine anion gap. The document also covers expected changes in respiratory and metabolic acid-base disorders and differentials for specific conditions.
The document discusses the interpretation of arterial blood gas (ABG) results. It provides:
1) Normal ABG value ranges for pH, PaCO2, PaO2 and HCO3.
2) A 6-step process to interpret ABG results, including analyzing pH, PaCO2, HCO3 levels and their relationships.
3) Examples of how to determine if an acid-base imbalance is respiratory or metabolic based on changes in pH, PaCO2 and HCO3. Conditions like respiratory acidosis, alkalosis and mixed disorders are explained.
4) Factors that indicate an acid-base imbalance is compensated or uncompensated.
5) How
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 provides a summary of an arterial blood gas interpretation presentation. It discusses the objectives, procedure, and precautions for arterial blood gas sampling. It then covers the interpretation of oxygenation status and acid-base status using a six step approach. The six steps include determining if acidemia or alkalemia is present, if the primary disturbance is respiratory or metabolic, if a respiratory disorder is acute or chronic, if compensation is adequate, evaluating the anion gap if metabolic, and identifying the cause of a high anion gap metabolic acidosis.
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
Metabolic acidosis is caused by an excess production of acids or loss of bicarbonate in the body. It results in a primary decrease in blood pH (acidemia) with low bicarbonate levels. The kidneys compensate by retaining bicarbonate to raise the pH. Causes include diabetic ketoacidosis, lactic acidosis, renal tubular acidosis, diarrhea, and uremia. An increased anion gap metabolic acidosis occurs when unmeasured anions like ketones and lactate are produced in excess. The clinical features include respiratory changes like Kussmaul breathing, as well as neurological symptoms. Arterial blood gas analysis is used to diagnose and classify the type and
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
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.
1. The document discusses acid-base balance and interpretation of arterial blood gases (ABGs). It covers definitions of pH, PCO2, and PO2 and their normal ranges.
2. Procedures for obtaining ABGs are outlined along with potential errors and complications.
3. A stepwise approach is provided for interpreting ABGs, identifying respiratory or metabolic acidosis or alkalosis and their underlying causes. Compensatory mechanisms are also addressed.
Metabolic alkalosis is a primary acid-base disturbance characterized by elevated serum bicarbonate and pH levels, along with increased PaCO2 levels. It can be caused by loss of stomach acid from vomiting or diarrhea, or by excessive intake of bicarbonate. The kidneys compensate by retaining bicarbonate, sodium, and chloride. Symptoms may include confusion, seizures, muscle cramps or weakness due to accompanying hypokalemia or hypocalcemia. Respiratory compensation occurs via hypoventilation and increased PaCO2 levels.
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.
Abg.2 Arterial blood gas analysis and example interpretationsamirelansary
This document provides an overview of different approaches to analyzing arterial blood gases (ABG), including the Copenhagen, Boston, and Stewart approaches. It discusses key parameters measured in an ABG such as pH, PaCO2, PaO2, HCO3, and oxygen saturation. The document also summarizes the steps involved in interpreting an ABG, including classifying acid-base disturbances as respiratory or metabolic, assessing compensation, and considering the anion gap in cases of metabolic acidosis.
Acid base abnormalities (causes and treatment)Vernon Pashi
This document provides an overview of acid-base abnormalities and their management. It defines key terms, outlines regulatory mechanisms like buffers and respiration, and describes different acid-base disorders including their causes and treatments. An example case is presented of a patient with metabolic and respiratory acidosis on admission, resolving to metabolic acidosis and respiratory alkalosis after treatment. Overall it reviews acid-base physiology and the approach to diagnosing and managing common acid-base imbalances.
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.
Short Review regarding Metabolic Acidosis
The Causes, anion gap,urine osmolal gap, Renal Tubular Acidosis, approach to Metabolic Acidosis in Final Slide
Lactic acidosis is defined as a serum lactate level greater than 5mmol/L accompanied by acidosis and a low serum pH. It occurs when lactate production exceeds utilization, commonly due to tissue hypoxia or impaired liver/kidney function. Management involves treating the underlying cause to restore oxygen delivery and lactate clearance. Bicarbonate therapy can raise the pH but risks hypercapnia and is not recommended in some cases. New therapies like dichloroacetate aim to increase lactate utilization but have not reduced mortality in clinical trials.
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.
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 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.
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
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 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 provides information on interpreting blood gas analysis (ABG). It discusses common errors in ABG sampling and outlines steps to analyze ABG results. Key points include checking if the pH indicates acidosis or alkalosis, identifying the primary disorder, assessing compensation, and calculating the anion and delta gaps to detect mixed disorders. Non-gap causes of acidosis are distinguished using urine anion gap. The document also covers expected changes in respiratory and metabolic acid-base disorders and differentials for specific conditions.
The document discusses the interpretation of arterial blood gas (ABG) results. It provides:
1) Normal ABG value ranges for pH, PaCO2, PaO2 and HCO3.
2) A 6-step process to interpret ABG results, including analyzing pH, PaCO2, HCO3 levels and their relationships.
3) Examples of how to determine if an acid-base imbalance is respiratory or metabolic based on changes in pH, PaCO2 and HCO3. Conditions like respiratory acidosis, alkalosis and mixed disorders are explained.
4) Factors that indicate an acid-base imbalance is compensated or uncompensated.
5) How
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 provides a summary of an arterial blood gas interpretation presentation. It discusses the objectives, procedure, and precautions for arterial blood gas sampling. It then covers the interpretation of oxygenation status and acid-base status using a six step approach. The six steps include determining if acidemia or alkalemia is present, if the primary disturbance is respiratory or metabolic, if a respiratory disorder is acute or chronic, if compensation is adequate, evaluating the anion gap if metabolic, and identifying the cause of a high anion gap metabolic acidosis.
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
Metabolic acidosis is caused by an excess production of acids or loss of bicarbonate in the body. It results in a primary decrease in blood pH (acidemia) with low bicarbonate levels. The kidneys compensate by retaining bicarbonate to raise the pH. Causes include diabetic ketoacidosis, lactic acidosis, renal tubular acidosis, diarrhea, and uremia. An increased anion gap metabolic acidosis occurs when unmeasured anions like ketones and lactate are produced in excess. The clinical features include respiratory changes like Kussmaul breathing, as well as neurological symptoms. Arterial blood gas analysis is used to diagnose and classify the type and
Arterial blood gas analysis in clinical practice (2)Mohit Aggarwal
This document provides information about arterial blood gases (ABGs), including what an ABG is, the components that are measured, normal ranges, reasons for ordering an ABG, how to interpret ABG results, and types of acid-base imbalances. An ABG is a blood test that measures pH, oxygen, and carbon dioxide levels to help diagnose respiratory and metabolic conditions. The document outlines the steps to interpret an ABG and explains various acid-base disorders like respiratory acidosis, metabolic alkalosis, and mixed disorders. Compensation mechanisms of the lungs and kidneys in response to acid-base imbalances are also discussed.
This document discusses arterial blood gas analysis (ABG), including:
1. The history and development of ABG analysis and ongoing issues with interpretation.
2. The indications, contraindications, and hazards of ABG sampling as well as the procedure.
3. How ABG parameters like pH, PaCO2, PaO2, HCO3 can be used to evaluate acid-base balance, ventilation, and oxygenation.
4. A stepwise approach to acid-base analysis including identifying primary vs secondary disorders and using gaps to evaluate metabolic acidosis.
This document provides an overview of arterial blood gas analysis. It discusses the history and development of blood gas analysis, indications for arterial blood gas sampling, and the procedure. It outlines normal values and how to interpret acid-base balance, oxygenation, and ventilation based on arterial blood gas parameters. A stepwise approach to acid-base analysis is presented, including how to identify primary versus secondary disorders and evaluate respiratory and renal responses.
This document discusses arterial blood gas analysis. It provides information on the indications, contraindications, and procedure for arterial blood sampling. Key points include assessing oxygenation and ventilation, establishing diagnoses of respiratory failure, and guiding treatment. Complications of sampling and normal ranges for analytes are outlined. Methods for calculating bicarbonate, anion gap, and other values are described. Causes and characteristics of metabolic and respiratory acid-base disorders are summarized.
This document provides information about arterial blood gases (ABGs), including what parameters are measured in an ABG, which artery is commonly used for sampling, cautions when obtaining an ABG, and conditions that can invalidate or modify ABG results. It also outlines the six step approach to evaluating acid-base disorders based on an ABG result, including identifying if the primary disturbance is respiratory or metabolic, ruling out combined disorders, checking the anion gap in metabolic acidosis, and calculating the delta anion gap. An illustrative case is provided where the ABG results indicate a mixed metabolic acidosis and respiratory acidosis based on application of the six step approach.
This document provides information on arterial blood gas (ABG) interpretation for medical professionals and trainees. It discusses the indications, equipment, and procedures for collecting an ABG sample. Key steps in the collection process include preparing the patient, selecting an appropriate artery site, and applying pressure after puncture. The document then covers interpreting ABG results through a stepwise approach considering pH, acid-base balance, compensation, oxygenation status, and identifying simple vs mixed disorders. Common abnormal values and their implications are presented. Examples of interpreted ABG reports are provided to demonstrate the evaluation process.
This document provides guidance on interpreting arterial blood gas (ABG) results. It discusses:
1. The normal ranges for pH, pCO2, pO2, HCO3, and other ABG components.
2. A step-by-step process for ABG interpretation, beginning with checking the validity of results, assessing oxygenation, identifying acid-base disturbances, and determining whether issues are respiratory or metabolic in nature.
3. How to evaluate the chronicity of any respiratory acid-base disturbances and how the kidneys will compensate metabolically.
4. How to classify metabolic acid-base disturbances based on anion gap and identify potential etiologies like lactic acidosis
This document discusses acid-base balance and interpreting arterial blood gas results. It provides an overview of how the respiratory and renal systems regulate acid-base homeostasis. It then outlines a step-wise approach to diagnosing acid-base disorders based on analyzing pH, bicarbonate, PCO2 and anion gap values. Primary disorders are distinguished as being either respiratory or metabolic based on the primary defect in bicarbonate or PCO2. Compensatory responses and whether they are appropriate are also evaluated.
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.
A blood gas analysis showed a pH of 7.27, pCO2 of 58 mmHg, and HCO3- of 26 mmol/L in a patient receiving 5L of oxygen. This represents a primary respiratory acidosis with appropriate chronic compensation, as the pH and pCO2 are low and HCO3- is elevated, consistent with long-standing respiratory acidosis. The anion gap and albumin are normal. This patient is experiencing chronic respiratory acidosis.
Interpretation of arterial blood gases:Traditional versus Modern Gamal Agmy
This document discusses the interpretation of arterial blood gases and acid-base disorders. It begins by outlining the Handerson-Hasselbalch equation and normal blood gas values. It then defines respiratory failure and describes the four types based on PaO2 and PaCO2 levels. The document details how to evaluate oxygen status, ventilation, and acid-base disorders from a blood gas analysis. It provides examples of metabolic and respiratory acidosis and alkalosis, explaining compensation mechanisms. Mixed disorders and a step-wise approach to interpretation are also outlined. Three sample problems are worked through as examples.
This document outlines an approach to diagnosing acid-base disorders presented by Dr. Abel Tenaw. It discusses basic acid-base concepts, the Henderson-Hasselbalch equation, compensatory mechanisms, arterial blood gas analysis including anion gap and delta ratio calculations, types of acid-base disorders and a stepwise approach to diagnosis. Key points covered include the importance of pH regulation, buffer systems, respiratory and renal compensation, and differentiating between simple and mixed acid-base disorders.
Arterial blood gas presentation in ICU/OTDrVANDANA17
This document discusses arterial blood gas (ABG) sampling and analysis. Some key points:
- ABG provides important information about respiratory, metabolic and mixed acid-base disorders through measurement of pH, pCO2 and HCO3 levels.
- It can help guide treatment, especially for critically ill patients, as results are rapidly available at the bedside.
- Samples must be taken and analyzed properly to avoid inaccuracies from factors like delayed analysis, air bubbles, excessive heparin or temperature changes.
- ABG interpretation involves classifying the primary acid-base disorder based on directional changes in pH and pCO2, and evaluating any secondary responses. This helps identify conditions like respiratory acid
This document provides an overview of arterial blood gas (ABG) analysis and interpretation. It discusses indications for ABG testing, appropriate sampling sites, and precautions. Key parameters measured in an ABG such as pH, PaCO2, PaO2, HCO3, and SaO2 are defined. Methods for interpreting ABG results, including evaluating for respiratory vs. metabolic causes and compensation, are outlined. Common errors in sampling technique and their effects are reviewed.
The document discusses acid-base balance and arterial blood gas (ABG) analysis. It defines normal blood pH and explains how changes can interfere with functions. It describes different acid-base imbalances including respiratory and metabolic acidosis and alkalosis. The procedure for ABG sampling and interpretation is explained in detail, including normal values and a step-by-step approach to analysis. Compensatory responses and examples of interpreted ABG results are also provided.
The document discusses arterial blood gas (ABG) analysis. It provides information on the uses and contraindications of ABG tests, as well as the procedure, normal values, and interpretation of ABG results. It discusses oxygenation, acid-base balance, definitions, regulation of acid-base balance, and a step-wise approach to interpreting ABG reports. Key points include how ABG analysis can help establish diagnoses and guide treatment for conditions like respiratory failure, and the importance of factors like temperature, oxygen levels, and timing when withdrawing and analyzing ABG samples.
1. The patient has a mixed disorder of metabolic acidosis with respiratory compensation and high anion gap metabolic acidosis.
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2. OBJECTIVES
• Understand correct sample handling
• Outline an interpretation strategy
• Describe causes for acid-base disturbances
• Delineate a workup strategy for common disorders
@ NKMishra23/07/18 2
3. ABG
• ABG is a very useful diagnostic tool in our day to day practice.
• The first arterial puncture was performed in 1912 by Hurter, a German
physician.
• Drawn from artery- Radial, Brachial, Femoral, Dorsalis pedis, Posterior
tibial
• It is an invasive procedure.
@ NKMishra23/07/18 3
4. Acid-Base Physiology
• pH is the negative logarithm to the base 10 of the hydrogen ion
concentration in mmol/L
• pH = - log10[H+]
• An increase in pH indicates a proportionate decrease in the [H+] and a
decrease in the pH indicates a proportionate increase in the [H+].
• H2CO3 generates 12,500 mmol H+ per day.
• Normal metabolism of proteins and nucleotides generates about 100
mmol H+ per day in the form of sulphuric and phosphoric acids.@ NKMishra23/07/18 4
5. Calculation of pH
• pH is calculated from Henderson-Hasselbalch
equation .
• pH = pK + log acid/bas
• pH = 6.1 + log HCO3-
H2CO3
Kassirer and Bliech modified equation
• H+ = 24 x PCO2/HCO3-
@ NKMishra23/07/18 5
6. Regulation of pH
pH is maintained in narrow range by
• 1) In seconds: buffer systems
• 2)In minutes: CO2 excretion by the lungs
• 3)In hours to days: renal excretion of H+,
reabsorption of HCO3
@ NKMishra23/07/18 6
7. Regulation of arterial pH
• 1.BUFFERS –Buffer systems minimize the change in pH resulting from
production of acid .
• Main buffer system in humans is HCO3- in ECF and protein and
phosphate buffers in ICF.
2.ROLE OF THE RESPIRATORY SYSTEM–Elimination of volatile acid CO2.
• a. Respiratory centers in the brain respond to changes in pH of CSF
and blood to affect ventilatory rate.
• b. Ventilation directly controls the elimination of CO2.
@ NKMishra23/07/18 7
8. ROLE OF KIDNEY
It retains and regenerate HCO3- thereby regenerating the
body buffer with the net effect of eliminating the non-
volatile acid load
a. H+ secretion
1. Free urinary H+ - minimal contribution
2. Ammonia
3. Phosphorus
b. HCO3- reabsorption
1. Proximal tubule – 90%
2. Distal tubule -10%
@ NKMishra23/07/18 8
9. Applications of ABG
• To document respiratory failure and assess its severity.
• To monitor patients on ventilators and assist in weaning.
• To assess acid base imbalance in critical illness.
• To assess response to therapeutic interventions and
mechanical ventilation.
• To assess pre-op patients.
@ NKMishra23/07/18 9
10. VENTILATION
PaCO2 = VCO2 x K
VA
Hypercapnea > 45 mm Hg (Hypoventilation)
Respiratory Acidosis
Hypocapnea < 35 mm Hg (Hyperventilation)
Respiratory Alkalosis
VA=Portion of total ventilation participate in gas
exchange with pulmonary blood
@ NKMishra23/07/18 10
11. OXYGENATION
• P(A-a)O2
• O2 content
• PaO2 / FiO2 ratio
• arterial-Alveolar O2 tension ratio
@ NKMishra23/07/18 11
12. P(A-a)O2= PAO2- PaO2
• PAO2- partial pressure of oxygen in alveolar gas
pAO2 = pIO2 – (paCO2 / R)
PAO2= (PB-P h2o) x FiO2- (paCO2/R)
Eg.:
=(760-47) x .21- (40/0.8) =100
PAO2-Pao2= 100-80=20
N= <15
PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric
pressure (760mmHg), Ph2o = water vapor pressure (47 mm Hg),
FiO2 = fraction of inspired oxygen, PCO2 = partial pressure of CO2
in the ABG, R = respiratory quotient (0.8)
@ NKMishra23/07/18 12
13. P(A-a)O2= PAO2- PaO2
• PaO2- partial pressure of oxygen in blood
PaO2 = FiO2 × 5
PaO2 = 109 - 0.4 (Age)
PaO2 is dependant upon Age, FiO2, Patm
HYPOXEMIA
Mild (60-80) mmHg
Moderate(40-60) mmHg
Severe <40 mmHg
@ NKMishra23/07/18 13
20. Technical Errors
Risk of alteration of results with:
1)size of syringe/needle
2)vol of sample
Syringes must have > 50% blood
Use only 3ml or less syringe
25% lower values if 1 ml sample taken in 10 ml syringe (0.25 ml heparin in
needle)
@ NKMishra23/07/18 20
21. Parameters Excessive Heparin Air bubbles
pH ↓ or remain the same ↑
PCO2 ↓ ↓
PO2 May altered May altered
HbO2% sat May altered May altered
HbCO2% sat Will not altered Will not altered
Hb content ↓ Is not altered
HCO3 ↓ ↓
Base Excess ↓ ↓
Oxygen content May be altered Maybe altered
@ NKMishra23/07/18 21
22. Technical Errors
WBC Counts
0.01 ml O2 consumed/dL/min
Marked increase in high TLC/plt counts : dec.pO2
Chilling / immediate analysis
ABG Syringe must be transported earliest via COLD CHAIN
Change/10 min Uniced 370C Iced 40C
pH 0.01 0.001
pCO2 1 mm Hg 0.1 mm Hg
pO2 0.1% 0.01%
@ NKMishra23/07/18 22
29. Contraindication
• No absolute contraindications
• Dialysis shunt – choose another site
• Patient on anticoagulant/aspirin therapy – may have to hold
pressure on puncture site longer than normal
@ NKMishra23/07/18 30
30. Site specific contraindication
Radial : Buergers disease
Raynauds
Absent Ulnar collateral circulation
AV dialysis shunt
Femoral: Local infection
@ NKMishra23/07/18 31
34. Step 1: Assess the internal consistency of the values using
the Henderseon-Hasselbach equation:
• [H+] = 24(PaCO2)
[HCO3-]
@ NKMishra23/07/18 35
35. pH Approximate [H+]
(mmol/L)
7.00 100
7.05 89
7.10 79
7.15 71
7.20 63
7.25 56
7.30 50
7.35 45
7.40 40
7.45 35
7.50 32
7.55 28
7.60 25
7.65 22
If the pH and the [H+] are inconsistent, the ABG is probably not valid.
@ NKMishra23/07/18 36
36. Step 2: Is there alkalemia or acidemia present?
• pH < 7.35 acidemia
pH > 7.45 alkalemia
• This is usually the primary disorder
• Remember: an acidosis or alkalosis may be present even if the pH is in
the normal range (7.35 – 7.45)
• You will need to check the PaCO2, HCO3- and anion gap
@ NKMishra23/07/18 37
37. • Step 3: Is the disturbance respiratory or metabolic?
• What is the relationship between the direction of change in the pH and the
direction of change in the PaCO2?
• In primary respiratory disorders, the pH and PaCO2 change in opposite directions;
in metabolic disorders the pH and PaCO2 change in the same direction.
Acidosis Respiratory pH ↓ PaCO2 ↑ ROME
Acidosis Metabolic& pH ↓ PaCO2 ↓ ROME
Alkalosis Respiratory pH ↑ PaCO2 ↓ ROME
Alkalosis Metabolic pH ↑ PaCO2 ↑ ROME
@ NKMishra23/07/18 38
38. • Step 4: Is there appropriate compensation for the primary disturbance?
• Usually, compensation does not return the pH to normal (7.35 – 7.45) except….?
Disorder Expected compensation Correction factor
Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ± 2
Acute respiratory acidosis Increase in [HCO3-]= ∆ PaCO2/10 ± 3
Chronic respiratory acidosis (3-5 days) Increase in [HCO3-]= 3.5(∆ PaCO2/10)
Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-)
Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆ PaCO2/10)
Chronic respiratory alkalosis Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆
PaCO2/10)
If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is
present. @ NKMishra23/07/18 39
39. • Step 5: Calculate the anion gap (if a metabolic acidosis exists):
• AG= [Na+]-( [Cl-] + [HCO3-] )=12 ± 2
• A normal anion gap is approximately 12 meq/L.
• In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the
“normal” anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for
each 1 gm/dL decrease in the plasma albumin concentration (for example, a patient
with a plasma albumin of 2.0 gm/dL would be approximately 7 meq/L.)
• If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical
situations.
• Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure
• Toxic ingestion is suspected
• OSM gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8
• The OSM gap should be < 10
@ NKMishra23/07/18 40
40. • Step 6: If an increased anion gap is present, assess the relationship between
the increase in the anion gap and the decrease in [HCO3-].
• Assess the ratio of the change in the anion gap (∆AG ) to the change in [HCO3-
] (∆[HCO3-]): ∆AG/∆[HCO3-]
• This ratio should be between 1.0 and 2.0 if an uncomplicated anion gap
metabolic acidosis is present.
• If this ratio falls outside of this range, then another metabolic disorder is
present:
• If ∆AG/∆[HCO3-] < 1.0, then a concurrent non-anion gap metabolic acidosis is
likely to be present.
• If ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic alkalosis is likely to be
present.
• It is important to remember what the expected “normal” anion gap for your
patient should be, by adjusting for hypoalbuminemia (see Step 5, above.)
@ NKMishra23/07/18 41
41. Disorder pH Primary problem Compensation
Metabolic acidosis ↓ ↓ in HCO3- ↓ in PaCO2
Metabolic alkalosis ↑ ↑ in HCO3- ↑ in PaCO2
Respiratory acidosis ↓ ↑ in PaCO2 ↑ in [HCO3-]
Respiratory alkalosis ↑ ↓ in PaCO2 ↓ in [HCO3-]
Table 1: Characteristics of acid-base disturbances
@ NKMishra23/07/18 42
42. Table 2: Selected etiologies of respiratory acidosis
oAirway obstruction
- Upper
- Lower
o COPD
o asthma
o other obstructive lung disease
oCNS depression
oSleep disordered breathing (OSA or OHS)
oNeuromuscular impairment
oVentilatory restriction
oIncreased CO2 production: shivering, rigors, seizures, malignant hyperthermia, hypermetabolism,
increased intake of carbohydrates
oIncorrect mechanical ventilation settings
@ NKMishra23/07/18 43
44. Table 4: Selected causes of metabolic alkalosis
oHypovolemia with Cl- depletion
o GI loss of H+
o Vomiting, gastric suction, villous adenoma,
diarrhea with chloride-rich fluid
o Renal loss H+
o Loop and thiazide diuretics, post-hypercapnia
(especially after institution of mechanical
ventilation)
oHypervolemia, Cl- expansion
o Renal loss of H+: edematous states (heart failure,
cirrhosis, nephrotic syndrome),
hyperaldosteronism, hypercortisolism, excess
ACTH, exogenous steroids, hyperreninemia,
severe hypokalemia, renal artery stenosis,
bicarbonate administration
@ NKMishra23/07/18 45
45. Table 5: Selected etiologies of metabolic acidosis
oElevated anion gap:
o Methanol intoxication
o Uremia
o Diabetic ketoacidosisa, alcoholic ketoacidosis,
starvation ketoacidosis
o Paraldehyde toxicity
o Isoniazid
o Lactic acidosisa
o Type A: tissue ischemia
o Type B: Altered cellular metabolism
o Ethanolb or ethylene glycolb intoxication
o Salicylate intoxication
a Most common causes of metabolic acidosis with an
elevated anion gap
b Frequently associated with an osmolal gap
oNormal anion gap: will have increase in [Cl-]
o GI loss of HCO3-
o Diarrhea, ileostomy, proximal colostomy,
ureteral diversion
o Renal loss of HCO3-
o proximal RTA
o carbonic anhydrase inhibitor (acetazolamide)
o Renal tubular disease
o ATN
o Chronic renal disease
o Distal RTA
o Aldosterone inhibitors or absence
o NaCl infusion, TPN, NH4+ administration
@ NKMishra23/07/18 46
46. Disorder Characteristics Selected situations
Respiratory acidosis with
metabolic acidosis
↓in pH
↓ in HCO3
↑ in PaCO2
•Cardiac arrest
•Intoxications
•Multi-organ failure
Respiratory alkalosis with
metabolic alkalosis
↑in pH
↑ in HCO3-
↓ in PaCO2
•Cirrhosis with diuretics
•Pregnancy with vomiting
•Over ventilation of COPD
Respiratory acidosis with
metabolic alkalosis
pH in normal range
↑ in PaCO2,
↑ in HCO3-
•COPD with diuretics, vomiting, NG suction
•Severe hypokalemia
Respiratory alkalosis with
metabolic acidosis
pH in normal range
↓ in PaCO2
↓ in HCO3
•Sepsis
•Salicylate toxicity
•Renal failure with CHF or pneumonia
•Advanced liver disease
Metabolic acidosis with metabolic
alkalosis
pH in normal range
HCO3- normal
•Uremia or ketoacidosis with vomiting, NG suction,
diuretics, etc.
Table 6: Selected mixed and complex acid-base disturbances
@ NKMishra23/07/18 47
50. Base excess and deficit
• The BE (or base deficit) is defined as the amount of acid (or base) required
to be added to whole blood to achieve a pH of 7.4 at 37˚C and paCO2 of
40mmHg.
If the base is in excess
• may be due to decrease in metabolic acids
• may be due to increase in buffers (e.g. HCO3-)
If the base is in deficit
• may be due to excess metabolic acids
@ NKMishra23/07/18 51
51. Step 1: is it reliable??
STEP -2 : Comprehensive history and physical
examination.
STEP -3 : Acidosis or alkalosis..???
See the pH (<7.35 or >7.45)
STEP -4 : Identify the primary disorder
See the change in PCo2 & HCO3
STEP -5 : Calculate the compensatory response
Is adequately compensated???
@ NKMishra23/07/18 52
52. STEP -6 : Calculate anion gap
STEP -7 : Calculate the delta gap (unmask hidden
mixed disorders)
STEP -8 : Calculate the osmolar gap (for high AG
acidosis)
STEP -9 : Calculate the urinary anion gap (Non AG
metabolic acidosis)
STEP -10 : Formulate differential diagnosis
@ NKMishra23/07/18 53
54. ANION GAP (AG)
• Normal value 8 – 12
• Primarily determined by negatively charged plasma proteins
• Albumin ↓ 1 g/dL (below 4/4.5) AG ↓ 2.5
• AG needs correction for hypoalbuminemia
@ NKMishra23/07/18 55
55. UNADJUSTED AG ADJUSTED AG
Decreased 26.7 %
Decreased 4.7 %
Normal 22.0 %
Normal 62.6 %
Normal 36.4 %
Increased 26.3 %
Increased 10.7 % Increased 10.7 %
J Lab Clin Med 2005;146:317–20 @ NKMishra23/07/18 56
56. Some quick clues:
• 1. if CO2 and HCO3 in opposite direction , it indicates mixed d/o
• 2. if pH and Co2 same direction, it indicates Metabolic d/o=ROME
• 3. if pH and Co2 same direction, it indicates Respiratory d/o= ROME
• If the difference between digits after decimal in PH and CO2 is
• <15= metabolic
• > 15= Respiratory
@ NKMishra23/07/18 57
64. 1. pH: ↓
2. PCO2: ↓
3. Anion Gap: Normal
- Delta ratio
4. Compensation
CASE 1
METABOLIC ACIDOSIS
NON-ANION GAP
ADEQUATE
COMPENSATION
@ NKMishra23/07/18 65
65. NON-ANION GAP ACIDOSIS
• Hyperchloremic: Net
Bicarbonate loss
• Two main different routes
• GI: diarrhea, fistulas
• Renal: RTAs, drugs
• What is used to differentiate?
Urine AG = Na+ + K+ - Cl-
UAG = Negative normally bcz CL- content is high in
urine.
• NAG Acidosis:
Diarrhea
NAG M.Acidosis
UAG= Neg
K+= dec
RTA
NAG M.Acidosis
UAG= Positive
K+= Inc
@ NKMishra23/07/18 66
74. DELTA RATIO
• Delta ratio = Δ anion gap / Δ bicarbonate
Actual AG – 12
Delta Ratio =
24 – HCO3
-
22 – 12 12
Delta Ratio = = = 1.7
24 – 17 7
@ NKMishra23/07/18 75
75. NON-ANION GAP ACIDOSIS
(↑↑ AG – 12)
Delta Ratio = -----------------------
(24-↓↓↓HCO3)
• Delta Ratio < 0.8
METABOLIC ALKALOSIS
(↑↑ AG – 12)
Delta Ratio = -----------------------
(24 - ≈↑HCO3)
• Delta Ratio > 1.5
Δ AG (↑AG-12)
Delta Ratio = ------------- = -----------------
Δ HCO3- (24-↓HCO3)
(0.8-1.5)1
@ NKMishra23/07/18 76
76. DELTA RATIO
Δ RATIO
< 0.8 0.8 - 1.5 > 1.5
Anion Gap metabolic acidosis
Anion Gap metabolic
acidosis
Anion Gap metabolic acidosis
Non anion gap acidosis Metabolic alkalosis
@ NKMishra23/07/18 77
77. 1. pH: ↓
2. PCO2: ↓
3. Anion Gap: ↑
- Delta Ratio = 1.7
4. Compensation
CASE 2
METABOLIC ACIDOSIS
ANION GAP
METABOLIC
ALKALOSIS
@ NKMishra23/07/18 78
80. HIGH ANION GAP
M ethanol
U remia
D iabetic Ketoacidosis: alcohol, starvation
P araldehyde, paracetamol
I ron, Isoniazid, inborn errors of metabolism
L actic Acidosis
E thylene glycol, Ethanol
S alicylates
@ NKMishra23/07/18 81
107. CASE 6
• pH 7.40
• PaCO2 38 mm Hg
• PaO2 106 mm Hg
• Na+ 141 mmol/L
• K+ 4.8 mmol/L
• Cl- 97 mmol/L
• HCO3
- 23 mmol/L
• Albumin 4.0 g/dL
ANION GAP = 21
@ NKMishra23/07/18 108
108. 1. pH: Normal
2. PCO2: Normal
3. Anion Gap: ↑
- Delta Ratio
4. Compensation
CASE 6
METABOLIC ACIDOSIS
ANION GAP
pH PaCO2 Disorder
↓ ↓ Metabolic Acidosis
↑ ↑ Metabolic Alkalosis
↓ ↑ Respiratory Acidosis
↑ ↓ Respiratory Alkalosis
@ NKMishra23/07/18 109
109. DELTA RATIO
• Delta ratio = Δ anion gap / Δ bicarbonate
Actual AG – 12
Delta Ratio =
24 – HCO3
-
21 – 12 9
Delta Ratio = = = 9
24 – 23 1
@ NKMishra23/07/18 110
110. DELTA RATIO
Δ RATIO
< 0.8 0.8 - 1.5 > 1.5
Anion Gap metabolic acidosis
Anion Gap metabolic
acidosis
Anion Gap metabolic acidosis
Non anion gap acidosis Metabolic alkalosis
@ NKMishra23/07/18 111
111. 1. pH: Normal
2. PCO2: Normal
3. Anion Gap: ↑
- Delta Ratio = 9
4. Compensation
CASE 6
METABOLIC ACIDOSIS
ANION GAP
METABOLIC
ALKALOSIS
@ NKMishra23/07/18 112
113. 1. pH: Normal
2. PCO2: Normal
3. Anion Gap: ↑
- Delta Ratio = 9
4. Compensation
CASE 6
METABOLIC ACIDOSIS
ANION GAP
METABOLIC
ALKALOSIS
RESPIRATORY
ALKALOSIS
@ NKMishra23/07/18 114
114. Case 7
• pH: 7.4
• PCO2: 40MM/HG
• HCO3: 25MMOL/L
• AG: 30
• M.AC with M.Alk with R.Alk
@ NKMishra23/07/18 115
115. • Case 8. A 54y/o male, Alcoholic presented to ER with c/o vomiting and
increased respiratory rate.
• PH: 7.4
• PCO2: 30
• HCO3:25
• AG: 30
• M. AC(Alcoholic Ketoacidosis)
• with M.Alk(Vomiting)
• with R. Alk( Hyperventilation due to hepatic dysfxn or alcohol withdrawal)
@ NKMishra23/07/18 116
120. Treat the patient not the ABG.
Thank you!!
Have a Nice Day!!
@ NKMishra23/07/18 121
121. Case-1
• 60 years old M, presents to the ED with rapid
breathing and less responsive than usual. No other
history available.
ABG results
pH 7.31
PCO₂ 10
HCO₃ 5
Na 123
K 5
Cl 99
@ NKMishra23/07/18 122
122. Stepwise interpretation
1. At pH 7.3 H+ conc. Should be ≈50nmol/L
• Calculated H+ = 24 × 10/5 = 24 × 2 = 48
• Both values corroborate, hence result is valid.
2. pH is 7.3, i.e Acidosis
3. HCO₃ value has gone down, primary process is
metabolic
4. Respiratory compensation:
• Calculated PCO₂ = (1.5 × 5)+8 ± 2 = 13.5 to 17.5
• Partially compensated M.Acidosis a/w respiratory
alkalosis :- Mixed disorder
@ NKMishra23/07/18 123
123. 5. Anion gap: (123+5) – (99 + 5) = 24
• High anion gap metabolic acidosis
Finally:- Mixed acid base disorder, with presence of high
AG metabolic acidosis and respiratory alkalosis.
@ NKMishra23/07/18 124
124. Case-2
• A k/c/o COPD with cor pulmonale on treatment
presented with progressive breathlessness.
ABG results
pH 7.42
PCO₂ 67
HCO₃ 42
Na 140
K 3.5
Cl 88
@ NKMishra23/07/18 125
125. • pH is normal; but PCO₂ & HCO₃ both are increased.
• Change in PCO₂ is 67-40 = 27
• Expected rise in HCO₃ should be 27 × 0.4 = 10.8
• Expected HCO₃ = 24+10.8 ≈ 35
• Actual HCO₃ = 42
• AG = 12 (N)
• Mixed disorder, both respiratory acidosis & metabolic
alkalosis.
@ NKMishra23/07/18 126
126. Case -3
• A known case of chronic kidney disease, discontinued
dialysis & presented to the emergency in an altered
state of sensorium. Attendants gave history of
repeated episodes of vomiting at home.
ABG results
pH 7.42
PCO₂ 40
HCO₃ 25
Na 140
K 3.0
Cl 95@ NKMishra23/07/18 127
127. • pH, PCO₂, HCO₃ all WNL
• AG = 23 (↑)
• Delta gap = 13 – 1 = 12 (↑)
• AG >> HCO3
–
• Mixed disorder with presence of both high AG
metabolic acidosis and metabolic alkalosis.
@ NKMishra23/07/18 128
128. Case-4
• 65 yrs old M, past h/o Acute MI on medication,
presented with high grade fever with, cough & yellowish
expectoration for 5 days. Acute increase in shortness of
breath.
ABG results
pH 7.3
PCO₂ 38
HCO₃ 16
Na 136
K 4
Cl 102
@ NKMishra23/07/18 129
144. Causes of High AG Met Acidosis
1. Ketoacidosis:
Diabetic
Alcoholic
Starvation
2. Lactic Acidosis:
Type A (Inadequate O2 Delivery to Cells)
Type B (Inability of Cells to utilise O2)
Type D (Abnormal bowel anatomy)
3. Toxicity:
Salicylates Paraldehyde
Methanol Toluene
Ethylene Glycol
4. Renal Failure
5. Rhabdomyolsis
@ NKMishra23/07/18 145
145. CAUSES OF NORMAL ANION GAP METABOLIC
ACIDOSIS
1.HCO3 loss:
GIT Diarrhoea
Pancreatic or biliary drainage
Urinary diversions
(ureterosigmoidostomy)
Renal Proximal (type 2) RTA
Ketoacidosis (during therapy)
Post-chronic hypocapnia
@ NKMishra23/07/18 146
149. RENAL LOSS : Diuretics
Post hypercapnic state
Hypercalcaemia
Recovery from LA/KA
Mg2+ deficiency
Bartters/Gitelmans syndr
Nonreabs anions – penicill
3. ECFV expansion, hypertension,K+ deficiency, and
mineralocorticoid excess:
HIGH RENIN : RAS
Accelerated hypertension
Renin sec tumor
@ NKMishra23/07/18 150
150. LOW RENIN :
PRIMARY ALDOSTERONISM –
Adenoma, hyperplasia , carcinoma
ADRENAL ENZYME DEFECTS –
11 b Hydroxylase
CUSHINGS SYNDROME OR DIS.
4. Gain of function mutation of renal sodium channel
with ECF expansion , hypertension , K+ deficiency
and hyporeninemic hypoaldosteronism : called as
LIDDLES SYNDROME
@ NKMishra23/07/18 151
157. • ABG is a very useful diagnostic tool for our day to day
practice.
• Approach to interpret should be step wise & in a
systematic manner.
• Any abnormal result should be analyzed cautiously in
light of clinical context.
• Appropriate use of this tool using clinical judgment is of
paramount importance
@ NKMishra23/07/18 158