1. The patient has a mixed disorder of metabolic acidosis with respiratory compensation and high anion gap metabolic acidosis.
2. The primary disorder is metabolic acidosis as pH and HCO3 are decreased while PCO2 is normal.
3. The anion gap is elevated indicating a high anion gap metabolic acidosis likely due to an unknown toxin given the clinical context.
This document discusses the Stewart approach to acid-base disorders. It provides 3 key points:
1. The Stewart approach examines the independent variables that determine pH: the strong ion difference (SID), total weak acids (ATOT), and partial pressure of carbon dioxide (pCO2). Imbalances in these variables can lead to acid-base disorders.
2. Strong ions like sodium, chloride, and lactate influence pH through their effect on water dissociation. Increased sodium or lactate can increase SID and cause alkalosis, while increased chloride decreases SID and causes acidosis.
3. The presence of unmeasured anions can be detected using the Fencl-Stewart approach by
The document provides information on 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.
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.
The document discusses acid-base homeostasis, which involves chemical and physiological processes that maintain the acidity of body fluids at optimal levels. The chemical processes include extracellular and intracellular buffers that provide the first line of defense against acid-base imbalances. Physiological processes like respiration and kidney function then modulate acid-base levels through changes in metabolism and the excretion of acids and bases. Multiple interconnected mechanisms are needed due to the importance of tightly regulating hydrogen ion concentrations for cellular functions and organ systems like the brain and heart.
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 analyzing arterial blood gas results. It discusses:
1. The key parameters measured in an arterial blood gas report including pH, pCO2, pO2, HCO3, oxygen saturation, and others.
2. How to interpret these parameters to determine a patient's acid-base status, oxygenation, and ventilation.
3. Formulas used to calculate derived values like oxygen content, alveolar-arterial difference, and base excess which provide additional insight.
4. Guidelines for properly collecting and handling arterial blood gas samples to avoid technical errors.
5. The importance of considering clinical context and using a systematic approach to integrate arterial blood gas results with
The document discusses acid-base balance and regulation in the human body. It covers:
1) Chemical compounds can act as proton donors (acids) or acceptors (bases), and acids and bases react to form salts. The body maintains blood pH through buffers like bicarbonate and proteins.
2) The lungs, kidneys, buffers and liver all play roles in regulating arterial pH. The lungs excrete carbon dioxide through respiration as compensation for metabolic acidosis or alkalosis. The kidneys reclaim bicarbonate and generate new bicarbonate through secretion of hydrogen ions.
3) Disturbances to acid-base balance result in acidosis or alkalosis,
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 the Stewart approach to acid-base disorders. It provides 3 key points:
1. The Stewart approach examines the independent variables that determine pH: the strong ion difference (SID), total weak acids (ATOT), and partial pressure of carbon dioxide (pCO2). Imbalances in these variables can lead to acid-base disorders.
2. Strong ions like sodium, chloride, and lactate influence pH through their effect on water dissociation. Increased sodium or lactate can increase SID and cause alkalosis, while increased chloride decreases SID and causes acidosis.
3. The presence of unmeasured anions can be detected using the Fencl-Stewart approach by
The document provides information on 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.
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.
The document discusses acid-base homeostasis, which involves chemical and physiological processes that maintain the acidity of body fluids at optimal levels. The chemical processes include extracellular and intracellular buffers that provide the first line of defense against acid-base imbalances. Physiological processes like respiration and kidney function then modulate acid-base levels through changes in metabolism and the excretion of acids and bases. Multiple interconnected mechanisms are needed due to the importance of tightly regulating hydrogen ion concentrations for cellular functions and organ systems like the brain and heart.
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 analyzing arterial blood gas results. It discusses:
1. The key parameters measured in an arterial blood gas report including pH, pCO2, pO2, HCO3, oxygen saturation, and others.
2. How to interpret these parameters to determine a patient's acid-base status, oxygenation, and ventilation.
3. Formulas used to calculate derived values like oxygen content, alveolar-arterial difference, and base excess which provide additional insight.
4. Guidelines for properly collecting and handling arterial blood gas samples to avoid technical errors.
5. The importance of considering clinical context and using a systematic approach to integrate arterial blood gas results with
The document discusses acid-base balance and regulation in the human body. It covers:
1) Chemical compounds can act as proton donors (acids) or acceptors (bases), and acids and bases react to form salts. The body maintains blood pH through buffers like bicarbonate and proteins.
2) The lungs, kidneys, buffers and liver all play roles in regulating arterial pH. The lungs excrete carbon dioxide through respiration as compensation for metabolic acidosis or alkalosis. The kidneys reclaim bicarbonate and generate new bicarbonate through secretion of hydrogen ions.
3) Disturbances to acid-base balance result in acidosis or alkalosis,
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.
The document discusses acid-base balance and disorders. It provides an introduction to acid-base chemistry and defines pH. It describes how the body regulates acids through buffer systems, respiration, and the kidneys. The document defines and discusses the causes, pathophysiology, diagnosis, and management of respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Arterial blood gas analysis is described as a key test to evaluate acid-base status.
Echocardiography uses ultrasound to produce images of the heart. Sound waves are sent through a transducer and reflected off heart structures, with the echoes converted into pictures seen on a monitor. It has several applications including assessing cardiac chamber size and function, valves, pericardium, aorta, and detecting tumors or clots. Views are obtained by positioning the transducer in different locations and angles around the chest to visualize the heart from multiple windows.
The document summarizes guidelines from the 2017 AHA/ACC for the prevention, detection, evaluation, and management of high blood pressure in adults. It defines categories of blood pressure, discusses evaluation for secondary hypertension, recommends non-pharmacologic and pharmacologic treatment options including drug classes and combinations, and provides treatment algorithms for specific conditions like stable ischemic heart disease and heart failure.
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.
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.
This document discusses the use of transesophageal echocardiography (TEE) as a powerful diagnostic tool that can decrease morbidity and increase survival in anesthetized patients. It describes how TEE works and provides various views that can be obtained. It also outlines applications of TEE during cardiac surgery and in the intensive care unit to assess hemodynamics and guide treatment. Contraindications and precautions for TEE are also mentioned.
This document provides an overview of a presentation on arterial blood gases (ABG) and acid-base balance. It includes the following:
1. Three main targets of the presentation: understanding acid-base disorders, making ABG interpretation easy, and treatment of acid-base disorders.
2. The presentation is divided into three parts: concepts, practice with case scenarios, and treatment of acid-base disorders.
3. Part 1 on concepts covers pulmonary gas exchange, acid-base balance disorders, ABG sampling and interpretation. It aims to explain the basics of gas exchange, acid-base balance, and ABG values.
4. Part 2 involves practicing ABG analysis through a series of case
This document provides an overview of acid-base disorders and their diagnosis and management. It discusses the regulation of acid-base balance and what arterial blood gases can reveal about a patient's condition. It then covers the diagnosis of acid-base disorders including sample handling and analysis. Key concepts around the Henderson-Hasselbalch equation and normal values are explained. The document breaks down simple and expected changes in various acid-base disorders. Case studies are presented and analyzed. Metabolic acidosis, alkalosis, respiratory compensation, and anion gaps are discussed in detail.
This document provides an overview of arterial blood gas analysis. It discusses the physiology of acid-base status including the basics of pH, acids, bases and buffers. The key buffers that help regulate acid-base balance are the bicarbonate buffer system and protein buffers. Respiratory regulation is also important as carbon dioxide production is a major factor influencing hydrogen ion concentration and pH. The kidneys play an important role in excretion of acids and bases to help maintain homeostasis.
This document discusses heart failure, including its causes, clinical presentation, assessment, and management. It provides information on hemodynamics in heart failure, how to clinically recognize and differentiate various types of heart failure based on volume status and perfusion. It outlines approaches for assessing severity, ordering appropriate tests, and managing patients with both acute and long-term heart failure through pharmacological therapies, procedures like CRT and LVAD, and potentially stem cell therapy or transplant. Key signs, symptoms, and treatments are summarized.
A 30-minute talk, presented as part of the weekly teaching activities in Alder Hey Children's Hospital (Liverpool, UK). It addresses PDA evaluation in children - starting with embryology & anatomy with the basis behind physiological closure versus patency after birth. What is the role of echo study in diagnosing/evaluating PDA? Modes used with some clear movies? Its limitations?
This document discusses hypernatremia and provides a stepwise approach to evaluating and treating patients with hypernatremia. It addresses four key questions:
1) Determining if hypernatremia is caused by water deficit or sodium gain.
2) Calculating a patient's water deficit based on their serum sodium level.
3) Choosing the appropriate fluid for administration based on a patient's volume status.
4) Estimating the reduction in serum sodium that would result from infusing 1 L of fluid over 1 hour.
Central hyperthermia can occur after stroke or brain injury due to damage to the hypothalamus or brainstem centers that regulate temperature. It causes rapid onset fever without evidence of infection. Diagnosis involves ruling out infection and treatment uses a multimodal approach including medications like bromocriptine or baclofen to reduce fever by acting on dopamine or GABA receptors in the brain.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and oxygen saturation. It outlines a 4 step method for ABG interpretation including identifying the primary disturbance, determining if it is respiratory or metabolic, and assessing for compensation. Several case examples are provided to demonstrate application of this analytical approach.
This document provides 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.
This document provides an introduction to hemodynamic monitoring, which involves measuring factors that influence blood flow and pressure. It defines hemodynamic monitoring and outlines its purposes, which include diagnosing and managing shock states, determining fluid status, and measuring cardiac output. The document discusses indications for hemodynamic monitoring as well as contraindications for invasive pulmonary artery catheters. It also reviews important hemodynamic values and concepts, pulmonary artery catheter insertion and positioning, waveform analysis, and removal of pulmonary artery catheters.
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.
Antibiotic Dosing in critical care Catherine mc kenzieisakakinada
- Antibiotics should be administered within the first hour of recognizing severe sepsis or septic shock. Broad-spectrum antibiotics with good penetration of the suspected infection site should be used.
- The antibiotic regimen should be reassessed daily to optimize efficacy, prevent resistance, avoid toxicity, and minimize costs. Extended or continuous infusions of beta-lactam antibiotics may improve outcomes for critically ill patients, especially those with infection from less susceptible organisms.
- Proper dosing of antibiotics in critical care requires considering each patient's individual situation and balancing optimal treatment with minimizing harm from adverse events like toxicity.
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.
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 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
The document discusses acid-base balance and disorders. It provides an introduction to acid-base chemistry and defines pH. It describes how the body regulates acids through buffer systems, respiration, and the kidneys. The document defines and discusses the causes, pathophysiology, diagnosis, and management of respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Arterial blood gas analysis is described as a key test to evaluate acid-base status.
Echocardiography uses ultrasound to produce images of the heart. Sound waves are sent through a transducer and reflected off heart structures, with the echoes converted into pictures seen on a monitor. It has several applications including assessing cardiac chamber size and function, valves, pericardium, aorta, and detecting tumors or clots. Views are obtained by positioning the transducer in different locations and angles around the chest to visualize the heart from multiple windows.
The document summarizes guidelines from the 2017 AHA/ACC for the prevention, detection, evaluation, and management of high blood pressure in adults. It defines categories of blood pressure, discusses evaluation for secondary hypertension, recommends non-pharmacologic and pharmacologic treatment options including drug classes and combinations, and provides treatment algorithms for specific conditions like stable ischemic heart disease and heart failure.
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.
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.
This document discusses the use of transesophageal echocardiography (TEE) as a powerful diagnostic tool that can decrease morbidity and increase survival in anesthetized patients. It describes how TEE works and provides various views that can be obtained. It also outlines applications of TEE during cardiac surgery and in the intensive care unit to assess hemodynamics and guide treatment. Contraindications and precautions for TEE are also mentioned.
This document provides an overview of a presentation on arterial blood gases (ABG) and acid-base balance. It includes the following:
1. Three main targets of the presentation: understanding acid-base disorders, making ABG interpretation easy, and treatment of acid-base disorders.
2. The presentation is divided into three parts: concepts, practice with case scenarios, and treatment of acid-base disorders.
3. Part 1 on concepts covers pulmonary gas exchange, acid-base balance disorders, ABG sampling and interpretation. It aims to explain the basics of gas exchange, acid-base balance, and ABG values.
4. Part 2 involves practicing ABG analysis through a series of case
This document provides an overview of acid-base disorders and their diagnosis and management. It discusses the regulation of acid-base balance and what arterial blood gases can reveal about a patient's condition. It then covers the diagnosis of acid-base disorders including sample handling and analysis. Key concepts around the Henderson-Hasselbalch equation and normal values are explained. The document breaks down simple and expected changes in various acid-base disorders. Case studies are presented and analyzed. Metabolic acidosis, alkalosis, respiratory compensation, and anion gaps are discussed in detail.
This document provides an overview of arterial blood gas analysis. It discusses the physiology of acid-base status including the basics of pH, acids, bases and buffers. The key buffers that help regulate acid-base balance are the bicarbonate buffer system and protein buffers. Respiratory regulation is also important as carbon dioxide production is a major factor influencing hydrogen ion concentration and pH. The kidneys play an important role in excretion of acids and bases to help maintain homeostasis.
This document discusses heart failure, including its causes, clinical presentation, assessment, and management. It provides information on hemodynamics in heart failure, how to clinically recognize and differentiate various types of heart failure based on volume status and perfusion. It outlines approaches for assessing severity, ordering appropriate tests, and managing patients with both acute and long-term heart failure through pharmacological therapies, procedures like CRT and LVAD, and potentially stem cell therapy or transplant. Key signs, symptoms, and treatments are summarized.
A 30-minute talk, presented as part of the weekly teaching activities in Alder Hey Children's Hospital (Liverpool, UK). It addresses PDA evaluation in children - starting with embryology & anatomy with the basis behind physiological closure versus patency after birth. What is the role of echo study in diagnosing/evaluating PDA? Modes used with some clear movies? Its limitations?
This document discusses hypernatremia and provides a stepwise approach to evaluating and treating patients with hypernatremia. It addresses four key questions:
1) Determining if hypernatremia is caused by water deficit or sodium gain.
2) Calculating a patient's water deficit based on their serum sodium level.
3) Choosing the appropriate fluid for administration based on a patient's volume status.
4) Estimating the reduction in serum sodium that would result from infusing 1 L of fluid over 1 hour.
Central hyperthermia can occur after stroke or brain injury due to damage to the hypothalamus or brainstem centers that regulate temperature. It causes rapid onset fever without evidence of infection. Diagnosis involves ruling out infection and treatment uses a multimodal approach including medications like bromocriptine or baclofen to reduce fever by acting on dopamine or GABA receptors in the brain.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and oxygen saturation. It outlines a 4 step method for ABG interpretation including identifying the primary disturbance, determining if it is respiratory or metabolic, and assessing for compensation. Several case examples are provided to demonstrate application of this analytical approach.
This document provides 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.
This document provides an introduction to hemodynamic monitoring, which involves measuring factors that influence blood flow and pressure. It defines hemodynamic monitoring and outlines its purposes, which include diagnosing and managing shock states, determining fluid status, and measuring cardiac output. The document discusses indications for hemodynamic monitoring as well as contraindications for invasive pulmonary artery catheters. It also reviews important hemodynamic values and concepts, pulmonary artery catheter insertion and positioning, waveform analysis, and removal of pulmonary artery catheters.
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.
Antibiotic Dosing in critical care Catherine mc kenzieisakakinada
- Antibiotics should be administered within the first hour of recognizing severe sepsis or septic shock. Broad-spectrum antibiotics with good penetration of the suspected infection site should be used.
- The antibiotic regimen should be reassessed daily to optimize efficacy, prevent resistance, avoid toxicity, and minimize costs. Extended or continuous infusions of beta-lactam antibiotics may improve outcomes for critically ill patients, especially those with infection from less susceptible organisms.
- Proper dosing of antibiotics in critical care requires considering each patient's individual situation and balancing optimal treatment with minimizing harm from adverse events like toxicity.
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.
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 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 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 an overview of arterial blood gas interpretation. It discusses the objectives, procedure and precautions for ABG sampling. It covers the interpretation of oxygenation status including how to determine PaO2 and the PaO2/FiO2 ratio. For acid-base status, it explains the bicarbonate buffer system, respiratory and renal regulation and how to assess primary acid-base disorders. A 6-step approach to ABG interpretation is presented covering evaluating authenticity, determining acidemia/alkalemia, respiratory vs. metabolic causes, compensation and using the anion gap to identify high anion gap metabolic acidosis.
This document provides guidance on arterial blood gas (ABG) interpretation. It discusses the indications for ABG testing, appropriate sampling sites, contraindications, and technical considerations. The normal ranges for pH, PCO2, PO2, HCO3, and other values are provided. A step-by-step process is outlined to interpret ABGs, including assessing oxygenation, identifying acid-base disturbances, evaluating respiratory vs. metabolic causes, and compensatory mechanisms. Common etiologies of respiratory and metabolic acidosis and alkalosis are also reviewed.
ABG intreptretation on clinical setup-1.pptxpugalrockzz1
This document provides guidance on arterial blood gas (ABG) interpretation. It discusses the indications for ABG testing, appropriate sampling sites, contraindications, and technical considerations. The normal ranges for pH, PCO2, PO2, HCO3, and other values are provided. A step-by-step process is outlined to interpret ABGs, including assessing oxygenation, identifying acid-base disturbances, evaluating respiratory vs. metabolic causes, and compensatory mechanisms. Common etiologies of respiratory and metabolic acidosis and alkalosis are also reviewed.
This document provides an overview of arterial blood gas interpretation. It discusses the objectives, procedure and precautions for ABG sampling. It covers the interpretation of oxygenation status including how to determine PaO2 and the PaO2/FiO2 ratio. For acid-base status, it discusses the bicarbonate buffer system, respiratory and renal regulation, and how to assess primary acid-base disorders. It provides a 6 step approach to ABG interpretation including determining if there is acidemia/alkalemia, if the primary disturbance is respiratory or metabolic, and if metabolic whether the anion gap is normal or high.
step by step approach to arterial blood gas analysisikramdr01
The document provides step-by-step information on interpreting an arterial blood gas (ABG) report. It describes the normal ranges for pH, PCO2, PO2, and other components in an ABG. It then explains how to identify metabolic vs respiratory acidosis and alkalosis based on changes in pH, PCO2, and HCO3 levels. The document also summarizes compensation mechanisms and gives formulas to predict expected pH and HCO3 levels based on primary acid-base disturbances.
This document discusses blood gas analysis and clinical interpretation. It begins by outlining common errors in blood gas sampling and discusses the components of a blood gas analysis. It then provides steps for analyzing blood gas results, including calculating the anion gap and delta gap to identify specific acid-base disorders. Examples are provided to demonstrate how to use these steps and calculations to interpret blood gas results and determine if findings indicate a respiratory or metabolic disorder and if compensation is appropriate. Causes of anion gap and non-anion gap metabolic acidosis are also reviewed.
This document outlines the key steps in analyzing blood gas results and interpreting acid-base disorders. It discusses factors that can affect blood gas values, such as delayed analysis, temperature changes, and air bubbles. The document then covers the components of a blood gas analysis and the central acid-base equation. It provides guidance on analyzing primary vs compensatory changes and calculating the anion gap and delta gap to determine the presence of mixed disorders. Differentials are given for specific acid-base imbalances like respiratory acidosis, metabolic acidosis, and non-gap metabolic acidosis.
This document discusses blood gas analysis and its clinical interpretation. It begins by outlining common errors in blood gas sampling and discusses the components of a blood gas analysis. It then provides steps for analyzing blood gas results, including calculating the anion gap and delta gap to identify specific acid-base disorders. Examples are provided to demonstrate how to use these steps and calculations to interpret blood gas results and determine if findings indicate a respiratory or metabolic disorder and if compensation is appropriate. Causes of anion gap and non-anion gap metabolic acidosis are also reviewed.
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 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 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.
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.
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.
1) The document discusses approaches to analyzing blood gases and acid-base disorders. It provides details on how the kidney regulates acid-base balance through bicarbonate reabsorption and secretion of hydrogen ions. Formulas for calculating compensation and identifying dominant acid-base disorders are presented.
2) Mechanisms of bicarbonate and hydrogen ion transport across renal tubular cells are illustrated through diagrams. Equations for calculating expected compensation in common acid-base imbalances are given to help identify the primary disorder.
3) Methods for evaluating systemic acid-base disorders are outlined, including using arterial blood gas results and serum electrolytes to identify
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ABG Interpretation.pptx
1. Arterial Blood Gas Analysis
Dr. Bikram K Gupta
MD,PDCC,EDIC,FACEE,FICCM
Professor & Head
Division of Critical Care Medicine
Dept. of Anaesthesiology
Heritage Institute of Medical Sciences
Email: – bikramgupta03@gmail.com
2. Application 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 for high risk surgeries
9. Alveolar Arterial Oxygen Gradient (AaDO2)
= 0.21 (760 - 47) – 40/0.8 = 100 mm Hg
AaDO2 = 0.21 (760 - 47) – 40/0.8 – 90 = 10 mm Hg
The normal A-aPO2 gradient increases 5 to 7 mm Hg for every 10% increase in FIO2.
10.
11. AaDO2 Implications…
Pramod Sood et al. Interpretation of arterial blood gas. IJCCM 2010;14:57-64.
Hypoxemic Respiratory Failure
12. • Unaffected by FIO2
• The normal a/A PO2 ratio is 0.74 to 0.77 when breathing room air, and 0.80 to 0.82
when breathing 100% oxygen.
13. • The oxygenation status of the patient is judged by the paO2;however,
never comment on the oxygenation status without knowing the
corresponding FiO2. Calculate the expected paO2 (generally five times
the FiO2).
19. Boston approach Vs. Copenhagen approach
• In reality, there is little difference between two; both equations and normograms were derived from in
vivo patient data.
• For most patients, either approach is accurate but misleading.
Boston approach Copenhagen approach
20. (Na + K + Ca + Mg) – (Cl + Lactate + SO4 + Keto ions) – (Albumin + Pi) - (HCO3) = 0
SID ATOT
Metabolic Acid – Base Abnormality
pCO2
So alterations in the SID or ATOT or Both affect dissociation of water Hence affect H+ ion
Conc.
Decreased SID (More anions) or Increased ATOT – Acidosis
Increased SID (More Cations) or Decreased ATOT – Alkalosis
Stewart Approach
23. Obtain a relevant clinical history..
• A patient with a history of hypotension, renal failure, uncontrolled
diabetic status, of treatment with drugs such as metformin is likely to
have metabolic acidosis.
• A patient, with a history of diuretic use, bicarbonate administration,
high-nasogastric aspirate, and vomiting, is likely to have metabolic
alkalosis.
• Respiratory acidosis would occur in COPD, muscular weakness,
postoperative cases, and opioid overdose.
• Respiratory alkalosis is likely to occur in sepsis, hepatic coma, and
pregnancy.
24. Check for Validity of Gas
A) First calculate H+ by putting PCO2 and HCO3 in the equation
H+ = 24 X (PaCO2/HCO3)
B )Then
• For every 0.1 decrease in PH, multiply H+ sequentially by 1.25
• For every 0.1 increase in PH, multiply H+ sequentially by 0.08
C) Match H+ by both A & B, if matches then ABG is valid
PH = 7.4 (H+ =40)
PH = 7.2
For PH 7.3, H+ = 40 X 1.25 = 50
Next
For PH 7.2, , H+ = 50 X 1.25 = 62.5
25. pH Concentration of
H+ ions
7.0 98
7.1 79
7.2 63
7.3 50
7.4 40
7.5 32
7.6 26
7.7 21
H+ = 80 – last two point of decimal
Check for Validity of Gas
26. Assess for Oxygenation
• Room air
• PAO2-PaO2 =5-15mm Hg
• PaO2 for age= 109-0.45xAge
• Ventilator/oxygen supplementation
• PaO2/FiO2 =400-500
PaO2
Normal 60-80
Mild 50-59
Moderate 40-49
Severe <40
P/F
Mild Hypoxemia 200-300
Moderate 100-200
Severe <100
27. Look at pH
• <7.35 (academia) / >7.45 (alkemia)
• pH is inversely proportional to H+ ions.
28. Identify the primary disorder
• In primary respiratory disorders, the pH and PaCO2 change
in opposite directions.
• In metabolic disorders the pH and PaCO2 change in the same direction.
In a normal ABG
• pH and paCO2 move in opposite directions.
• HCO3
-and paCO2 move in same direction.
29. Identify the primary disorder
• When the pH and paCO2 change in the same direction (which normally should not),
the primary problem is metabolic; when pH and paCO2 move in opposite directions
and paCO2 is abnormal, then the primary problem is respiratory.
• Mixed Disorder – if HCO3
- and paCO2 change in opposite direction (which they
normally should not), then it is a mixed disorder: pH may be normal with abnormal
paCO2 or abnormal pH and normal paCO2.
30. Mixed Acid Base Disorders
• Presence of more than one acid base disorder simultaneously
• Clues to a mixed disorder :-
• Normal PH with abnormal HCO3 or PCO2
• PCO2 and HCO3 move in opposite directions
• PH changes in an opposite direction for a known primary disorder
31. Identify the primary disorder……..
• If the trend of change in paCO2 and HCO3
- is the same, check the percent difference. The one, with
greater % difference, between the two is the one that is the dominant disorder.
e.g.: pH = 7.25 HCO3
-=16 paCO2=60
Here, the pH is acidotic and both paCO2 and HCO3
- explain its acidosis: so look at the % difference
• HCO3
-% difference = (24 - 16)/24 = 0.33
• paCO2% difference = (60 - 40)/40 = 0.5
Therefore, respiratory acidosis as the dominant disorder.
32. Respiratory : is it Acute or Chronic ?
• Respiratory disturbance: Acute /Chronic
• Acute: pH changes by 0.008 with each changes in CO2
(For every 10 change in PaCO2 ; pH will change by 0.08)
• Chronic: pH changes by 0.003 with each changes in PaCO2
(For every 10 change in PaCO2 ;pH will change by 0.03)
• Acute on Chronic : For every 10 change in PaCO2 ;pH will change in between
0.03 – 0.08.
33.
34. Is there appropriate compensation for the primary
disturbance? Usually, compensation does not return the pH
to normal (7.35 – 7.45).
Disorder CO2 change HCO3 change
Acute respiratory acidosis For every 10 mmHg rise in
CO2
HCO3 will rise by 1 mmol/l
Chronic respiratory acidosis For every 10 mmHg rise in
CO2
HCO3 will rise by 4 mmol/l
Disorder CO2 change HCO3 change
Acute respiratory alkalosis For every 10 mmHg fall in CO2 HCO3 will fall by 2 mmol/l
Chronic respiratory alkalosis For every 10 mmHg fall in CO2 HCO3 will fall by 5 mmol/l
35. • If paCO2↓ and HCO3
- is also ↓→ primary metabolic acidosis
• Calculate Anion Gap
38. • If metabolic acidosis, then Anion Gap (AG) should be examined.
• AG= Na+ - (Cl-+HCO3-) , normal value : – 12 ± 2
• In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L.
• Correction factor = 2.5 X {4 – albumin (gm/dl)}
• Corrected AG = Correction factor + AG
• If AG is unchanged → then it is hyperchloremic metabolic acidosis/ NAGMA.
• If AG is ↑ → then it is High AG acidosis (HAGMA).
39.
40. • If the anion gap is elevated, consider calculating the osmolar gap in compatible
clinical situations.
• Elevation in AG is not explained by an obvious case (DKA, renal failure etc)
• Toxic ingestion is suspected
• Osmolar gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8)
• The OSM gap should be < 10
• If osmolar gap >10 then suspect ingestion of an alcohol, including ethanol,
methanol, ethylene glycol, diethylene glycol, propylene glycol, and
isopropanol (isopropyl alcohol)
42. • If paCO2↓ and HCO3
- is also ↓→ primary metabolic acidosis
• Expected PaCO2 (Winters Formulae) = 1.5 x HCO3 + 8 ± 2
• Calculate expected paCO2 as follows:
• paCO2 = [1.5 × HCO3+ 8] ± 2 metabolic acidosis only.
• paCO2 < expected paCO2→ concomitant respiratory alkalosis.
• paCO2 > expected paCO2→ concomitant respiratory acidosis.
43.
44. • If paCO2 ↑ and HCO3
- also ↑ → then it is primary metabolic alkalosis.
• Calculate the expected paCO2
• paCO2 = [0.7 × HCO3-+ 21] ± 2 Or 40 + [0.7 ΔHCO3] → metabolic
alkalosis only
• paCO2 < expected paCO2 → concomitant respiratory alkalosis.
• paCO2 > expected paCO2 → concomitant respiratory acidosis
45.
46. Check urinary chloride
• If urinary chloride < 20 → chloride responsive or ECV depletion
• If urinary chloride > 20→ chloride resistant
47. STEP 1 Validity of gas
STEP 2 Assess for Oxygenation
STEP 3 Look at pH
STEP 4 Identify the primary disorder
STEP 5 Respiratory acute or chronic
STEP 6 Metabolic Compensation
STEP 7 Metabolic Acidosis – Anion gap
STEP 8 Respiratory compensation
STEP 9 Concomitant/Mixed disorder
STEP 10 Metabolic alkalosis – Urinary Chloride
48. Case 1
• A 22-year-old man who had been previously healthy was brought to the emergency
room early on a Monday morning, with agitation, fever, tachycardia, and hypertension.
• He was confused and incapable of providing a meaningful history.
• Examination revealed pulse 124 and regular; respirations 30; blood pressure 180/118;
and temperature 101.6°F.
• Pulse oximetry was consistent with oxygen saturation of 95%.
BE=-5.8 mmol/l; Albumin =4 gm/dL; Hb=15 gm %
49. • Step : 1 – Validity
a) H+= 24 x 40/18 = 53.33,
b) for every 0.1 decrease in PH, multiply H+ sequentially by 1.25, here PH is 7.27
Hence H+ CONC = 40 x 1.25 = 50.
A & B matched hence ABG is valid
• Step : 2 – Oxygenation 84 mm Hg means normal on room air
• Step: 3 – PH is 7.27 i.e. academia
• Step: 4 - Identify the primary disorder (PCO2 – 40, HCO3 -18); Metabolic acidosis
• Step: 7 - Metabolic Acidosis, see Anion gap (AG) = Na+ - (Cl-+HCO3-) = 128 – (88 + 18) = 22 (HAGMA)
• Step: 8 – Respiratory compensation = (1.5x 18)+8±2 = 35±2
• Step: 9 – Mixed disorder see Gap-gap ratio= (22-12)/(24-18)=1.66
Interpretation: High anion gap metabolic acidosis having respiratory compensation with normal oxygenation
50. • Treat the patient not the gas; correlate with clinical condition
• Always follow the essential Ten steps for ABG interpretation
• Compensation tries to bring pH towards normal but never near normal
• If pH is near normal then coexisting disorder is present
Editor's Notes
Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygenation status and acid–base balance. The usefulness of this diagnostic tool is dependent on being able to correctly interpret the results.
Never to forget to Look at the oxygenation status of the patient, purposefully I have discuss at first about how to see oxygenation status
The three widely used approaches to acid–base physiology are the HCO3- (in the context of pCO2), standard base excess (SBE), and strong ion difference (SID).
By convention acid base disorders are divided into respiratory (PCO2) and Metabolic (Non PCO2). PCO2 IS THE UNDISPUTED INDEX OF RESPIRATORY ACID BASE STATUS. TWO SCHOOLS, Boston and COPENHAGEN HAVE FORMED AROUND THE IDENTIFICATION & QUANTITIFICATION OF METABOLIC ACID BASE DISTURBANCES. IF USED CORRECTLY. The bicarbonate used in these equations is the "actual bicarbonate", as calculated from the pCO2 and pH using the Henderson-Hasselbalch equation. The baseline bicarbonate value is assumed to be 24mmol/L, and the baseline "normal" CO2 is assumed to be 40mmHg.
The Copenhagen method rests on the use of Standard Base Excess to separate the respiratory and metabolic influences on in vivo acid base balance.
Stewart’s approach neither invalidate nor supplement the traditional approaches.
While making an interpretation of an ABG, never comment on the ABG without obtaining a relevant clinical history of the patient, which gives a clue to the etiology of the given acid–base disorder. For example
Then look at paCO2 which is a respiratory acid, whether it is increased, i.e., >40 (acidosis) or decreased <40 (alkalosis) and if this explains the change of pH, then it is respiratory disorder; otherwise, see the trend of change of HCO3-(whether increased in alkalosis or decreased in acidosis)–if it explains the change of pH, then it is a metabolic disorder.
H+= 24x40/18=53.33, 7.3=50
Oxygenation is fine
Acidemia
High AG Metabolic acidosiswith gap gap 22-12-24-18=4
Resp acidosis35+2