This document provides an overview of arterial blood gas interpretation. It begins by discussing the proper procedure for obtaining an ABG sample and interpreting the results. It then covers the components measured by ABG electrodes and how the body maintains acid-base homeostasis through buffer systems, respiratory regulation, and renal regulation. Key terms are defined and the characteristics of primary acid-base disorders are described. A step-wise approach to ABG interpretation is presented, beginning with validating the results, determining if acidosis or alkalosis is present, and identifying if the cause is respiratory or metabolic by examining compensation.
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.
The document discusses pulmonary circulation and ventilation-perfusion relationships in the lungs. It provides information on:
1. The pulmonary circulation has low pressure, low resistance, and high compliance compared to the systemic circulation in order to efficiently oxygenate blood and accommodate shifts in blood volume.
2. Ventilation and perfusion are unevenly distributed in the lungs, with more ventilation and perfusion occurring in the lower zones due to gravitational effects. A mismatch between ventilation and perfusion can result in dead space or shunts.
3. Shunts occur when blood is perfused but not ventilated, resulting in hypoxemia. The magnitude of shunt can be estimated by measuring venous admixture.
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.
Cardio Pulmonary Interactions during Mechanical VentilationDr.Mahmoud Abbas
Lecture presented by Dr.Lluis Blanch at Pulmonary Critical Care Egypt, the leading critical care medical event and exhibition organized by the Egyptian College of Critical Care Physicians.www.pccmegypt.com
1) Hypoxia can lead to decreased ATP synthesis, lactic acidosis, impaired protein synthesis, and irreversible cell changes due to increased cytosolic calcium.
2) Pao2, Sao2, and oxygen content are important measures of oxygen levels in the blood. Pulse oximetry can monitor Sao2 non-invasively but has limitations.
3) Arterial blood gas analysis precisely measures oxygen, carbon dioxide, pH, bicarbonate, and base excess levels to evaluate oxygenation and ventilation.
The document discusses basic principles of mechanical ventilation including factors that can lead to ventilatory failure, airway resistance, lung compliance, hypoventilation, V/Q mismatch, intrapulmonary shunting, and diffusion defects. It also covers different types of ventilator waveforms including pressure, volume, flow and pressure/volume loops which can be used to assess a patient's respiratory status and response to therapy.
Capnography is a technique that monitors carbon dioxide (CO2) in exhaled breath to provide information about respiratory and circulatory functions. It has become an important monitoring tool to detect hypoxia and respiratory depression earlier than other methods. Capnography works by measuring the absorption of infrared light by CO2 and can detect changes in end-tidal CO2, respiratory rate, and the shape of the CO2 waveform/capnogram. Analyzing the capnogram provides insights into ventilation, perfusion matching in the lungs, and cardiopulmonary physiology. Capnography is useful for monitoring patients during procedures like surgery and anesthesia to detect complications like respiratory depression, air embolism, or carbon dioxide embolism
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.
The document discusses pulmonary circulation and ventilation-perfusion relationships in the lungs. It provides information on:
1. The pulmonary circulation has low pressure, low resistance, and high compliance compared to the systemic circulation in order to efficiently oxygenate blood and accommodate shifts in blood volume.
2. Ventilation and perfusion are unevenly distributed in the lungs, with more ventilation and perfusion occurring in the lower zones due to gravitational effects. A mismatch between ventilation and perfusion can result in dead space or shunts.
3. Shunts occur when blood is perfused but not ventilated, resulting in hypoxemia. The magnitude of shunt can be estimated by measuring venous admixture.
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.
Cardio Pulmonary Interactions during Mechanical VentilationDr.Mahmoud Abbas
Lecture presented by Dr.Lluis Blanch at Pulmonary Critical Care Egypt, the leading critical care medical event and exhibition organized by the Egyptian College of Critical Care Physicians.www.pccmegypt.com
1) Hypoxia can lead to decreased ATP synthesis, lactic acidosis, impaired protein synthesis, and irreversible cell changes due to increased cytosolic calcium.
2) Pao2, Sao2, and oxygen content are important measures of oxygen levels in the blood. Pulse oximetry can monitor Sao2 non-invasively but has limitations.
3) Arterial blood gas analysis precisely measures oxygen, carbon dioxide, pH, bicarbonate, and base excess levels to evaluate oxygenation and ventilation.
The document discusses basic principles of mechanical ventilation including factors that can lead to ventilatory failure, airway resistance, lung compliance, hypoventilation, V/Q mismatch, intrapulmonary shunting, and diffusion defects. It also covers different types of ventilator waveforms including pressure, volume, flow and pressure/volume loops which can be used to assess a patient's respiratory status and response to therapy.
Capnography is a technique that monitors carbon dioxide (CO2) in exhaled breath to provide information about respiratory and circulatory functions. It has become an important monitoring tool to detect hypoxia and respiratory depression earlier than other methods. Capnography works by measuring the absorption of infrared light by CO2 and can detect changes in end-tidal CO2, respiratory rate, and the shape of the CO2 waveform/capnogram. Analyzing the capnogram provides insights into ventilation, perfusion matching in the lungs, and cardiopulmonary physiology. Capnography is useful for monitoring patients during procedures like surgery and anesthesia to detect complications like respiratory depression, air embolism, or carbon dioxide embolism
Heliox therapy involves breathing a gas mixture of helium (80%) and oxygen (20%). It was discovered in 1934. Physiologically, heliox has a lower density than air, which reduces airflow resistance in the lungs and decreases the work of breathing. Its mechanism of action involves increasing laminar flow and decreasing turbulent flow resistance. Clinically, heliox therapy can be used for various upper airway and lung conditions involving increased respiratory effort or resistance, such as COPD exacerbations. Potential hazards include anoxia if oxygen levels are too low and hypothermia in infants.
The document discusses arterial blood gas analysis and interpretation. It provides an overview of gas exchange, acid-base homeostasis, and the basics of acid-base balance. It describes how to interpret an arterial blood gas report, including how to diagnose acid-base disorders and examples. Technical aspects like sampling technique and potential errors or complications are covered. Compensation mechanisms in response to primary acid-base disturbances are explained.
Acid base balance & ABG interpretation,Dept of anesthesiology,JJMMC,DavangereGopan Gopalakrisna Pillai
Acid base balance and ABG interpretation presented by Dr.Gopan.G,Post-Graduate student. Chairperson : Dr.Ravi.R,Professor, Department of Anaesthesiology & Critical care,JJMMC,Davangere.
1) Recruitment maneuvers (RMs) aim to reopen collapsed alveoli in ARDS patients through temporarily increasing transpulmonary pressure. Common types include sighs, sustained inflations, and stepwise increases in pressure.
2) While RMs often improve short-term oxygenation, clinical trials have found no evidence of reduced mortality or improved outcomes. One large trial found RMs may actually increase mortality.
3) Not all ARDS patients respond equally to RMs due to factors like etiology, severity, and lung recruitability. RMs should only be considered for hypoxemic individuals based on an individual risk-benefit assessment.
1. Hypoxemia, defined as low oxygen levels in arterial blood, can be caused by hypoventilation, low inspired oxygen, right-to-left shunts, ventilation-perfusion mismatching, or diffusion impairment in the lungs.
2. Physical exam and arterial blood gas analysis are used to diagnose hypoxemia and its underlying causes. Treatment focuses on oxygen supplementation, treating the underlying condition, correcting acid-base imbalances, and mechanical ventilation if needed.
3. The causes, mechanisms, diagnosis and management of hypoxemia are complex but critical for treatment of respiratory failure.
Mechanical ventilation graphics provide important information to interpret patient response, disease status, and ventilator function. Scalars plot pressure, volume, or flow over time, while loops plot pressure versus volume or flow versus volume with no time component. Common waveforms include square, ramp, and sine waves. Pressure modes result in square pressure waves while volume modes produce ramp waves. Loops can indicate breath type and assess issues like air trapping, resistance, compliance, and asynchrony. Graphical analysis is a critical tool for ventilator management and optimization.
Use of bedside ultrasound in shock: RUSH protocolSCGH ED CME
This document outlines the RUSH protocol for using bedside ultrasound to evaluate undifferentiated shock. The RUSH protocol examines four areas: the pump (heart), the tank (intravascular volume status via IVC scan), the pipes (vessels for leaks or blocks via abdominal, lower extremity scans), and lung sliding. It then presents four case examples where ultrasound identified cardiogenic shock, hypovolemic shock, pulmonary embolism, and aortic dissection as the causes of undifferentiated hypotension. The RUSH protocol aims to rapidly identify the cause of shock through focused bedside ultrasound exams of the heart, vessels, lungs and IVC to guide resuscitation efforts.
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.
Anesthesia For Congenital Diaphragmatic Herniakrishna dhakal
This document discusses congenital diaphragmatic hernia (CDH), a birth defect where organs protrude into the chest cavity due to a hole in the diaphragm. It covers the embryology, pathophysiology, diagnosis, and management of CDH. Surgical repair is the only treatment, but stabilization of the patient's respiratory and general status is needed first. Extracorporeal membrane oxygenation (ECMO) has improved survival for CDH. Long-term follow up is also important due to potential complications. A regional anesthesia method without opioids allowed early operating room extubation for CDH repair in one study.
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.
Point of critical care Ultrasound play a pivotal role in management of critically ill patients admitted in ICU . Its usage in this regard is ever growing . Here we discus about pearls and pitfalls of POCUS in Intensive care medicine.
This document provides an overview of arterial blood gas analysis. It discusses the history and development of blood gas analysis, indications for arterial blood gas sampling, and the procedure. It outlines normal values and how to interpret acid-base balance, oxygenation, and ventilation based on arterial blood gas parameters. A stepwise approach to acid-base analysis is presented, including how to identify primary versus secondary disorders and evaluate respiratory and renal responses.
This document provides an overview of using ultrasound (ECHO/FOCUS) in the intensive care unit (ICU). It discusses using ultrasound to assess cardiac function, volume status, and diagnose medical emergencies at the bedside. Ultrasound can be used to monitor hemodynamics, fluid responsiveness, and detect issues like cardiac tamponade. The document reviews ultrasound views of the heart and techniques for assessing volume status using the inferior vena cava. It also discusses using chest ultrasound to identify pleural effusions, pneumothorax, consolidation and quantify pleural fluid. The summary provides a concise high-level view of the key applications and techniques discussed in the document.
This document discusses mechanical ventilation waveforms. It begins by stating the objectives are to discuss commonly used waveforms, their applications, and combined waveforms. It then provides an outline and introduction on waveforms and how they represent ventilator data graphically over time or against each other. The majority of the document discusses specific commonly used waveforms including pressure-time, flow-time, and volume-time curves and how to interpret each to evaluate the patient and ventilator settings.
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 provides an overview of capnography, which is the noninvasive measurement of exhaled carbon dioxide levels. It discusses the history and use of capnography, the physiology of carbon dioxide transport and the capnographic waveform. Key benefits of capnography include verifying endotracheal tube placement, assessing effectiveness of CPR and detecting changes in ventilation early. Therapeutic hypothermia for cardiac arrest patients has shown benefits in studies, improving neurological outcomes. Capnography can help monitor patients during therapeutic hypothermia protocols.
This document discusses the use of lung ultrasound in the intensive care unit (ICU). It begins with an introduction and outline. It then covers techniques for imaging the lungs and pleura, and describes normal findings such as lung sliding, A-lines, and diaphragm movement. Abnormal findings including B-lines indicating pulmonary edema, pleural effusions, consolidations, and pneumothorax are also discussed. The document explores the use of lung ultrasound in clinical scenarios to differentiate causes of hypoxemia and respiratory failure. It emphasizes how lung ultrasound can aid procedures and follow clinical conditions. In conclusion, the author hopes to present again on this topic next year.
The document provides an overview of ventilation and perfusion matching in the lungs. It discusses how inadequate matching between ventilation and blood flow can lead to hypoxemia. Specifically, it covers the consequences of shunt physiology where blood is perfused but not ventilated, resulting in low oxygen levels. It also addresses how gravity affects regional differences in ventilation and perfusion in the upright posture.
This document provides a summary of an arterial blood gas interpretation presentation. It discusses the objectives, procedure, and precautions for arterial blood gas sampling. It then covers the interpretation of oxygenation status and acid-base status using a six step approach. The six steps include determining if acidemia or alkalemia is present, if the primary disturbance is respiratory or metabolic, if a respiratory disorder is acute or chronic, if compensation is adequate, evaluating the anion gap if metabolic, and identifying the cause of a high anion gap metabolic acidosis.
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.
Heliox therapy involves breathing a gas mixture of helium (80%) and oxygen (20%). It was discovered in 1934. Physiologically, heliox has a lower density than air, which reduces airflow resistance in the lungs and decreases the work of breathing. Its mechanism of action involves increasing laminar flow and decreasing turbulent flow resistance. Clinically, heliox therapy can be used for various upper airway and lung conditions involving increased respiratory effort or resistance, such as COPD exacerbations. Potential hazards include anoxia if oxygen levels are too low and hypothermia in infants.
The document discusses arterial blood gas analysis and interpretation. It provides an overview of gas exchange, acid-base homeostasis, and the basics of acid-base balance. It describes how to interpret an arterial blood gas report, including how to diagnose acid-base disorders and examples. Technical aspects like sampling technique and potential errors or complications are covered. Compensation mechanisms in response to primary acid-base disturbances are explained.
Acid base balance & ABG interpretation,Dept of anesthesiology,JJMMC,DavangereGopan Gopalakrisna Pillai
Acid base balance and ABG interpretation presented by Dr.Gopan.G,Post-Graduate student. Chairperson : Dr.Ravi.R,Professor, Department of Anaesthesiology & Critical care,JJMMC,Davangere.
1) Recruitment maneuvers (RMs) aim to reopen collapsed alveoli in ARDS patients through temporarily increasing transpulmonary pressure. Common types include sighs, sustained inflations, and stepwise increases in pressure.
2) While RMs often improve short-term oxygenation, clinical trials have found no evidence of reduced mortality or improved outcomes. One large trial found RMs may actually increase mortality.
3) Not all ARDS patients respond equally to RMs due to factors like etiology, severity, and lung recruitability. RMs should only be considered for hypoxemic individuals based on an individual risk-benefit assessment.
1. Hypoxemia, defined as low oxygen levels in arterial blood, can be caused by hypoventilation, low inspired oxygen, right-to-left shunts, ventilation-perfusion mismatching, or diffusion impairment in the lungs.
2. Physical exam and arterial blood gas analysis are used to diagnose hypoxemia and its underlying causes. Treatment focuses on oxygen supplementation, treating the underlying condition, correcting acid-base imbalances, and mechanical ventilation if needed.
3. The causes, mechanisms, diagnosis and management of hypoxemia are complex but critical for treatment of respiratory failure.
Mechanical ventilation graphics provide important information to interpret patient response, disease status, and ventilator function. Scalars plot pressure, volume, or flow over time, while loops plot pressure versus volume or flow versus volume with no time component. Common waveforms include square, ramp, and sine waves. Pressure modes result in square pressure waves while volume modes produce ramp waves. Loops can indicate breath type and assess issues like air trapping, resistance, compliance, and asynchrony. Graphical analysis is a critical tool for ventilator management and optimization.
Use of bedside ultrasound in shock: RUSH protocolSCGH ED CME
This document outlines the RUSH protocol for using bedside ultrasound to evaluate undifferentiated shock. The RUSH protocol examines four areas: the pump (heart), the tank (intravascular volume status via IVC scan), the pipes (vessels for leaks or blocks via abdominal, lower extremity scans), and lung sliding. It then presents four case examples where ultrasound identified cardiogenic shock, hypovolemic shock, pulmonary embolism, and aortic dissection as the causes of undifferentiated hypotension. The RUSH protocol aims to rapidly identify the cause of shock through focused bedside ultrasound exams of the heart, vessels, lungs and IVC to guide resuscitation efforts.
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.
Anesthesia For Congenital Diaphragmatic Herniakrishna dhakal
This document discusses congenital diaphragmatic hernia (CDH), a birth defect where organs protrude into the chest cavity due to a hole in the diaphragm. It covers the embryology, pathophysiology, diagnosis, and management of CDH. Surgical repair is the only treatment, but stabilization of the patient's respiratory and general status is needed first. Extracorporeal membrane oxygenation (ECMO) has improved survival for CDH. Long-term follow up is also important due to potential complications. A regional anesthesia method without opioids allowed early operating room extubation for CDH repair in one study.
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.
Point of critical care Ultrasound play a pivotal role in management of critically ill patients admitted in ICU . Its usage in this regard is ever growing . Here we discus about pearls and pitfalls of POCUS in Intensive care medicine.
This document provides an overview of arterial blood gas analysis. It discusses the history and development of blood gas analysis, indications for arterial blood gas sampling, and the procedure. It outlines normal values and how to interpret acid-base balance, oxygenation, and ventilation based on arterial blood gas parameters. A stepwise approach to acid-base analysis is presented, including how to identify primary versus secondary disorders and evaluate respiratory and renal responses.
This document provides an overview of using ultrasound (ECHO/FOCUS) in the intensive care unit (ICU). It discusses using ultrasound to assess cardiac function, volume status, and diagnose medical emergencies at the bedside. Ultrasound can be used to monitor hemodynamics, fluid responsiveness, and detect issues like cardiac tamponade. The document reviews ultrasound views of the heart and techniques for assessing volume status using the inferior vena cava. It also discusses using chest ultrasound to identify pleural effusions, pneumothorax, consolidation and quantify pleural fluid. The summary provides a concise high-level view of the key applications and techniques discussed in the document.
This document discusses mechanical ventilation waveforms. It begins by stating the objectives are to discuss commonly used waveforms, their applications, and combined waveforms. It then provides an outline and introduction on waveforms and how they represent ventilator data graphically over time or against each other. The majority of the document discusses specific commonly used waveforms including pressure-time, flow-time, and volume-time curves and how to interpret each to evaluate the patient and ventilator settings.
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 provides an overview of capnography, which is the noninvasive measurement of exhaled carbon dioxide levels. It discusses the history and use of capnography, the physiology of carbon dioxide transport and the capnographic waveform. Key benefits of capnography include verifying endotracheal tube placement, assessing effectiveness of CPR and detecting changes in ventilation early. Therapeutic hypothermia for cardiac arrest patients has shown benefits in studies, improving neurological outcomes. Capnography can help monitor patients during therapeutic hypothermia protocols.
This document discusses the use of lung ultrasound in the intensive care unit (ICU). It begins with an introduction and outline. It then covers techniques for imaging the lungs and pleura, and describes normal findings such as lung sliding, A-lines, and diaphragm movement. Abnormal findings including B-lines indicating pulmonary edema, pleural effusions, consolidations, and pneumothorax are also discussed. The document explores the use of lung ultrasound in clinical scenarios to differentiate causes of hypoxemia and respiratory failure. It emphasizes how lung ultrasound can aid procedures and follow clinical conditions. In conclusion, the author hopes to present again on this topic next year.
The document provides an overview of ventilation and perfusion matching in the lungs. It discusses how inadequate matching between ventilation and blood flow can lead to hypoxemia. Specifically, it covers the consequences of shunt physiology where blood is perfused but not ventilated, resulting in low oxygen levels. It also addresses how gravity affects regional differences in ventilation and perfusion in the upright posture.
This document provides a summary of an arterial blood gas interpretation presentation. It discusses the objectives, procedure, and precautions for arterial blood gas sampling. It then covers the interpretation of oxygenation status and acid-base status using a six step approach. The six steps include determining if acidemia or alkalemia is present, if the primary disturbance is respiratory or metabolic, if a respiratory disorder is acute or chronic, if compensation is adequate, evaluating the anion gap if metabolic, and identifying the cause of a high anion gap metabolic acidosis.
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.
The document provides information on blood gas interpretation, including the components measured in a blood gas analysis, normal values, indications for obtaining a blood gas, possible abnormalities, and a stepwise approach to interpreting blood gas results. Key points include that blood gas values can differ in preterm infants compared to normal ranges for adults, the four primary acid-base disorders are respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis, and a three step approach is outlined to analyze a blood gas result and determine if any acid-base imbalance is primarily respiratory or metabolic in nature. Several case examples are provided as a quiz to test interpretation skills.
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 discusses acid-base disorders and interpretation of arterial blood gases (ABGs). It defines acidosis and alkalosis, and describes respiratory and metabolic causes. Simple and mixed acid-base disorders are explained. Compensation by the lungs and kidneys in response to primary disorders is discussed. A stepwise approach to ABG interpretation is provided, including determining the primary disorder, checking for compensation, calculating the anion gap, and identifying specific etiologies. Characteristics of simple acid-base disturbances and combined disorders are summarized.
This document provides information on interpreting blood gases, including normal values for pH, PaCO2, PaO2, HCO3, and base excess. It describes causes and features of respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Various treatments are discussed for different acid-base imbalances. A section on arterial blood sampling and the Allen test is also included. The document ends with sample case studies to test the reader's understanding of interpreting blood gas results.
Arterial Blood Gas Interpretation By Dr. Prashant KumarDr. Prashant Kumar
This document provides an overview of arterial blood gas interpretation. It begins by defining pH and listing normal arterial blood gas values. It then discusses the importance of interpreting an ABG rather than relying solely on pulse oximetry. The document outlines the Henderson-Hasselbalch equation and describes how to approach ABG interpretation using a 7-step method. It provides examples of interpreting common acid-base disorders and mixed disorders. The key physiological processes of alveolar ventilation, oxygenation, and acid-base balance are summarized.
This document discusses arterial blood gas (ABG) analysis and interpretation. It covers:
- Why ABGs are important for clinical insight and picking up issues like hypercarbia that pulse oximetry cannot.
- Key principles like acid-base balance, recognizing simple vs. complex disorders.
- When to request ABGs, such as for serious illness, respiratory distress, or suspected metabolic issues.
- Factors that can influence ABG results like medications, electrolytes, and compensation time.
- Ten "commandments" for proper ABG technique, analysis, and interpretation in the clinical context.
- Several case examples are presented and analyzed to demonstrate applying the commandments.
This document provides information about arterial blood gases (ABG), including how ABG samples are collected, normal ABG values, interpreting ABG results, and the principles of oxygen saturation and pulse oximetry. It discusses analyzing primary versus compensatory acid-base imbalances based on pH, pCO2, and HCO3 levels. Ventilation-perfusion imbalance is a major cause of low pO2. Pulse oximetry indirectly measures oxygen saturation but cannot detect carboxyhemoglobin or methemoglobin.
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.
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 discusses acid-base disorders and ABG analysis. It defines acids and bases, describes the mechanisms that regulate acid-base balance, and classifies different types of acid-base imbalances including respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Causes, compensatory mechanisms, and treatments are provided for each type of imbalance. The document also covers ABG analysis, normal values, interpretation of results, and provides two sample problems to identify acid-base disturbances.
A 15-year-old male underwent craniotomy surgery and was transferred to the ICU. His initial ABG results showed a pH of 7.22, pCO2 of 36.7, and lactate of 7.8, indicating combined metabolic and respiratory acidosis due to lactic acidosis from possible hypothermia during surgery. The patient's lactic acidosis resolved after IV fluids and 12 hours, likely ruling out other causes of lactic acidosis such as medical conditions or toxins.
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
The blood gas report shows a pH of 7.436, pCO2 of 47.6 mm Hg, HCO3 of 31.2 mmol/L, and BE of 6.6 mmol/L. This indicates a primary metabolic alkalosis with partial respiratory compensation, as the HCO3 is high and the pH is also high but the pCO2 has risen, though not fully, to compensate. Further analysis of the clinical context is needed to determine the underlying cause of the metabolic alkalosis.
This document summarizes blood gas analysis and acid-base balance. It describes how pH is maintained between 7.36-7.44 through bicarbonate and phosphate buffer systems. Respiratory and metabolic acidosis and alkalosis are explained in relation to changes in CO2 and bicarbonate levels. Key factors in analyzing acid-base disturbances including anion gap, predicted respiratory pH, and metabolic components are outlined. Different types of acid-base disorders and their diagnoses are also summarized.
Arterial Blood Bas (ABG) Procedure and InterpretationLouie Ray
The document provides information about arterial blood gas (ABG) testing including the procedure, common terms, normal values, indications, contraindications, and complications. It describes how to perform an arterial puncture to obtain a blood sample including gathering supplies, locating the radial artery, administering local anesthesia, inserting the needle, applying pressure after removal to stop bleeding, and proper handling and labeling of the sample. The goals are to assess acid-base status, oxygenation, levels of carbon dioxide and bicarbonate, and to determine if issues lie with ventilation, oxygenation or metabolism.
This document provides an overview of arterial blood gas (ABG) interpretation. It discusses ABG sampling procedures and indications, oxygenation and acid-base status evaluation, and a step-wise approach to ABG interpretation. It also presents examples of clinical cases and discusses metabolic and respiratory acid-base disorders and their compensatory responses.
Este documento describe diferentes técnicas y materiales para el tratamiento de urgencias veterinarias, incluyendo fluidoterapia, vendajes, férulas y ortesis. Explica cómo colocar vendajes compresivos, de contención, de protección y el vendaje Robert-Jones, así como los tipos de férulas y su función de estabilizar fracturas y lesiones. Resalta la importancia de que los veterinarios cuenten con personal capacitado especialmente en el área de urgencias de pequeñas especies.
This document provides information on arterial blood gas analysis, including contraindications for arterial puncture, reasons to order an ABG, normal values, equations, and approaches to interpreting ABG results. It discusses how to determine if a patient has acidosis or alkalosis, whether it is respiratory or metabolic, and if the compensation is adequate. It provides steps to classify the acid-base disorder, consider anion and osmolal gaps, and evaluate for mixed disorders. Causes and treatments of different acid-base imbalances are outlined.
This document provides information on interpreting arterial blood gas results. It discusses sampling procedures and precautions for ABG tests. The six-step approach to ABG interpretation is outlined, covering assessing acid-base and oxygenation status. Key points include determining if the ABG is authentic, identifying if the primary disturbance is respiratory or metabolic, and assessing compensation. Causes of respiratory acidosis, respiratory alkalosis, and metabolic alkalosis are briefly summarized.
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 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.
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
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.
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 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 normal ranges for arterial blood gas values
Approach to arterial blood gas interpretation
Arterial blood gas abnormalities in special circumstances
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.
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 document discusses acid-base disorders. It begins by explaining that the human body maintains a slightly basic pH through various buffering mechanisms. It then describes the bicarbonate buffer system and how the lungs, kidneys, and buffers work to regulate pH. It discusses the causes, classifications, and clinical features of metabolic acidosis and alkalosis. Key points include how to interpret arterial blood gases, calculate anion and urine gaps, and determine compensations and mixed disorders. The document provides an in-depth overview of acid-base physiology and pathophysiology.
This document provides an overview of arterial blood gas analysis. It discusses how ABG provides information about ventilation, oxygenation, and acid-base balance. The key points covered include indications for ABG, contraindications, sample collection sites and techniques, complications, acid-base physiology including buffer systems and compensation mechanisms, and a stepwise approach to ABG interpretation.
The document discusses acid-base physiology and regulation. It covers 3 key topics:
1) Chemical buffering systems help resist changes in pH, with the HCO3-/CO2 system being the most important extracellular buffer.
2) Pulmonary regulation finely controls CO2 levels through respiration, helping normalize pH.
3) The kidneys play a major role in long-term pH regulation by adjusting HCO3- reabsorption and excretion over hours to days.
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 arterial blood gas analysis and acid-base physiology. It provides indications for obtaining an ABG such as respiratory or metabolic disorders, hypoxia, shock, sepsis, and decreased cardiac output. It then defines the components of an ABG - pH, PaCO2, PaO2, HCO3, and base excess - and their normal ranges. It explains the Henderson-Hasselbalch equation and how the kidneys and respiratory system work to regulate pH levels and compensate for acid-base imbalances through bicarbonate and CO2 elimination. Various acid-base disorders like respiratory acidosis, metabolic acidosis, and mixed disorders are covered.
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
ABG interpret in critical care 16-1-2024Anwar Yusr
This document discusses arterial blood gas analysis and acid-base physiology. It provides indications for obtaining an ABG such as respiratory or metabolic disorders, hypoxia, shock, sepsis, and decreased cardiac output. It then defines the components of an ABG - pH, PaCO2, PaO2, HCO3, and base excess - and their normal ranges. It explains the Henderson-Hasselbalch equation and how the bicarbonate-carbonic acid buffer system regulates pH. Compensation by the respiratory and renal systems is described. Causes of metabolic acidosis and alkalosis are listed. The six step method for analyzing acid-base disorders is outlined.
acid base and electrolye disorder in ICU.pptMisganawMengie
This document provides an overview of acid-base disorders and electrolyte imbalances that are commonly seen in critically ill patients in the intensive care unit (ICU). It begins with definitions of pH, acid-base balance, and the three buffering systems (respiratory, blood, and renal) that help maintain homeostasis. It describes the four main types of acid-base disorders (respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis) and how to interpret arterial blood gases. Rules for identifying primary vs compensated disorders and evaluating the adequacy of compensatory responses are also outlined. Equations are provided to calculate expected pH and bicarbonate levels based on PCO2 values in respiratory
1. Arterial Blood Gas
Interpretation
PRESENTER- Dr. Shankerdeep Sondhi
Resident IIInd Yr
Department of Medicine
2. OBJECTIVES
ABG Sampling
Interpretation of ABG
Case Scenarios
3. ABG – Procedure and Precautions
Site- (Ideally) Radial Artery
Brachial Artery
Femoral Artery
Ideally - Pre-heparinised ABG syringes
- Syringe should be FLUSHED with 0.5ml
of 1:1000 Heparin solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN THE
SYRINGE
HEPARIN DILUTIONAL HCO3
EFFECT PCO2
Only small 0.5ml Heparin for flushing and discard it
Syringes must have > 50% blood.
4. Ensure No Air Bubbles. Syringe must be sealed immediately
after withdrawing sample.
◦ Contact with AIR BUBBLES
Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
Air Bubble + Blood = PO2 PCO2
ABG Syringe must be transported at the earliest to the
laboratory for EARLY analysis via COLD CHAIN
5. ABG ELECTRODES
A. pH (Sanz Electrode)
Measures H+ ion concentration of sample against a
known pH in a reference electrode, hence potential
difference. Calibration with solutions of known pH (6.384
to 7.384)
B. P CO2 (Severinghaus Electrode)
CO2 reacts with solution to produce H+
higher C02- more H+ higher P CO2 measured
C. P 02 (Clark Electrode)
02 diffuses across membrane producing an electrical
current measured as P 02.
7. Acid Base Homeostasis
1. Plasma Acid Homeomostasis: Chemical
buffering
◦ H+ influenced by
Rate of endogenous production
Rate of excretion
Buffering capacity of body
◦ Buffers effective at physiologic pH are
Hemoglobin
Phosphate
Proteins
Bicarbonate
8. 2. Alveolar Ventilation:
pCO2 action is immediate. Stimulation of respiratory
center washes off the excess CO2 increasing pH, and
vice versa
3. Excretion:
Liver: uses HCO3– to make urea which further
prevents accumulation of ammonia and traps H+ in
renal distal tubule
Kidney: regulate plasma [HCO3–] through three main
processes:
• reabsorption of filtered HCO3–
• formation of titratable acid
• excretion of NH4+ in the urine.
Proximal tubule reclaims 85% filtered HCO3–
Distal tubule reclaims 15%, and excretes H+
40–60 mmol/d of protons is excreted to maintain balance
9. Acid Base Balance
H+ ion concentration in the body is
precisely regulated
The body understands the importance of H+
and hence devised DEFENCES against any
change in its concentration-
BICARBONATE RESPIRATORY RENAL
BUFFER REGULATION REGULATION
SYSTEM Acts in few Acts in hours to
Acts in few minutes days
seconds
10. BUFFER SYSTEM
1st line of defence in pH regulation.
Determine capacity of ECF to
transport acids from site of production
to site of excretion without undue
change in pH.
They resist change in pH on addition
of acid/alkali in media wherever they
are.
12. BICARBONATE BUFFER
NAHCO3/H2CO3 = 20/1 = Alkali reserve.
conversion of strong & non volatile acid
in ECF, in weak & volatile acid at the
expense of NaHCO3 component of
buffer.
H2CO3 thus formed is eliminated by lung
as CO2.Directly linked with respiration &
healthy lungs essential for its function.
High concentration in blood,so very good
physiological buffer.
Weak chemical buffer.
13. Bicarbonate Buffer System
CO2 + H2O carbonic anhydrase H2CO3 H+ + HCO3-
In Acidosis - Acid = H+
H+ + HCO3 H2CO3 CO2 + H2O
In Alkalosis - Alkali + Weak Acid = H2CO3
CO2 + H20 H2CO3 HCO3- + H+
+
ALKALI
14. PHOSPHATE BUFFER
Na2HPO4/NaH2PO4 =
AlkPO4/AcidPO4 = 4/1.
NaH2PO4 excreted by kidneys.
Directly linked with kidneys & healthy
kidneys necessary for its functioning.
Concentration in blood is low so not
good physiological buffer.
Very good chemical buffer as pKa
aprroches pH.
15. PROTEIN BUFFER
Na+Pr- / H+Pr- = salt/acid.
Proteins can act as a base In acidic
medium nd as an acid in basic
medium..with COOH& NH2 group.
Buffering capacity of plasma proteins
is much less than Hb.
16. Respiratory Regulation of Acid Base
Balance-
ALVEOLAR
H+ VENTILATION PaCO2
ALVEOLAR
H+ VENTILATION PaCO2
17. Renal Regulation of Acid Base Balance
Kidneys control the acid-base balance by excreting
either an acidic or a basic urine,
This is achieved in the following ways-
Reabsorption Secretion of H+
of HCO3 ions in tubules
in blood and excretion
PCO2 K+
in ECF
Aldosterone
H+ ion •Proximal Convulated
Tubules (85%)
•Thick Ascending Limb of
ECF Volume Loop of Henle (10%)
Angiotensin II
•Distal Convulated Tubule
•Collecting Tubules(5%)
18. Definitions and Terminology
ACIDOSIS – presence of a process which tends to
pH by virtue of gain of H + or loss of HCO3-
ALKALOSIS – presence of a process which tends
to pH by virtue of loss of H+ or gain of HCO3-
If these changes, change pH, suffix ‘emia’ is added
ACIDEMIA – reduction in arterial pH (pH<7.35)
ALKALEMIA – increase in arterial pH (pH>7.45)
19. Simple Acid Base Disorder/ Primary Acid Base
disorder – a single primary process of acidosis or
alkalosis due to an initial change in PCO2 and HCO3.
Compensation - The normal response of
the respiratory system or kidneys to change in pH
induced by a primary acid-base disorder
The Compensatory responses to a primary Acid Base
disturbance are never enough to correct the change in
pH , they only act to reduce the severity.
Mixed Acid Base Disorder – Presence of more than
one acid base disorder simultaneously .
22. Compensation
Metabolic Disorders – Compensation in these disorders leads to
a change in PCO2
METABOLIC
ACIDOSIS • For every 1mmol/l in HCO3 the
PCO2 falls by 1.25 mm Hg
METABOLIC
ALKALOSIS • For every 1mol/l in HCO3 the
PCO2 by 0.75 mm Hg
23. In Respiratory Disorders
PCO2 Kidney HCO3 Reabsorption
Compensation begins to appear in 6 – 12 hrs and is fully
developed only after a few days.
1.ACUTE
Before the onset of compensation
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.2 meq/l
2.CHRONIC (>24 hrs)
After compensation is fully developed
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
24. Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit
Full compensation
Partial compensation
No compensation…. (uncompensated)
BUT never overshoots,
If a overshoot pH is there,
Take it granted it is a MIXED disorder
26. Normal Values
ANALYTE Normal Value Units
pH 7.35 - 7.45
PCO2 35 – 45 mm Hg
PO2 80 – 100 mm Hg`
[HCO3] 22 – 26 meq/L
SaO2 95-100 %
Anion Gap 10 + 2 meq/L
∆HCO3 +2 to -2 meq/L
27. STEP 0 • Is this ABG Authentic?
STEP 1 • ACIDEMIA or ALKALEMIA?
• RESPIRATORY or METABOLIC?
STEP 2
STEP 3 • Is COMPENSATION adequate?
STEP 4 • If METABOLIC – ANION GAP?
• If High gap Metabolic Acidosis–
STEP 5 GAP GAP?
28. Step 0 – Authentic or Not?
Verify that the ABG values are internally
accurate.
◦ The accuracy of the values can be established
by confirming that they satisfy a simplified form
of the Henderson-Hasselbalch equation:
[H+](nmol/L) = 24 × pCO2(mm Hg) ∕ [HCO3-]
(mEq/L)
◦ [H+] = 10 exp(-pH). Within the pH range of 7.26
to 7.45 [H+] in nmol/L = 80 − the decimal of the
pH
(e.g., for pH = 7.25, [H+] = 80 − 25 = 55
30. STEP 1 ACIDEMIA OR ALKALEMIA?
Look at pH
<7.35 - acidemia
>7.45 – alkalemia
RULE – An acid base abnormality is present even if
either the pH or PCO2 are Normal.
31. STEP 2 RESPIRATORY or METABOLIC?
IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC?
pH HCO3 or pH HCO3 METABOLIC
pH PCO2 or pH PCO2 RESPIRATORY
RULE- If either the pH or PCO2 is Normal, there is a
mixed metabolic and respiratory acid base disorder.
33. Disorder Prediction of Compensation pH HCO3– PaCO2
Metabolic PaCO2 will 1.25 mmHg per mmol/L in
acidosis [HCO3-] Low Low Low
Metabolic PaCO2 will 0.75 mmHg per mmol/L in High High High
alkalosis [HCO3-]
34. Disorder Prediction of Compensation pH HCO3– PaCO2
Respiratory High Low Low
alkalosis
Acute [HCO3-] will 0.2 mmol/L per mmHg in
PaCO2
Chronic [HCO3-] will 0.4 mmol/L per mmHg in
PaCO2
Respiratory Low High High
acidosis
Acute [HCO3-] will 0.1 mmol/L per mmHg in
PaCO2
Chronic [HCO3-] will 0.4 mmol/L per mmHg in
PaCO2
35. STEP 0 • Is this ABG Authentic?
STEP 1 • ACIDEMIA or ALKALEMIA?
• RESPIRATORY or METABOLIC?
STEP 2
STEP 3 • If Respiratory – ACUTE or CHRONIC?
STEP 4 • Is COMPENSATION adequate?
STEP 4 • If METABOLIC – ANION GAP?
• If High gap Metabolic Acidosis–
STEP 6 GAP GAP?
36. Electrochemical Balance in Blood
100% UC
UA
90%
80% HCO3
Na Sulfate
70% Phosphate
60% Mg- OA
Cl
50% K - Proteins
40% Ca-HCO3
30% Na- Cl
20%
10%
0%
CATIONS ANIONS
37. Anion Gap
AG based on principle of electroneutrality:
Total Serum Cations = Total Serum Anions
M cations + U cations = M anions + U anions
Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
Na + UC = HCO3 + Cl + UA
But in Blood there is a relative abundance of Anions, hence
Anions > Cations
Na – (HCO3 + Cl) = UA – UC
Na – (HCO3 + Cl) = Anion Gap
38. METABOLIC ACIDOSIS-
STEP 4
ANION GAP?
IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP?
ANION GAP(AG) = Na – (HCO3 + Cl)
Normal Value = 10 + 2
Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin)
50% in S. Albumin 75% in Anion Gap !!!
High Anion Gap Metabolic Acidosis
Metabolic Acidosis
Normal Anion Gap Acidosis
39. STEP 5 CO EXISTANT METABOLIC
DISORDER – “Gap Gap‖?
C/O HGAG METABOLIC ACIDOSIS,ANOTHER DISORDER?
∆ Anion Gap = Measured AG – Normal AG
Measured AG – 12
∆ HCO3 = Normal HCO3 – Measured HCO3
24 – Measured HCO3
Ideally, ∆Anion Gap = ∆HCO3
For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L
∆AG/ HCO3- = 1 Pure High AG Met Acidosis
AG/ HCO3- > 1 Assoc Metabolic Alkalosis
AG/ HCO3- < 1 Assoc N AG Met Acidosis
41. Case Scenario
A patient with a severe postoperative
ileus requires the insertion of a
nasogastric (NG) tube for
decompression. After several days on
the floor, he develops a line infection and
is moved to the ICU once he becomes
pressor dependent. The patient's ABG
reveals a pH = 7.44, pCO2 = 12, and
[HCO3-] = 8. The [Na+] = 145 with [Cl-] =
102.
42. ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8,
[Na+] = 145 with [Cl-] = 102
◦ With knowledge of the common clinical
scenarios leading to acid-base
disturbances, this patient is at risk for
developing a metabolic alkalosis from NG
suction and a metabolic acidosis and
respiratory alkalosis from sepsis.
◦ Step 1. [H+] = 80 − 44 = 36.
Does 36 = 24 × 12 / 8? It does.
◦ Step 2. The patient is mildly alkalemic, which
can be explained by the low pCO2 but not by
the low [HCO3-], suggesting that a respiratory
alkalosis may be the primary derangement.
43. ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8,
[Na+] = 145 with [Cl-] = 102
◦ Step 3
a. The drop in [HCO3-] might be an appropriate
compensation for a chronic respiratory alkalosis
([HCO3-] is 0.4 mmol/L per mmHg in PaCO2)
However, 24 − [(40 − 12) × 0.4] = 12.8, which is not
close to the observed [HCO3-] of 8. A mixed disorder is
implied.
b. AG = 145 − 102 − 8 = 35. There is an elevated
AG, suggests a concomitant metabolic acidosis.
c. Delta anion gap=35 − 10 = 25.
d. Delta bicarbonate= 24 − 8 =16.
Ratio of above two is more than 1 suggestive of
associated metabolic alkalosis. This has proven to be
a triple acid-base disorder with an elevated anion
gap acidosis, a metabolic alkalosis, and a
respiratory alkalosis, as was alluded to in Step 1
44. Metabolic Acidosis
Metabolic acidosis can occur because of
◦ increase in endogenous acid production (lactate and ketoacids)
◦ loss of bicarbonate (as in diarrhea)
◦ accumulation of endogenous acids (as in renal failure).
Effects on the respiratory, cardiac, and nervous
systems.
◦ Kussmaul respiration
◦ Intrinsic cardiac contractility may be depressed, but inotropic
function can be normal because of catecholamine release.
◦ Both peripheral arterial vasodilation and central
venoconstriction can be present
◦ The decrease in central and pulmonary vascular compliance
predisposes to pulmonary edema with even minimal volume
overload.
◦ Central nervous system function is depressed, with
headache, lethargy, stupor, and, in some cases, even coma.
45. Metabolic Acidosis: Essentials of
Diagnosis
Decreased HCO3– with acidemia.
Classified into high anion gap acidosis
and normal anion gap (hyperchloremic)
acidosis.
The high anion gap acidoses are seen in
lactic acidosis, ketoacidosis, renal failure
or toxins.
Normal anion gap acidosis is mainly
caused by gastrointestinal HCO3– loss or
RTA.
Urinary anion gap may help distinguish
between these causes.
46. Causes of High-Anion-Gap
Metabolic Acidosis
1. Lactic acidosis
Poor tissue perfusion (type A)
Aerobic disorders (type B)
2. Ketoacidosis
Diabetic
Alcoholic
Starvation
3. Toxins
Ethylene glycol
Methanol
Salicylates
Propylene glycol: as vehicle of medications
Pyroglutamic acid: acetaminophen toxicity
4. Renal failure (acute and chronic)
47. Ketacidosis –
Diabetic Ketoacidosis (DKA):
DKA is caused by increased fatty acid
metabolism and the accumulation of ketoacids
(acetoacetate and -hydroxybutyrate).
DKA usually occurs in insulin-dependent
diabetes mellitus in association with
cessation of insulin or
an intercurrent illness, such as an
infection, gastroenteritis, pancreatitis, or
myocardial infarction, which increases insulin
requirements temporarily and acutely.
The accumulation of ketoacids accounts for the
increment in the Anion Gap and is
accompanied most often by hyperglycemia
[glucose > 17 mmol/L (300 mg/dL)].
48. Glucose,a mmol/L (mg/dL) 13.9–33.3 (250–600)
Sodium, meq/L 125–135
Potassiuma Normal to ↑
Magnesiuma Normal ( plasma levels may be normal or high at
presentation, total-body stores are usually
depleted)
Chloridea Normal
Phosphatea ↓
Creatinine Slightly ↑
Osmolality (mOsm/mL) 300–320
Plasma ketonesa ++++
Serum bicarbonate,a meq/L <15 meq/L
Arterial pH 6.8–7.3
Arterial PCO2,a mmHg 20–30
Anion gapa[Na - (Cl + HCO3)] ↑
49. Management
Confirm diagnosis (plasma glucose, positive serum
ketones, metabolic acidosis).
Admit to hospital; intensive-care setting may be necessary for
frequent monitoring or if pH < 7.00 or unconscious.
Assess:
Serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate)
Acid-base status—pH, HCO3-, PCO2, b-hydroxybutyrate
Renal function (creatinine, urine output)
Replace fluids:
2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour);
subsequently, 0.45% saline at 150–300 mL/h;
change to 5% glucose and 0.45% saline at 100–200 mL/h when
plasma glucose reaches 250 mg/dL (14 mmol/L).
Administer short-acting insulin:
IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by
continuous IV infusion;
increase 2- to 3-fold if no response by 2–4 h.
If initial serum potassium is < 3.3 mmol/L (3.3 meq/L), do not
administer insulin until the potassium is corrected to > 3.3 mmol/L
50. Management
Assess patient: What precipitated the episode
(noncompliance, infection, trauma, infarction, cocaine)?
Initiate appropriate workup for precipitating event
(cultures, CXR, ECG).
Measure
capillary glucose every 1–2 h;
electrolytes (especially K+, bicarbonate, phosphate) and anion
gap every 4 h for first 24 h.
Monitor blood pressure, pulse, respirations, mental
status, fluid intake and output every 1–4 h.
Replace K+:
10 meq/h when plasma K+ < 5.5 meq/L, ECG normal, urine flow
and normal creatinine documented;
administer 40–80 meq/h when plasma K+ < 3.5 meq/L or if
bicarbonate is given.
Continue above until patient is stable, glucose goal is 150–
250 mg/dL, and acidosis is resolved. Insulin infusion may be
decreased to 0.05–0.1 units/kg per hour.
Administer intermediate or long-acting insulin as soon as
patient is eating. Allow for overlap in insulin infusion and
51. since insulin prevents production of
ketones, bicarbonate therapy is rarely
needed except with extreme acidemia (pH <
7.1), and then in only limited amounts.
Patients with DKA are typically volume
depleted and require fluid resuscitation with
isotonic saline.
Volume overexpansion is not uncommon
after IV fluid administration, and contributes
to the development of a hyperchloremic
acidosis during treatment of DKA because
volume expansion increases urinary
ketoacid anion excretion (loss of potential
bicarbonate).
The mainstay for treatment of this condition
is IV regular insulin
52. Drug, Toxin-Induced Acidosis
Plasma osmolality is calculated according to the following
expression:
Posm = 2Na+ + Glu + BUN (all in mmol/L)
Posm = 2Na+ + Glu/18 + BUN/2.8 (milligrams per deciliter)
The calculated and determined osmolality should be within
10–15 mmol/kg H2O
When the measured osmolality exceeds the calculated
osmolality by >15–20 mmol/kg H2O, either prevails.
Either the serum sodium is spuriously low, as with
hyperlipidemia or hyperproteinemia
(pseudohyponatremia)
Osmolytes other than sodium salts, glucose, or urea
have accumulated in plasma. Examples include
mannitol, radiocontrast media, isopropyl
alcohol, ethylene glycol, propylene
53. In this situation, the difference between the
calculated osmolality and the measured osmolality
(osmolar gap) is proportional to the concentration of
the unmeasured solute.
Alcohols: With an appropriate clinical history and index
of suspicion, identification of an osmolar gap is helpful
in identifying the presence of poison-associated AG
acidosis. Three alcohols may cause fatal intoxications:
ethylene glycol, methanol, and isopropyl alcohol
Salicylates: Salicylate intoxication in adults usually
causes respiratory alkalosis or a mixture of high-AG
metabolic acidosis and respiratory alkalosis. Only a
portion of the AG is due to salicylates. Lactic acid
production is also often increased
54. Renal failure Acidosis
The hyperchloremic acidosis of moderate renal
insufficiency is eventually converted to the
high-AG acidosis of advanced renal failure.
At GFRs below 20 mL/min, the inability to
excrete H+ with retention of acid anions such
as PO43– and SO42– results in an increased
anion gap acidosis
[HCO3–] rarely falls to <15 mmol/L, and the AG
is rarely >20 mmol/L, indicating that the acid
retained in chronic renal disease is buffered by
alkaline salts from bone.
Results in significant loss of bone mass due to
reduction in bone calcium carbonate and
increases urinary calcium excretion.
55. Treatment of high anion gap
acidosis
Treatment is aimed at the underlying disorder, such as
insulin and fluid therapy for diabetes and appropriate
volume resuscitation to restore tissue perfusion. The
metabolism of lactate will produce HCO3– and increase
pH.
Controversy regarding administration of large
amounts of HCO3–
may have deleterious effects, including hypernatremia and
hyperosmolality.
Intracellular pH may decrease because administered HCO3–
is converted to CO2, which easily diffuses into cells, combines
with water to create additional hydrogen ions and worsening
of intracellular acidosis and this could impair cellular function
Alkali administration is known to stimulate
phosphofructokinase activity, thus exacerbating lactic acidosis
via enhanced lactate production. Ketogenesis is also
augmented by alkali therapy.
56. Treatment of high anion gap
acidosis…..
◦ In salicylate intoxication, alkali therapy must be started unless blood
pH is already alkalinized by respiratory alkalosis, since the
increment in pH converts salicylate to more impermeable salicylic
acid and thus prevents central nervous system damage.
◦ In DKA, alkali must be administered in extreme alkalemia (pH<7.1)
◦ In alcoholic ketoacidosis, thiamine should be given together with
glucose to avoid the development of Wernicke's encephalopathy.
The amount of HCO3– deficit can be calculated as follows:
Amount of HCO3– deficit = 0.5 X body weight X (24 - HCO3–)
◦ Half of the calculated deficit should be administered within the first
3–4 hours to avoid overcorrection and volume overload.
In methanol intoxication
◦ ethanol has been used as a competitive substrate for alcohol
dehydrogenase, which metabolizes methanol to formaldehyde
◦ or through direct inhibition of alcohol dehydrogenase by fomepizole
57. Hyperchloremic (Nongap)
Metabolic Acidoses: causes
I. Gastrointestinal bicarbonate loss
Diarrhea
External pancreatic or small-bowel drainage
Ureterosigmoidostomy, jejunal loop, ileal loop
Drugs - Calcium chloride , Magnesium sulfate
(diarrhea), Cholestyramine (bile acid diarrhea)
II. Renal acidosis
Hypokalemia
Proximal RTA (type 2)
Distal (classic) RTA (type 1)
Hyperkalemia
Generalized distal nephron dysfunction (type 4 RTA)
a. Mineralocorticoid deficiency
b. Mineralocorticoid resistance (autosomal dominant PHA I)
c. Voltage defect (autosomal dominant PHA I and PHA II)
d. Tubulointerstitial disease
58. III. Drug-induced hyperkalemia (with renal insufficiency)
◦ Potassium-sparing diuretics
(amiloride, triamterene, spironolactone)
◦ Trimethoprim
◦ Pentamidine
◦ ACE-Is and ARBs
◦ Nonsteroidal anti-inflammatory drugs
◦ Cyclosporine and tacrolimus
IV. Other
◦ Acid loads (ammonium chloride, hyperalimentation)
◦ Loss of potential bicarbonate: ketosis with ketone excretion
◦ Expansion /dilutional acidosis (rapid saline administration)
◦ Hippurate
◦ Cation exchange resins
59. Approach: Urinary Anion Gap
Increased renal NH4+Cl– excretion to enhance H+ removal is a normal
physiologic response to metabolic acidosis. NH3 reacts with H+ to
form NH4+, which is accompanied by the anion Cl– for excretion.
Urinary anion gap from a random urine sample ([Na++ K+]– Cl–)
reflects the ability of the kidney to excrete NH4Cl as in the following
equation:
Na+ + K+ + NH4+ = Cl– + 80
urinary anion gap is equal to (80 – NH4+)
Gastrointestinal HCO3– loss (diarrhea), the renal acidification ability
remains normal and NH4Cl excretion increases in response to the
acidosis. urinary anion gap is negative (eg, –30 mEq/L).
Distal RTA, the urinary anion gap is positive (eg, +25 mEq/L), since
the basic lesion in the disorder is the inability of the kidney to excrete
H+ and thus the inability to increase NH4Cl excretion.
Proximal (type II) RTA, the kidney has defective HCO3–
reabsorption, leading to increased HCO3– excretion rather than
decreased NH4Cl excretion. Thus, the urinary anion gap is negative
60. Urinary pH may not as readily differentiate
between the two causes because volume
depletion or potassium depletion, which can
accompany diarrhea (and surreptitious laxative
abuse) may impair renal acidification.
Thus, when volume depletion is present, the
urinary anion gap is a better measurement of
ability to acidify the urine than urinary pH.
When large amounts of other anions are present
in the urine, the urinary anion gap may not be
reliable. In such a situation, NH4+ excretion can
be estimated using the urinary osmolar gap.
NH4+ excretion (mmol/L) = 0.5 x Urinary osmolar
gap = 0.5 [U osm – 2(U Na++U K+) + U urea + U
glucose]
where urinary (U) concentrations and osmolality
are in millimoles per liter.
61. Renal Serum Urinary Titratable Urinary Treatment
Defect [K+] NH4+ Plus Acid Anion
Minimal Gap
Urine pH
Gastrointestinal None ↓ < 5.5 ↑↑ Negative Na+, K+, and
HCO3– loss HCO3– as
required
Renal tubular
acidosis
I. Classic distal Distal H+ ↓ > 5.5 ↓ Positive NaHCO3 (1–3
secretion mEq/kg/d)
II. Proximal Proximal ↓ < 5.5 Normal Negative NaHCO3 or
secretion HCO3– KHCO3 (10–15
abspn mEq/kg/d),
thiazide
IV. Distal Na+ ↑ < 5.5 ↓ Positive Fludrocortisone
Hyporeninemic reabsorption (0.1–0.5 mg/d),
+ dietary K+ rstrn,
hypoaldosteroni K secretion,
and H+ furosemide (40–
sm
secretion 160 mg/d),
NaHCO3 (1–3
mEq/kg/d)
62. Treatment of normal Anion gap
Acidosis
Gastrointestinal: Correction of the contracted ECFV with NaCl
and repair of K+ deficits corrects the acid-base disorder, and
chloride deficiency.
RTA : administration of alkali (either as bicarbonate or citrate) to
correct metabolic abnormalities and prevent nephrocalcinosis and
renal failure.
◦ Proximal RTA : Large amounts of alkali (10–15 mEq/kg/d) may
be required to treat proximal RTA because most of the alkali is
excreted into the urine, which exacerbates hypokalemia. Thus, a
mixture of sodium and potassium salts, such as K-Shohl
solution, is preferred. The addition of thiazides may reduce the
amount of alkali required, but hypokalemia may develop.
◦ Distal RTA : Correction of type 1 distal RTA requires a smaller
amount of alkali (1–3 mEq/kg/d) and potassium supplementation
as needed.
◦ Type IV RTA: dietary potassium restriction may be needed and
potassium-retaining drugs should be withdrawn. Fludrocortisone
may be effective in cases with hypoaldosteronism, but should be
used with care, preferably in combination with loop diuretics.
alkali supplementation (1–3 mEq/kg/d) may be required.
63.
64. Metabolic Alkalosis
Essentials of Diagnosis
◦ High HCO3– with alkalemia.
◦ Evaluate effective circulating volume by
physical examination and check urinary
chloride concentration. This will help
differentiate saline-responsive metabolic
alkalosis from saline-unresponsive
alkalosis
65. Metabolic Alkalosis
Occurs as a result of net gain of [HCO3–] or loss
of nonvolatile acid (usually HCl by vomiting) from
the extracellular fluid.
The disorder involves
a generative stage, in which the loss of acid usually
causes alkalosis
maintenance stage, in which the kidneys fail to
compensate by excreting HCO3–.
Classified based on "saline responsiveness" or
urinary Cl–, which are markers for volume status
Saline-responsive metabolic alkalosis is a sign
of extracellular volume contraction
Saline-unresponsive alkalosis implies a volume-
expanded state
66. Symptoms
With metabolic alkalosis, changes in central and
peripheral nervous system function are similar to
those of hypocalcemia : symptoms include
Mental confusion
Obtundation
Predisposition to seizures
Paresthesia
Muscular cramping
Tetany
Aggravation of arrhythmias
Hypoxemia in chronic obstructive pulmonary
disease.
Related electrolyte abnormalities include
Hypokalemia- Weakness and hyporeflexia
hypophosphatemia.
67. Classification and etiology
I. Saline-Responsive (UCl < 10 mEq/d)
Excessive body bicarbonate content
Renal alkalosis
Diuretic therapy
Poorly reabsorbable anion therapy:
carbenicillin, penicillin, sulfate, phosphate
Posthypercapnia
Gastrointestinal alkalosis
Loss of HCl from vomiting or nasogastric suction
Intestinal alkalosis: chloride diarrhea
Exogenous alkali
NaHCO3 (baking soda)
Sodium citrate, lactate, gluconate, acetate
Transfusions
Antacids
Normal body bicarbonate content
"Contraction alkalosis"
68. II. Saline-Unresponsive (UCl > 10 mEq/d)
Excessive body bicarbonate content
Renal alkalosis
Normotensive
Bartter's syndrome (renal salt wasting and
secondary hyperaldosteronism)
Severe potassium depletion
Refeeding alkalosis
Hypercalcemia and hypoparathyroidism
Hypertensive
Endogenous mineralocorticoids
Primary aldosteronism
Hyperreninism
Adrenal enzyme deficiency: 11- and 17-
hydroxylase
Liddle's syndrome
Exogenous mineralocorticoids
Licorice
69.
70. Treatment
Mild alkalosis is generally well tolerated. Severe or
symptomatic alkalosis (pH > 7.60) requires urgent
treatment.
Saline-Responsive Metabolic Alkalosis
◦ Aimed at correction of extracellular volume
deficit.
◦ Depending on the degree of
hypovolemia, adequate amounts of 0.9%
NaCl and KCl should be administered.
◦ Discontinuation of diuretics and
administration of H2-blockers in patients
whose alkalosis is due to nasogastric suction
can be useful.
◦ If impaired pulmonary or cardiovascular
status prohibits adequate volume
repletion, acetazolamide, 250–500 mg
intravenously every 4–6 hours, can be used.
71. Treatment…..
One must be alert to the possible development of
hypokalemia, since potassium depletion can be
induced by forced kaliuresis via bicarbonaturia.
Administration of acid can be used as emergency
therapy. HCl, 0.1 mol/L, is infused via a central vein
(the solution is sclerosing). Dosage is calculated to
decrease the HCO3– level by 50% over 2–4
hours, assuming an HCO3– volume of distribution (L)
of 0.5% body weight (kg).
Patients with marked renal failure may require dialysis.
Saline-Unresponsive Metabolic Alkalosis
surgical removal of a mineralocorticoid-producing
tumor
blockage of aldosterone effect with an ACE inhibitor or
with spironolactone.
primary aldosteronism can be treated only with
potassium repletion.
72. Respiratory Acidosis
Results from decreased alveolar ventilation and hypercapnia
both due to pulmonary and non pulmonary disorders
Central Neuromuscular
◦ Drugs ◦ Poliomyelitis
(anesthetics, morphine, sedatives) ◦ Kyphoscoliosis
◦ Stroke ◦ Myasthenia
◦ Infection ◦ Muscular dystrophies
Airway Miscellaneous
◦ Obstruction ◦ Obesity
◦ Asthma ◦ Hypoventilation
Parenchyma ◦ Permissive hypercapnia
◦ Emphysema
◦ Pneumoconiosis
◦ Bronchitis
◦ Adult respiratory distress
syndrome
◦ Barotrauma
73. Respiratory Acidosis
Acute respiratory failure
associated with severe acidosis and only a small increase
in the plasma bicarbonate.
After 6–12 hours, the primary increase in PCO2 evokes a
renal compensatory response to generate more HCO3–
, which tends to ameliorate the respiratory acidosis. This
takes several days to complete.
Chronic respiratory acidosis
seen in patients with underlying lung disease, such as
chronic obstructive pulmonary disease.
Urinary excretion of acid in the form of NH4+ and Cl– ions
results in the characteristic hypochloremia of chronic
respiratory acidosis.
When chronic respiratory acidosis is corrected
suddenly, especially in patients who receive mechanical
ventilation, there is a 2- to 3-day lag in renal bicarbonate
excretion, resulting in posthypercapnic metabolic
alkalosis.
74. Symptoms and Signs
◦ With acute onset, there is somnolence and confusion, and
myoclonus with asterixis
◦ Coma from CO2 narcosis may ensue
◦ Severe hypercapnia increases cerebral blood flow and
cerebrospinal fluid pressure. Signs of increased intracranial
pressure (papilledema, pseudotumor cerebri) may be seen.
Laboratory Findings
◦ Arterial pH is low
◦ PCO2 is increased
◦ Serum HCO3– is elevated, but not enough to completely
compensate for the hypercapnia.
◦ If the disorder is chronic, hypochloremia is seen.
Treatment
◦ In all forms of respiratory acidosis, treatment is directed at the
underlying disorder to improve ventilation.
◦ Because opioid drug overdose is an important reversible cause of
acute respiratory acidosis, naloxone, 0.04–2 mg intravenously is
administered to all such patients if no obvious cause for
respiratory depression is present.
◦ Mechanical ventilation for oxygenation till it restores back to
normal maybe needed
75. Respiratory Alkalosis(Hypocapnia)
Respiratory alkalosis, or hypocapnia, occurs when hyperventilation
reduces the PCO2, which increases the pH
Symptoms and Signs
In acute cases (hyperventilation), there is light-headedness,
anxiety, paresthesias, numbness about the mouth, and a tingling
sensation in the hands and feet. Tetany occurs in more severe
alkalosis from a fall in ionized calcium.
In chronic cases, findings are those of the responsible condition.
Laboratory Findings
Arterial blood pH is elevated, and PCO2 is low. Serum
bicarbonate is decreased in chronic respiratory alkalosis.
Determination of appropriate compensatory changes in the
HCO3– is useful to sort out the presence of an associated
metabolic disorder
the changes in HCO3– values are greater if the respiratory
alkalosis is chronic
Although serum HCO3– is frequently below 15 mEq/L in
metabolic acidosis, it is unusual to see such a low level in
respiratory alkalosis, and its presence would imply a
superimposed (noncompensatory) metabolic acidosis.
78. Treatment
Treatment is directed toward the underlying cause.
In acute hyperventilation syndrome from
anxiety, reassurance , attention to underlying psychological
stress and rebreathing into a paper bag will increase the
PCO2.
The processes are usually self-limited since muscle
weakness caused by hyperventilation-induced alkalemia will
suppress ventilation.
Sedation may be necessary if the process persists however
Antidepressants and sedatives should be avoided
Adrenergic blockers may ameliorate peripheral
manifestations of the hyperadrenergic state.
Rapid correction of chronic respiratory alkalosis may result
in metabolic acidosis as PCO2 is increased in the setting of
previous compensatory decrease in HCO3–.
If respiratory alkalosis complicates ventilator
management, changes in dead space, tidal volume, and
frequency can minimize the hypocapnia
79. Conclusion
Clinical suspicion according to scenario
Primary disorder from pH and bicarbonate or CO2
values
Degree of compensation…? Inappropriate? mixed
disorder
Anion gap (corrected for serum albumin
change)…? Primary metabolic acidosis
Corrected bicarbonate levels…?
More than normal- associated metabolic alkalosis
Less - associated metabolic non-anion gap acidosis
Review compensation for metabolic ds…confirm if
initially suspected respiratory disorder exists
80. Metabolic acidosis: ..see AG
High AG: …plasma osmolal gap
more.. Toxins
Less.. KA, RF, LA,
Normal AG acidosis:
urine AG….negative..GI
urinary pH ….high..RTA 1
serum potassium….high..RTA4
Metabolic alkalosis:
◦ Urinary Chloride…
Less..saline responsive…ECF contraction
more ..saline non responsive
Plasma Potassium…low..K depletion
High…Blood pressure
Plasma renin
81. 1.PaCO2 equation:
VCO2 x 0.863 VCO2 = CO2 production
PaCO2 = ----------------- VA = VE – VD
VA VE = minute (total) ventilation
VD = dead space ventilation
0.863 converts units to mm Hg
Condition State of
PaCO2 in blood alveolar ventilation
>45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal ventilation
<35 mm Hg Hypocapnia Hyperventilation
PaCO2 reflects ratio of metabolic CO2 production to alveolar
ventilation
82. Hypercapnia
VCO2 x 0.863
PaCO2 = ------------------
VA
The only physiologic reason for elevated PaCO2 is
inadequate alveolar ventilation (VA) for the amount of the
body‘s CO2 production (VCO2). Since alveolar ventilation
(VA) equals minute ventilation (VE) minus dead space
ventilation (VD), hypercapnia can arise from insufficient
VE, increased VD, or a combination.
83. Hypercapnia
VCO2 x 0.863
PaCO2 = ------------------
VA VA = VE – VD
Examples of inadequate VE leading to decreased VA and
increased PaCO2: sedative drug overdose; respiratory muscle
paralysis; central hypoventilation
Examples of increased VD leading to decreased VA and
increased PaCO2: chronic obstructive pulmonary disease;
severe pulmonary embolism, pulmonary edema.
84. Physiologic effects of
hypercapnia
◦ 1) An elevated PaCO2 will lower the PAO2 (see Alveolar gas
equation), and as a result lower the PaO2.
◦ 2) An elevated PaCO2 will lower the pH (see Henderson-
Hasselbalch equation).
◦ 3) The higher the baseline PaCO2, the greater it will rise for a
given fall in alveolar ventilation, e.g., a 1 L/min decrease in
VA will raise PaCO2 a greater amount when baseline PaCO2
is 50 mm Hg than when it is 40 mm Hg.
86. Oxygenation
-----XXXX Diagnostics----- Parameters: /limitations
Blood Gas Report
328
Pt ID
03:44
3245 / 00
Feb 5 2006 O2 Content of blood:
(Hb x1.34x O2 Sat + 0.003x Dissolved O2 )
Measured 37.0 0C
pH 7.452 Remember Hemoglobin
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
Corrected 38.6 0C Oxygen Saturation:
pH 7.436
pCO2 47.6 mm Hg ( remember this is calculated …error prone)
pO2 122.4 mm Hg
Calculated Data Alveolar / arterial gradient:
HCO3 act 31.2 mmol / L ( classify respiratory failure)
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 ct 15.8 mL / dl
O2 Sat 98.4 % Arterial / alveolar ratio:
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg Proposed to be less variable
pO2 (a/A) 0.78
Same limitations as A-a gradient
Entered Data
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl
87. Alveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)
where PAO2 is the average alveolar PO2, and PIO2 is the partial pressure
of inspired oxygen in the trachea
PIO2 = FIO2 (PB – 47 mm Hg)
FIO2 is fraction of inspired oxygen and PB is the barometric pressure. 47
mm Hg is the water vapor pressure at normal body temperature.
88. Alveolar Gas Equation
If FIO2 and PB are constant, then as PaCO2 increases
both PAO2 and PaO2 will decrease (hypercapnia causes
hypoxemia).
If FIO2 decreases and PB and PaCO2 are constant, both
PAO2 and PaO2 will decrease.
If PB decreases (e.g., with altitude), and PaCO2 and FIO2
are constant, both PAO2 and PaO2 will decrease
(mountain climbing causes hypoxemia).
89. P(A-a)O2
P(A-a)O2 is the alveolar-arterial difference in partial pressure of
oxygen. It is commonly called the ―A-a gradient‖. It results from
gravity-related blood flow changes within the lungs (normal
ventilation-perfusion imbalance).
Normal P(A-a)O2 ranges from 5 to 25 mm Hg breathing room air
(it increases with age). A higher than normal P(A-a)O2 means the
lungs are not transferring oxygen properly from alveoli into the
pulmonary capillaries. Except for right to left cardiac shunts, an
elevated P(A-a)O2 signifies some sort of problem within the lungs.
90. Physiologic causes of low PaO2
NON-RESPIRATORY P(A-a)O2
Cardiac right to left shunt Increased
Decreased PIO2 Normal
RESPIRATORY
Pulmonary right to left shunt Increased
Ventilation-perfusion imbalance Increased
Diffusion barrier Increased
Hypoventilation (increased PaCO2) Normal
91. Ventilation-Perfusion imbalance
A normal amount of ventilation-perfusion (V-Q)
imbalance accounts for the normal P(A-a)O2.
By far the most common cause of low PaO2 is an
abnormal degree of ventilation-perfusion imbalance
within the hundreds of millions of alveolar-capillary
units. Virtually all lung disease lowers PaO2 via V-Q
imbalance, e.g., asthma, pneumonia, atelectasis,
pulmonary edema, COPD.
Diffusion barrier is seldom a major cause of low PaO2
(it can lead to a low PaO2 during exercise).
92. SaO2 and oxygen content
How much oxygen is in the blood? Oxygen content = CaO2 (mlO2/dl).
CaO2 = quantity O2 bound + quantity O2 dissolved
to hemoglobin in plasma
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of
Hb; SaO2 is percent saturation of hemoglobin with oxygen; .003 is
solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg
PO2.
93. Given arterial oxygen saturation (SpO2) =
100%, Hb = 15 g/100 ml and arterial partial
pressure of oxygen (PaO2) = 13.3 kPa, then
the oxygen content of arterial blood (CaO2) is:
CaO2 = 20.1 +0.3 = 20.4 ml/100 ml
Similarly the oxygen content of mixed venous
blood can be calculated. Given normal
values of mixed venous oxygen saturation
(SvO2) = 75% and venous partial pressure of
oxygen (PvO2) = 6 kPa, so:
CvO2 = 15.2 + 0.1 = 15.2 ml/100 ml
94. Oxygen dissociation curve: SaO2 vs. PaO2
Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm%
and 10 gm%. CaO2 units are ml O2/dl. P50 is the PaO2 at which SaO2 is 50%.
95. SaO2 – is it calculated or measured?
SaO2 is measured in a ‗co-oximeter‘. The traditional ‗blood gas
machine‘ measures only pH, PaCO2 and PaO2,, whereas the co-
oximeter measures SaO2, carboxyhemoglobin, methemoglobin and
hemoglobin content. Newer ‗blood gas‘ consoles incorporate a co-
oximeter, and so offer the latter group of measurements as well as
pH, PaCO2 and PaO2.
Always make sure the SaO2 is measured, not calculated. If it is
calculated from the PaO2 and the O2-dissociation curve, it
provides no new information, and could be inaccurate --
especially in states of CO intoxication or excess
methemoglobin. CO and metHb do not affect PaO2, but do lower
the SaO2.
96. Carbon monoxide – an important cause
of hypoxemia
Normal %COHb in the blood is 1-2%, from metabolism and small
amount of ambient CO (higher in traffic-congested areas)
All smokers have excess CO in their blood.
CO binds @ 200x more avidly to hemoglobin than O2, displacing O2
from the heme binding sites.
CO : 1) decreases SaO2 by the amount of %COHb present, and 2)
shifts the O2-dissociation curve to the left, retarding unloading of
oxygen to the tissues.
CO does not affect PaO2, only SaO2. To detect CO
poisoning, SaO2 and/or COHb must be measured (requires co-
oximeter). In the presence of excess CO, SaO2 (when measured)
will be lower than expected from the PaO2.
97. CO does not affect PaO2!
A patient presented to the ER with headache and dyspnea.
His first blood gases showed PaO2 80 mm Hg, PaCO2 38 mm Hg, pH
7.43. SaO2 on this first set was calculated from the O2-dissociation
curve at 97%, and oxygenation was judged normal.
He was sent out from the ER and returned a few hours later with mental
confusion; this time both SaO2 and COHb were measured (SaO2 shown
by ‗X‘): PaO2 79 mm Hg, PaCO2 31 mm Hg, pH 7.36, SaO2
53%, carboxyhemoglobin 46%.
CO poisoning was missed on the first set of blood gases
because SaO2 was not measured!
98. Causes of Hypoxia
1. Hypoxemia (=low PaO2 and/or low CaO2)
◦ a. reduced PaO2 – usually from lung disease (most common
physiologic mechanism: V-Q imbalance)
◦ b. reduced SaO2 -- most commonly from reduced PaO2; other
causes include carbon monoxide
poisoning, methemoglobinemia, or rightward shift of the O2-
dissociation curve
◦ c. reduced hemoglobin content -- anemia
2. Reduced oxygen delivery to the tissues
◦ a. reduced cardiac output -- shock, congestive heart failure
◦ b. left to right systemic shunt (as may be seen in septic shock)
3. Decreased tissue oxygen uptake
◦ a. mitochondrial poisoning (e.g., cyanide poisoning)
◦ b. left-shifted hemoglobin dissociation curve (e.g., from acute
alkalosis, excess CO, or abnormal hemoglobin structure)
99. Arterial Oxygen Tension (PaO2)
Normal value in healthy adult breathing
room air at sea level 97 mm Hg.
progressively with age
Dependant upon
1. FiO2
2. Patm
Hypoxemia is PaO2 < 80 mm Hg at RA
Most pts who need ABG usually req O2
therapy
O2 therapy should not be
withheld/interrupted ‗to determine PaO2
on RA‘
100. Acceptable PaO2 Values on Room
Air
Age Group Accepable PaO2
(mm Hg)
Adults upto 60 yrs > 80
& Children
Newborn 40-70
70 yrs > 70
80 yrs > 60
90 yrs > 50
60 yrs 80 mm Hg 1mm Hg/yr
101. Inspired O2 – PaO2 Relationship
FIO2 (%) Predicted Min
PaO2 (mm Hg)
30 150
40 200
50 250
80 400
100 500
If PaO2 < FIO2 x 5, pt probably hypoxemic at RA
102. Hypoxemia on O2 therapy
Uncorrected: PaO2 < 80 mm Hg
(< expected on RA & FIO2)
Corrected: PaO2 = 80-100 mm Hg
(= expected on RA but < expected for FIO2)
Excessively Corrected: PaO2 > 100 mm Hg
(> expected on RA but < expected for FIO2)
PaO2 > expected for FIO2:
1. Error in sample/analyzer
2. Pt‘s O2 consumption reduced
3. Pt does not req O2 therapy (if 1 & 2 NA)