This document provides detailed information about arterial blood gases (ABGs), including:
- The main components of an ABG (pH, PCO2, HCO3) and their normal values.
- How to interpret abnormal ABG readings, distinguishing between compensated and uncompensated disturbances, and identifying the primary acid-base disorder.
- Examples of mixed acid-base disorders and clinical causes of metabolic and respiratory acid-base disorders.
- Practice questions to assess the ability to interpret ABG results.
The document discusses arterial blood gas analysis and interpretation. It provides guidelines for deciding when to intubate based on clinical assessment rather than strict ABG value cutoffs. It also presents two scenarios to determine which case would warrant immediate ventilatory support. The key is that the decision to intubate should be based primarily on clinical factors, not just ABG values alone.
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
1. The patient presented with drowsiness and sluggish respiration after overdosing on sleeping pills. An ABG revealed a pH of 7.1, HCO3 of 28 mEq/L, PaCO2 of 72 mmHg, and PaO2 of 78 mmHg.
2. These results indicate a primary respiratory acidosis, seen by the elevated PaCO2 and low pH. The HCO3 is also elevated, showing compensation for the chronic respiratory acidosis through bicarbonate retention.
3. Overdosing on sleeping pills can cause respiratory depression leading to respiratory acidosis from failure of carbon dioxide elimination, as seen in this case.
The document discusses arterial blood gas (ABG) analysis. It provides 3 key points:
1. ABG analysis aids in establishing diagnoses and assessing the severity of respiratory failure by measuring oxygenation, ventilation, and acid-base balance.
2. The normal values for pH, PCO2, PO2, HCO3, and other components are outlined.
3. A step-wise approach to interpreting an ABG report is described, including assessing whether it indicates a respiratory or metabolic disorder, whether compensation is adequate, and evaluating other acid-base parameters like anion gap.
This document provides an overview of acid-base balance and homeostasis. It discusses the bicarbonate buffer system, respiratory regulation through alveolar ventilation, and renal regulation through reabsorption and secretion of bicarbonate and hydrogen ions. The steps for analyzing an arterial blood gas are described, including looking at pH, identifying the primary disturbance, assessing compensation, and correlating clinically. Examples of acid-base disorders and their classifications are provided.
This document provides information on acid-base balance and interpretation of arterial blood gases (ABGs). It discusses terminology, how ABG analysis is performed, indications for ABGs, limitations, and an 8-step approach to evaluating acid-base disorders. Key points covered include the relationship between pH, acids, bases, acidosis, and alkalosis. Compensation in respiratory and metabolic acidosis/alkalosis is explained. Causes, evaluation, and treatment of different acid-base imbalances such as respiratory acidosis, metabolic acidosis, and lactic acidosis are summarized. Organ systems involved in acid-base regulation like the respiratory and renal systems are also overviewed.
This document provides an overview of arterial blood gas (ABG) analysis including normal parameters, definitions of acid-base disturbances, and a systematic approach to interpreting ABG results. It discusses the three mechanisms that maintain pH homeostasis: chemical buffering, alveolar ventilation, and renal handling of acids and bases. The four primary acid-base disorders are defined as metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. A stepwise approach is outlined including establishing the primary disorder, assessing compensation, and evaluating for mixed disturbances. Examples of common ABG interpretations are also provided.
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.
The document discusses arterial blood gas analysis and interpretation. It provides guidelines for deciding when to intubate based on clinical assessment rather than strict ABG value cutoffs. It also presents two scenarios to determine which case would warrant immediate ventilatory support. The key is that the decision to intubate should be based primarily on clinical factors, not just ABG values alone.
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
1. The patient presented with drowsiness and sluggish respiration after overdosing on sleeping pills. An ABG revealed a pH of 7.1, HCO3 of 28 mEq/L, PaCO2 of 72 mmHg, and PaO2 of 78 mmHg.
2. These results indicate a primary respiratory acidosis, seen by the elevated PaCO2 and low pH. The HCO3 is also elevated, showing compensation for the chronic respiratory acidosis through bicarbonate retention.
3. Overdosing on sleeping pills can cause respiratory depression leading to respiratory acidosis from failure of carbon dioxide elimination, as seen in this case.
The document discusses arterial blood gas (ABG) analysis. It provides 3 key points:
1. ABG analysis aids in establishing diagnoses and assessing the severity of respiratory failure by measuring oxygenation, ventilation, and acid-base balance.
2. The normal values for pH, PCO2, PO2, HCO3, and other components are outlined.
3. A step-wise approach to interpreting an ABG report is described, including assessing whether it indicates a respiratory or metabolic disorder, whether compensation is adequate, and evaluating other acid-base parameters like anion gap.
This document provides an overview of acid-base balance and homeostasis. It discusses the bicarbonate buffer system, respiratory regulation through alveolar ventilation, and renal regulation through reabsorption and secretion of bicarbonate and hydrogen ions. The steps for analyzing an arterial blood gas are described, including looking at pH, identifying the primary disturbance, assessing compensation, and correlating clinically. Examples of acid-base disorders and their classifications are provided.
This document provides information on acid-base balance and interpretation of arterial blood gases (ABGs). It discusses terminology, how ABG analysis is performed, indications for ABGs, limitations, and an 8-step approach to evaluating acid-base disorders. Key points covered include the relationship between pH, acids, bases, acidosis, and alkalosis. Compensation in respiratory and metabolic acidosis/alkalosis is explained. Causes, evaluation, and treatment of different acid-base imbalances such as respiratory acidosis, metabolic acidosis, and lactic acidosis are summarized. Organ systems involved in acid-base regulation like the respiratory and renal systems are also overviewed.
This document provides an overview of arterial blood gas (ABG) analysis including normal parameters, definitions of acid-base disturbances, and a systematic approach to interpreting ABG results. It discusses the three mechanisms that maintain pH homeostasis: chemical buffering, alveolar ventilation, and renal handling of acids and bases. The four primary acid-base disorders are defined as metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. A stepwise approach is outlined including establishing the primary disorder, assessing compensation, and evaluating for mixed disturbances. Examples of common ABG interpretations are also provided.
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.
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 discusses acid-base balance and disorders. It provides an overview of how the lungs and kidneys work to maintain acid-base homeostasis by regulating carbon dioxide and bicarbonate levels. It then outlines the steps for diagnosing and classifying acid-base disorders as either respiratory or metabolic in nature, and as compensated or uncompensated. Examples of respiratory alkalosis and its causes and manifestations are also provided.
The document discusses arterial blood gas interpretation and key concepts related to pH, PaCO2, PaO2, and bicarbonate levels. It covers the four equations used to interpret blood gases, focusing on the PaCO2 equation and how it relates to alveolar ventilation and carbon dioxide production. Hypercapnia, or elevated PaCO2, is explained as resulting from inadequate alveolar ventilation. Clinical assessment of hypercapnia is shown to be unreliable.
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.
1) Arterial blood gas analysis measures gases in arterial blood and helps diagnose acid-base disorders.
2) It involves puncturing an artery with a needle to draw a small volume of blood, which is then analyzed to determine pH, oxygen and carbon dioxide levels.
3) This provides information about a patient's acid-base and respiratory status, and can help monitor conditions and treatment effectiveness.
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.
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.
This document provides information about arterial blood gas (ABG) interpretation. It discusses the procedure and precautions for ABG sampling, how the body maintains acid-base balance through bicarbonate buffering and respiratory and renal regulation. It explains the anatomy of an ABG report, including measured, calculated and entered values. Key areas of interpretation are oxygenation parameters like PaO2, A-a gradient and oxygen saturation, as well as acid-base status through pH, PCO2 and bicarbonate levels. The document provides examples of interpreting ABG results to assess for respiratory and metabolic acid-base disorders.
1. The document discusses acid-base balance and arterial blood gases (ABGs), including definitions of pH, the Henderson-Hasselbalch equation, and the three main mechanisms of acid-base regulation: chemical buffers, respiration, and renal.
2. It examines the causes, classifications, and compensation mechanisms of metabolic and respiratory acidosis and alkalosis. Mixed acid-base disorders are also addressed.
3. The importance of considering the patient's history and clinical presentation when interpreting ABG results is emphasized to help identify underlying etiologies and guide treatment.
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.
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.
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.
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 discusses arterial blood gases (ABG) and venous blood gases (VBG), including their normal values, physiology of acid-base balance, interpretation, and factors that can affect results. ABG provides information about acid-base balance, alveolar ventilation, and oxygenation status, while VBG is less invasive and can be used for frequent monitoring. The document outlines the steps to analyze ABG, describes various acid-base imbalances like respiratory acidosis and metabolic alkalosis, and provides examples of ABG values for different conditions.
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.
VBG vs ABG (replacement of venous blood sample instead of arterial one for an...Reza Aminnejad
This document discusses the use of venous blood gas measurements compared to arterial blood gas measurements. It finds that central venous blood gases most closely correlate with arterial measurements, while peripheral venous measurements vary more. Specifically, venous pH is typically 0.02-0.05 lower, PCO2 is typically 3-8 mmHg higher, and bicarbonate may be up to 2 mEq/L higher compared to arterial values. Venous measurements can be used for monitoring patients without arterial access, but arterial measurements are still preferred, especially for hypotensive patients. Periodic correlation of venous and arterial values is recommended when using venous measurements serially.
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 provides an overview of arterial blood gas (ABG) analysis, including:
1. ABG analysis measures oxygen, carbon dioxide, pH, and bicarbonate levels in arterial blood to evaluate respiratory and metabolic function.
2. It is ordered to assess patients with breathing issues, lung disease, or those on oxygen therapy to monitor treatment effectiveness.
3. Normal ABG results include a pH of 7.35-7.45, PaO2 of 80-100 mmHg, PaCO2 of 35-45 mmHg, and bicarbonate of 22-26 mmol/L.
Abnormal results can indicate respiratory or metabolic acidosis/alkalosis helping clinicians
1) An arterial blood gas test measures oxygen, carbon dioxide, acidity and bicarbonate levels in arterial blood to detect acid-base imbalances.
2) Metabolic acidosis occurs when the body produces excessive acid or the kidneys cannot remove enough acid. Respiratory acidosis occurs when the lungs cannot remove enough carbon dioxide from the body.
3) The body compensates for acid-base imbalances through respiratory or renal systems to restore the pH to normal levels. Respiratory compensation is faster acting than renal compensation.
An arterial blood gas (ABG) analysis measures pH, oxygen, and carbon dioxide levels in arterial blood. It is used to assess respiratory and metabolic function. The document outlines how to perform an ABG, including using a syringe to draw blood from the radial, brachial, or femoral artery. It discusses components measured in an ABG and their normal ranges, as well as factors that can affect results. Common acid-base imbalances like respiratory acidosis and metabolic alkalosis are also summarized, along with their primary and compensatory responses.
This document provides information on arterial blood gas analysis including acid-base terminology, clinical terminology criteria, the anion gap, prediction of compensatory changes, primary acid-base disorders, mixed acid-base disorders, examples of acid-base disorders, and causes of various disorders. Key points include definitions of acidemia, acidosis, alkalemia, and alkalosis. Normal values for pH, PaCO2, and HCO3 are provided. Respiratory and metabolic acidosis and alkalosis are described along with expected compensatory changes.
This presentation discuss about acid-base-gas normal ratio and its indication in relation to varying abnormal level and how to manage it. This includes clinical analysis practice.
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 discusses acid-base balance and disorders. It provides an overview of how the lungs and kidneys work to maintain acid-base homeostasis by regulating carbon dioxide and bicarbonate levels. It then outlines the steps for diagnosing and classifying acid-base disorders as either respiratory or metabolic in nature, and as compensated or uncompensated. Examples of respiratory alkalosis and its causes and manifestations are also provided.
The document discusses arterial blood gas interpretation and key concepts related to pH, PaCO2, PaO2, and bicarbonate levels. It covers the four equations used to interpret blood gases, focusing on the PaCO2 equation and how it relates to alveolar ventilation and carbon dioxide production. Hypercapnia, or elevated PaCO2, is explained as resulting from inadequate alveolar ventilation. Clinical assessment of hypercapnia is shown to be unreliable.
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.
1) Arterial blood gas analysis measures gases in arterial blood and helps diagnose acid-base disorders.
2) It involves puncturing an artery with a needle to draw a small volume of blood, which is then analyzed to determine pH, oxygen and carbon dioxide levels.
3) This provides information about a patient's acid-base and respiratory status, and can help monitor conditions and treatment effectiveness.
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.
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.
This document provides information about arterial blood gas (ABG) interpretation. It discusses the procedure and precautions for ABG sampling, how the body maintains acid-base balance through bicarbonate buffering and respiratory and renal regulation. It explains the anatomy of an ABG report, including measured, calculated and entered values. Key areas of interpretation are oxygenation parameters like PaO2, A-a gradient and oxygen saturation, as well as acid-base status through pH, PCO2 and bicarbonate levels. The document provides examples of interpreting ABG results to assess for respiratory and metabolic acid-base disorders.
1. The document discusses acid-base balance and arterial blood gases (ABGs), including definitions of pH, the Henderson-Hasselbalch equation, and the three main mechanisms of acid-base regulation: chemical buffers, respiration, and renal.
2. It examines the causes, classifications, and compensation mechanisms of metabolic and respiratory acidosis and alkalosis. Mixed acid-base disorders are also addressed.
3. The importance of considering the patient's history and clinical presentation when interpreting ABG results is emphasized to help identify underlying etiologies and guide treatment.
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.
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.
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.
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 discusses arterial blood gases (ABG) and venous blood gases (VBG), including their normal values, physiology of acid-base balance, interpretation, and factors that can affect results. ABG provides information about acid-base balance, alveolar ventilation, and oxygenation status, while VBG is less invasive and can be used for frequent monitoring. The document outlines the steps to analyze ABG, describes various acid-base imbalances like respiratory acidosis and metabolic alkalosis, and provides examples of ABG values for different conditions.
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.
VBG vs ABG (replacement of venous blood sample instead of arterial one for an...Reza Aminnejad
This document discusses the use of venous blood gas measurements compared to arterial blood gas measurements. It finds that central venous blood gases most closely correlate with arterial measurements, while peripheral venous measurements vary more. Specifically, venous pH is typically 0.02-0.05 lower, PCO2 is typically 3-8 mmHg higher, and bicarbonate may be up to 2 mEq/L higher compared to arterial values. Venous measurements can be used for monitoring patients without arterial access, but arterial measurements are still preferred, especially for hypotensive patients. Periodic correlation of venous and arterial values is recommended when using venous measurements serially.
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 provides an overview of arterial blood gas (ABG) analysis, including:
1. ABG analysis measures oxygen, carbon dioxide, pH, and bicarbonate levels in arterial blood to evaluate respiratory and metabolic function.
2. It is ordered to assess patients with breathing issues, lung disease, or those on oxygen therapy to monitor treatment effectiveness.
3. Normal ABG results include a pH of 7.35-7.45, PaO2 of 80-100 mmHg, PaCO2 of 35-45 mmHg, and bicarbonate of 22-26 mmol/L.
Abnormal results can indicate respiratory or metabolic acidosis/alkalosis helping clinicians
1) An arterial blood gas test measures oxygen, carbon dioxide, acidity and bicarbonate levels in arterial blood to detect acid-base imbalances.
2) Metabolic acidosis occurs when the body produces excessive acid or the kidneys cannot remove enough acid. Respiratory acidosis occurs when the lungs cannot remove enough carbon dioxide from the body.
3) The body compensates for acid-base imbalances through respiratory or renal systems to restore the pH to normal levels. Respiratory compensation is faster acting than renal compensation.
An arterial blood gas (ABG) analysis measures pH, oxygen, and carbon dioxide levels in arterial blood. It is used to assess respiratory and metabolic function. The document outlines how to perform an ABG, including using a syringe to draw blood from the radial, brachial, or femoral artery. It discusses components measured in an ABG and their normal ranges, as well as factors that can affect results. Common acid-base imbalances like respiratory acidosis and metabolic alkalosis are also summarized, along with their primary and compensatory responses.
This document provides information on arterial blood gas analysis including acid-base terminology, clinical terminology criteria, the anion gap, prediction of compensatory changes, primary acid-base disorders, mixed acid-base disorders, examples of acid-base disorders, and causes of various disorders. Key points include definitions of acidemia, acidosis, alkalemia, and alkalosis. Normal values for pH, PaCO2, and HCO3 are provided. Respiratory and metabolic acidosis and alkalosis are described along with expected compensatory changes.
This presentation discuss about acid-base-gas normal ratio and its indication in relation to varying abnormal level and how to manage it. This includes clinical analysis practice.
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.
This document discusses acid-base disorders and provides definitions, regulatory mechanisms, causes, and approaches to diagnosis. It defines acids, bases, and pH. The body tightly regulates blood pH between 7.35-7.45 through buffer systems, respiratory control of carbon dioxide levels, and renal regulation of bicarbonate. Causes of acid-base disorders include things like ketoacidosis, renal failure, diarrhea, and respiratory depression. Diagnosis involves determining if the primary disturbance is acidosis or alkalosis, whether it is respiratory or metabolic in nature, and assessing compensation through formulas like the anion gap and Winters formula.
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
The normal ranges for arterial blood gas values
Approach to arterial blood gas interpretation
Arterial blood gas abnormalities in special circumstances
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.
The document provides information on interpreting arterial blood gases (ABGs). It discusses:
- How the lungs and kidneys work to maintain acid-base balance by regulating carbon dioxide and bicarbonate levels.
- Key terms like pH, acidosis, alkalosis and how changes in pCO2 and HCO3 impact acid-base status.
- The process for drawing an ABG sample and analyzing the results, including calculating values like oxygen saturation and alveolar-arterial gradient.
- How to assess for primary acid-base disorders by looking at pH, pCO2 and HCO3 levels and whether compensation is appropriate.
- Formulas like Winter's equation and those for calculating
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 the biochemical aspects of pH imbalance and acid-base disorders. It begins by explaining how the body maintains pH balance through various buffer systems and respiratory and renal regulation. It then describes the types of acid-base disorders (metabolic acidosis, respiratory acidosis, metabolic alkalosis, respiratory alkalosis) and their primary abnormalities and compensatory mechanisms. The document also discusses arterial blood gas measurement and analysis to assess acid-base status and the major clinical causes of different acid-base disorders.
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.
1. The document discusses acid-base disturbances and homeostasis. It defines acids and bases, and how the body maintains pH levels through buffers, respiration, and the kidneys.
2. Specific acid-base disorders are described in detail, including metabolic acidosis, alkalosis and respiratory acidosis, alkalosis. Causes, clinical presentations, diagnoses, and treatments are provided for each.
3. Case studies are presented and acid-base status can be determined by reviewing arterial blood gases to measure pH, PaCO2 and HCO3 levels.
The document provides information about arterial blood gas analysis, including:
1. It outlines the objectives of arterial blood gas analysis such as assessing ventilation, oxygenation, acid-base homeostasis, and guiding treatment.
2. It describes important considerations for arterial blood sampling such as ensuring the patient is in a steady state.
3. It explains how to interpret an arterial blood gas report by analyzing parameters like pH, PCO2, HCO3 to classify if any acid-base disturbances are present and whether they are respiratory or metabolic in nature.
PRESENT: Acid base balance hossam (1).pptMbabazi Theos
This document discusses acid-base balance and interpreting arterial blood gas results. It begins by outlining the objectives of understanding acid-base physiology and the roles of pH, PaCO2, and bicarbonate. Normal values for arterial blood gases are defined. Causes, signs, and treatments of respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis are reviewed. The document explains how to interpret an arterial blood gas report using a multi-step process of analyzing pH, PaCO2, and bicarbonate levels to determine if an acid-base imbalance is respiratory or metabolically-driven. Two case examples are provided and interpreted using the outlined steps.
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 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 ratio of anion gap to bicarbonate change.
- Tables listing normal ABG values and expected compensation patterns for different acid-base disorders.
- Explanations of key ABG components like pH, partial pressures, bicarbonate, and base excess and how they relate to acid-base status.
- Causes and characteristics of respiratory and metabolic acidosis and alkalosis.
This document provides an overview of blood gas interpretation. It defines the components of a blood gas analysis and normal arterial blood gas values. Blood gas analysis is indicated to assess ventilation and oxygenation in respiratory diseases and acid-base imbalances in other conditions. There are four primary acid-base disturbances: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. The document outlines a stepwise approach to analyzing arterial blood gas results and interpreting acid-base status.
1. The document provides normal values for arterial blood gases and discusses the interpretation and significance of various blood gas measurements. It covers topics like respiratory and metabolic acidosis/alkalosis, oxygen content, carbon monoxide poisoning, and ventilation/perfusion imbalance.
2. Causes, treatments, and compensatory mechanisms for different acid-base imbalances are explained. Various equations used in blood gas analysis are also presented, such as the Henderson-Hasselbalch and alveolar gas equations.
3. The role of the kidneys, lungs, and hemoglobin in maintaining acid-base balance is described. Factors that can cause hypoxemia and how to determine oxygen adequacy from blood gases are discussed.
The document provides historical background on the development of peritoneal dialysis (PD) and outlines its use in acute kidney injury (AKI). It discusses:
1. The first experiments using the peritoneal cavity for uremia removal in the 1920s.
2. The development of intermittent PD in the 1960s and continuous ambulatory PD in the 1970s.
3. Evidence that high doses of continuous PD can provide appropriate metabolic control in AKI, with survival and renal recovery rates similar to other renal replacement therapies.
4. Indications for acute PD include hemodynamic instability and bleeding risks, while contraindications include recent abdominal surgery and severe peritonitis.
This document summarizes a presentation on therapeutic plasma exchange (PEX) given by Kamal Mohamed Okasha. It provides an overview of the PEX procedure and potential indications for PEX, including Goodpasture's Syndrome, thrombotic thrombocytopenic purpura, cryoglobulinemia, multiple myeloma, and ANCA disease. It discusses complications of PEX and guidelines for efficacy based on recent studies. In particular, it examines the use of PEX for Goodpasture's Syndrome, noting that PEX aims to remove circulating anti-GBM antibodies and that studies have found improved outcomes, including renal function and survival, for patients receiving PEX treatment.
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This document discusses acute kidney injury (AKI). It notes that AKI is often not recognized or coded for correctly. The incidence of AKI is increasing globally due to factors like comorbidities. Treatment for AKI is mainly supportive as there are no effective preventative or curative treatments. Several studies discussed found that diuretics and mannitol did not prevent AKI and may increase the risk of contrast-induced nephropathy. Hydration with sodium bicarbonate or saline was compared, with meta-analyses finding sodium bicarbonate may reduce the risk of AKI compared to saline. Dopamine and fenoldopam were also discussed but did not show clear benefits for preventing or treating AK
This document summarizes key information about lupus nephritis (LN) from a lecture given by Dr. Hussein Sheashaa. It begins with an outline of topics to be covered, including histopathology/biopsy, predictors of outcome, treatment approaches, and special situations. Regarding biopsy findings, it indicates that class IV LN is most common and describes revised classification guidelines. Treatment principles focus on early, aggressive therapy to achieve remission and prevent flares/progression. Standard induction therapies are discussed as well as new options like voclosporin. Maintenance strategies and treatment algorithms are presented. Predictors of poor outcome and management of special cases like pregnancy and refractory LN are also summarized.
This document summarizes key aspects of fluid management in peritoneal dialysis (PD) patients. It discusses optimizing PD prescriptions to balance adequate solute clearance while avoiding excess dialysis fluid exposure. Factors like residual renal function, membrane characteristics, fill volume and dwell time are considered. Monitoring adequacy includes measuring clearances and adjusting therapy if targets are not met. Guidelines recommend strategies to preserve renal function like ACEi/ARB use and avoiding dehydration.
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This document summarizes a presentation on membranous nephropathy (MN). The presentation discusses: 1) The pathogenesis and pathology of MN, focusing on its autoimmune nature. 2) Immunosuppression treatments for MN including calcineurin inhibitors (CNIs), rituximab, and newer therapies. 3) Algorithms and guidelines for the management and treatment of MN. 4) Recent 2019 clinical studies on treatments like rituximab and CNIs. 5) Recurrent MN after kidney transplantation. 6) The use of circulating anti-PLA2R antibody levels to diagnose and monitor MN noninvasively.
This document discusses different modalities for treating acute kidney injury (AKI) in critically ill patients, including continuous renal replacement therapy (CRRT) and intermittent hemodialysis. It provides pros and cons of each modality and factors to consider in determining the optimal treatment for an individual patient. While CRRT allows for more gradual fluid removal and hemodynamic stability, clearance is better with intermittent therapies. The document concludes that hemodynamic stability is the main determinant of treatment choice and clearance is optimized through combination of diffusion and convection methods.
This document provides an outline and summary of a presentation on diabetic kidney disease (DKD). It discusses:
1. The epidemiology, presentation, and trends of DKD.
2. The pathology and biomarkers of DKD.
3. The management of DKD, including the use of RAAS blockers, anti-hyperglycemic drugs like SGLT2 inhibitors and GLP1 RAs, and renal replacement therapies.
4. It concludes with a discussion of taking a holistic approach to DKD and lessons that can be learned from basic research on autophagy.
The document discusses several cases of glomerular disease:
1) A 27-year-old male with nephrotic syndrome and a kidney biopsy showing IgG and C3 deposits along the glomerular basement membrane consistent with membranous nephropathy.
2) A 78-year-old female admitted with nephrotic syndrome after a history of NSAID use, with a biopsy showing focal segmental glomerulosclerosis.
3) A 26-year-old male with nephrotic syndrome and renal impairment, whose biopsy demonstrated membranoproliferative glomerulonephritis with C3 deposition and subendothelial electron dense deposits. Follow up showed elevated
A 30-year-old man presented with lower limb swelling, shortness of breath, and decreased urine output for 2 weeks. He had a history of drug abuse including heroin, tramadol, and marijuana. Initial labs showed severe kidney dysfunction with a creatinine of 7.5 mg/dl. A renal biopsy was performed which showed acute tubular injury, focal interstitial nephritis with eosinophil infiltrate, and mesangial proliferative glomerulonephritis. He was started on hemodialysis and steroids. After treatment, his kidney function improved and he was discharged with a creatinine of 1.5 mg/dl.
A 19-year-old male gym player presented with decreased urine output, fatigue, loss of appetite, joint pain, nausea, and vomiting for one week. Lab results showed impaired renal function. He has a history of artheralgia treated with long-acting penicillin. Investigations showed positive ANA and anti-ds DNA. A renal biopsy was done which revealed lupus nephritis class 4, indicating an active inflammation. The treatment plan includes high dose steroids, immunosuppressants, and supplements.
This document discusses tubulointerstitial nephritis (TIN), a pattern of renal injury characterized by inflammation and edema of the renal tubules and interstitium. TIN is most commonly caused by drugs (71% of cases) and infections (15% of cases). On biopsy, TIN shows lymphocytic infiltration of the tubules and interstitium with tubular atrophy and normal glomeruli and vessels. Treatment involves withdrawing the offending agent and supportive care. Corticosteroids may aid recovery but their effectiveness is debated. Prognosis depends on factors like duration of the insult and degree of fibrosis - complete recovery is more likely if treatment begins early.
Fasting ramadan nephrology prospective prof. osama el shahateFarragBahbah
Dr. Osama El-Shahat is the head of the nephrology department at New Mansoura General Hospital and vice president of the Dakahlia Nephrology Group. The document discusses kidney disease (CKD), transplantation, dialysis, and recommendations. It provides examples of how some animals fast during certain periods by not eating and reducing activity. It also discusses fasting guidelines for patients with illnesses, noting that those with more severe illnesses should generally be exempted from fasting. The document analyzes a study on the effects of Ramadan fasting on renal function in CKD patients and notes that more large studies are needed. It also reviews a case of a hypertensive patient wanting to fast for Ramadan
Ramadan fasting & kidney disease may 2019FarragBahbah
Ramadan fasting is a unique metabolic model that consists of alternating periods of fasting and feasting rather than continuous fasting. During the fast, the body breaks down fat stores and releases fatty acids into the bloodstream to be used for energy. This process can help eliminate toxins from the fatty acids. Fasting has also been shown to help reduce inflammation and support the immune system. However, fasting also carries risks and may not be appropriate for certain groups like pregnant women, those with medical conditions, or people on medication. Proper hydration and electrolyte replacement is important when fasting to avoid health issues.
- Short-term catheters should only be used for acute dialysis or limited hospital use. Non-cuffed femoral catheters are only for bed-bound patients.
- Long-term catheters should be used with a plan for permanent access and prefer those capable of high flow rates. Choice depends on local experience and goals.
- Long-term catheters should avoid the same side as a maturing arteriovenous access, if possible.
This document summarizes the medical history and treatment of a 55-year-old male patient with end-stage renal disease on hemodialysis for 17 years and secondary hyperparathyroidism. Medical treatment with cinacalcet and calcitriol was unsuccessful in lowering his high calcium, phosphorus, and PTH levels. Consultations with ENT and cardiology found no issues. The doctor decided that parathyroidectomy was the best option to treat his tertiary hyperparathyroidism that was not responding to medical treatment.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
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Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
- 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
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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).
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
4. ABGs: What You Get
• Arterial PO2
• Arterial PCO2
• Arterial pH
• Some electrolytes (e.g., Na+, K+, Ca++)
• Lactate
• [HCO3
-]
• SaO2
• Other assorted calculated results
5.
6.
7.
8.
9.
10.
11.
12. Main Components of ABG
• pH-Measures hydrogen ion (H+) concentration
• PCO2-Partial pressure of CO2 in arteries
• HCO3-Measures serum bicarbonate
13. Normal Values of ABG
• pH-7.35-7.45
• PCO2-35-45mmHg
• HCO3-22-26 mEq/l
14.
15.
16.
17. Abnormal ABG Readings
• The body will work hard to balance any
abnormal values within the acid-base system
• How the body works to do this depends on
the issue:
• CO2 is controlled by the lungs
• HCO3 is controlled by the kidneys
18.
19. Compensated Vs Uncompensated
• If the body can work to balance the issue
through the lungs or kidneys it will result in a
normal pH
• Other values in the ABG will be ABNL however
do not matter since there not an overall effect
on the pH
• This is a compensated ABG
20. Step 1
• Acidosis (7.35 _ 7.45) Alkalosis
7.4
• Look at the pH-if abnormal you have an
uncompensated disturbance
• Now figure out if the disturbance is acidosis or
alkalosis-this will determine the treatment
• Acidosis is pH below7.35 and results from
adding H+ an acid
• Alkalosis is pH above 7.45 and results from
decrease in H+ an acid
22. Step 2: What is the primary disorder?
What disorder is present? pH pCO2 or HCO3
Respiratory Acidosis pH low pCO2 high
Metabolic Acidosis pH low HCO3 low
Respiratory Alkalosis pH high pCO2 low
Metabolic Alkalosis pH high HCO3 high
23. Step 3
• Put all your findings together to determine the
overall imbalance
• Example: pH 7.29 PCO2 50 HCO3 26
• What is this patient’s condition?
25. Acid-base Terminology
Acidemia: blood pH < 7.35
Acidosis: a primary physiologic process that, occurring alone, tends
to cause acidemia. Examples: metabolic acidosis from decreased
perfusion (lactic acidosis); respiratory acidosis from hypoventilation.
If the patient also has an alkalosis at the same time, the resulting
blood pH may be low, normal, or high.
Alkalemia: blood pH > 7.45
Alkalosis: a primary physiologic process that, occurring alone,
tends to cause alkalemia. Examples: metabolic alkalosis from
excessive diuretic therapy; respiratory alkalosis from acute
hyperventilation. If the patient also has an acidosis at the same
time, the resulting blood pH may be high, normal, or low.
26. Acid-base Terminology (cont.)
Primary acid-base disorder: One of the four acid-base disturbances that is
manifested by an initial change in HCO3
- or PaCO2. They are: metabolic
acidosis (MAc), metabolic alkalosis (MAlk), respiratory acidosis (RAc), and
respiratory alkalosis (RAlk). If HCO3
- changes first, the disorder is either
MAc (reduced HCO3
- and acidemia) or MAlk (elevated HCO3
- and
alkalemia). If PaCO2 changes first, the problem is either RAlk (reduced
PaCO2 and alkalemia) or RAc (elevated PaCO2 and acidemia).
Compensation: The change in HCO3
- or PaCO2 that results from the
primary event. Compensatory changes are not classified by the terms used
for the four primary acid-base disturbances. For example, a patient who
hyperventilates (lowers PaCO2) solely as compensation for MAc does not
have a RAlk, the latter being a primary disorder that, alone, would lead to
alkalemia. In simple, uncomplicated MAc the patient will never develop
alkalemia.
27. Primary Acid-base Disorders:
Respiratory Alkalosis
Respiratory alkalosis - A primary disorder where the first change is a
lowering of PaCO2, resulting in an elevated pH. Compensation
(bringing the pH back down toward normal) is a secondary lowering
of bicarbonate (HCO3) by the kidneys; this reduction in HCO3
- is not
metabolic acidosis, since it is not a primary process.
Primary Event Compensatory Event
HCO3
- ↓HCO3
-
↑ pH ~ ------- ↑ pH ~ --------
↓ PaCO2 ↓ PaCO2
28. Primary Acid-base Disorders:
Respiratory Acidosis
Respiratory acidosis - A primary disorder where the first change is
an elevation of PaCO2, resulting in decreased pH. Compensation
(bringing pH back up toward normal) is a secondary retention of
bicarbonate by the kidneys; this elevation of HCO3
- is not metabolic
alkalosis since it is not a primary process.
Primary Event Compensatory Event
HCO3
- ↑ HCO3
-
↓ pH ~ --------- ↓ pH ~ ---------
↑PaCO2 ↑ PaCO2
29. Primary Acid-base Disorders:
Metabolic Acidosis
Metabolic acidosis - A primary acid-base disorder where the first
change is a lowering of HCO3
-, resulting in decreased pH.
Compensation (bringing pH back up toward normal) is a secondary
hyperventilation; this lowering of PaCO2 is not respiratory alkalosis
since it is not a primary process.
Primary Event Compensatory Event
↓ HCO3
- ↓HCO3
-
↓ pH ~ ------------ ↓ pH ~ ------------
PaCO2 ↓ PaCO2
30. Primary Acid-base Disorders:
Metabolic Alkalosis
Metabolic alkalosis - A primary acid-base disorder where the first change is
an elevation of HCO3
-, resulting in increased pH. Compensation is a
secondary hypoventilation (increased PaCO2), which is not respiratory
acidosis since it is not a primary process. Compensation for metabolic
alkalosis (attempting to bring pH back down toward normal) is less
predictable than for the other three acid-base disorders.
Primary Event Compensatory Event
↑ HCO3
- ↑HCO3
-
↑ pH ~ ------------ ↑ pH ~ ---------
PaCO2 ↑PaCO2
31. Metabolic Acid-base Disorders:
Some Clinical Causes
METABOLIC ACIDOSIS ↓HCO3
- & ↓ pH
- Increased anion gap
• lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethylene
glycol, methanol)
- Normal anion gap
• diarrhea; some kidney problems (e.g., renal tubular acidosis,
interstitial nephritis)
METABOLIC ALKALOSIS ↑ HCO3
- & ↑ pH
Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis,
diuretics, corticosteroids, gastric suctioning, vomiting
Chloride resistant: any hyperaldosterone state (e.g., Cushing’s syndrome,
Bartter’s syndrome, severe K+ depletion)
32. RESPIRATORY ACIDOSIS ↑PaCO2 & ↓pH
Central nervous system depression (e.g., drug overdose)
Chest bellows dysfunction (e.g., Guillain-Barré syndrome, myasthenia
gravis)
Disease of lungs and/or upper airway (e.g., chronic obstructive lung
disease, severe asthma attack, severe pulmonary edema)
RESPIRATORY ALKALOSIS ↓PaCO2 & ↑ pH
Hypoxemia (includes altitude)
Anxiety
Sepsis
Any acute pulmonary insult (e.g., pneumonia, mild asthma attack, early
pulmonary edema, pulmonary embolism)
Respiratory Acid-base Disorders:
Some Clinical Causes
33. Mixed Acid-base Disorders
In chronically ill respiratory patients, mixed disorders are probably
more common than single disorders, e.g., RAc + MAlk, RAc + Mac,
Ralk + MAlk.
In renal failure (and other conditions) combined MAlk + MAc is also
encountered.
Always be on the lookout for mixed acid-base disorders. They can
be missed!
34. Expected changes in pH and HCO3
- for a 10-mm Hg change in PaCO2
resulting from either primary hypoventilation (respiratory acidosis) or
primary hyperventilation (respiratory alkalosis):
ACUTE CHRONIC
Resp Acidosis
pH ↓ by 0.07 pH ↓ by 0.03
HCO3
- ↑ by 1* HCO3
- ↑ by 3 - 4
Resp Alkalosis
pH ↑ by 0.08 pH ↑ by 0.03
HCO3
- ↓ by 2 HCO3
- ↓ by 5
* Units for HCO3
- are mEq/L
35.
36.
37. Predicted changes in HCO3
- for a directional change in
PaCO2 can help uncover mixed acid-base disorders.
a) A normal or slightly low HCO3
-
in the presence of hypercapnia
suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO2 50
mm Hg, HCO3
-
22 mEq/L. Based on the rule for increase in HCO3
-
with hypercapnia, it should be at least 25 mEq/L in this example;
that it is only 22 mEq/L suggests a concomitant metabolic acidosis.
b) A normal or slightly elevated HCO3
-
in the presence of hypocapnia
suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO2 30
mm Hg, HCO3
-
26 mEq/L. Based on the rule for decrease in HCO3
-
with hypocapnia, it should be at least 23 mEq/L in this example; that
it is 26 mEq/L suggests a concomitant metabolic alkalosis.
38. How much oxygen is in the blood?
PaO2 vs. SaO2 vs. CaO2
OXYGEN PRESSURE: PaO2
Since PaO2 reflects only free oxygen molecules dissolved in plasma and not those bound to hemoglobin,
PaO2 cannot tell us “how much” oxygen is in the blood; for that you need to know how much oxygen is also
bound to hemoglobin, information given by the SaO2 and hemoglobin content.
OXYGEN SATURATION: SaO2
The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen
saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn’t reveal how much oxygen is in the
blood; for that we also need to know the hemoglobin content.
OXYGEN CONTENT: CaO2
Tissues need a requisite amount of O2 molecules for metabolism. Neither the PaO2 nor the SaO2 provide
information on the number of oxygen molecules, i.e., how much oxygen is in the blood. (Neither PaO2 nor
SaO2 have units that denote any quantity.) Only CaO2 (units ml O2/dl) tells us how much oxygen is in the
blood; this is because CaO2 is the only value that incorporates the hemoglobin content. Oxygen content
can be measured directly or calculated by the oxygen content equation:
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
39. ABG Practice
• pH 7.36
• PaCO2 43
• HCO3 22
• Interpretation?
A. Normal
B. Respiratory acidosis
C. Compensated respiratory
acidosis
D. Respiratory Alkalosis
E. Compensated respiratory
alkalosis
F. Metabolic acidosis
G. Compensated metabolic
acidosis
H. Metabolic alkalosis
I. Compensated metabolic
alkalosis
Answer: A. Normal
40. ABG Practice
• pH 7.45
• PaCO2 30
• HCO3 19
• Interpretation?
Answer: E. Compensated Respiratory Alkalosis
PaCO2 is low
HCO3 is low
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
41. ABG Practice
• pH 7.52
• PaCO2 43
• HCO3 31
• Interpretation?
Answer: H. Metabolic Alkalosis
PaCO2 is normal
HCO3 is high
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
42. ABG Practice
• pH 7.3
• PaCO2 72
• HCO3 24
• Interpretation?
Answer: B. Respiratory Acidosis
PaCO2 is high
HCO3 is normal
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
43. ABG Practice
• pH 7.35
• PaCO2 28
• HCO3 18
• Interpretation?
Answer: G. Compensated Metabolic Acidosis
PaCO2 is low
HCO3 is low
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
44. ABG Practice
• pH 7.51
• PaCO2 28
• HCO3 23
• Interpretation?
Answer: D. Respiratory Alkalosis
PaCO2 is normal
HCO3 is low
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
45. ABG Practice
• pH 7.35
• PaCO2 65
• HCO3 31
• Interpretation?
Answer: C. Compensated Respiratory Acidosis
PaCO2 is high
HCO3 is high
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
46. ABG Practice
• pH 7.26
• PaCO2 45
• HCO3 16
• Interpretation?
Answer: F. Metabolic Acidosis
PaCO2 is normal
HCO3 is low
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
47. 47
ABG Practice
• pH 7.49
• PaCO2 42
• HCO3 29
• Interpretation?
Answer: H. Metabolic Alkalosis
PaCO2 is normal
HCO3 is high
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
48. ABG Practice
• pH 7.3
• PaCO2 59
• HCO3 24
• Interpretation?
Answer: B. Respiratory Acidosis
PaCO2 is high
HCO3 is normal
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
49. ABG Practice
• pH 7.44
• PaCO2 53
• HCO3 31
• Interpretation?
Answer: I. Compensated Metabolic Alkalosis
PaCO2 is high
HCO3 is high
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
50. ABG Practice
• pH 7.39
• PaCO2 42
• HCO3 23
• Interpretation?
Answer: A. Normal
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
51. ABG Practice
• pH 7.31
• PaCO2 36
• HCO3 18
• Interpretation?
Answer: F. Metabolic Acidosis
PaCO2 is normal
HCO3 is low
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
52. ABG Practice
• pH 7.17
• PaCO2 89
• HCO3 22
• Interpretation?
Answer: B. Respiratory Acidosis
PaCO2 is high
HCO3 is normal
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis
53. ABG Practice
• pH 7.43
• PaCO2 38
• HCO3 24
• Interpretation?
Answer: A. Normal
A. Normal
B. Respiratory acidosis
C. Compensated respiratory acidosis
D. Respiratory Alkalosis
E. Compensated respiratory alkalosis
F. Metabolic acidosis
G. Compensated metabolic acidosis
H. Metabolic alkalosis
I. Compensated metabolic alkalosis