1. An arterial blood gas (ABG) analysis can provide information about oxygenation, ventilation, and acid-base status. It answers questions like how severe hypoxia or hypercarbia is and what acid-base abnormalities may be present.
2. The document provides templates for interpreting ABG results and analyzing acid-base disturbances and their compensation. It also includes several case scenarios where ABG results are used to diagnose conditions like respiratory acidosis from narcotic overdose or metabolic acidosis and hyperventilation from pneumonia.
3. Key steps in ABG interpretation involve checking for hypoxemia and quantifying any shunt fraction, evaluating ventilation and dead space, identifying primary acid-base disturbances and compensation
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.
Interpretation of the Arterial Blood Gas analysisVishal Golay
The document discusses the basics of acid-base balance, the role of kidneys in homeostasis, and a step-wise approach to diagnosing acid-base disorders from arterial blood gas results including evaluating pH, PCO2, HCO3, and other electrolytes and looking at changes from normal values. It also covers proper sampling techniques for arterial blood gases and interpreting various values calculated from the measured results.
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 strategies for optimizing preoxygenation prior to endotracheal intubation. It notes that conventional preoxygenation techniques provide safe intubation for most ED patients but that a subset may still desaturate. To safely intubate this higher risk group, the document recommends optimizing preoxygenation through techniques like non-invasive ventilation, apneic oxygenation through nasal cannula, positioning patients in a head-up position, and breaking the sequence of rapid sequence intubation administration. The goal is to prevent deoxygenation and extend the safe apneic period for patients undergoing endotracheal intubation.
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.
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 perioperative fluid therapy. It covers topics such as total body water, fluid compartments, preoperative fluid status evaluation, intravenous fluids including crystalloids like normal saline and lactated ringer's solution and colloids like albumin, gelatin and hydroxyethyl starches. It provides guidelines on calculating fluid requirements including maintenance fluids, deficits, third spacing losses and blood loss replacement. The document emphasizes using crystalloids over colloids for resuscitation and limiting colloid volumes due to lack of evidence for their continued use in acute illness.
This document outlines the steps for analyzing arterial blood gases (ABGs) and determining the underlying acid-base disorder. The key steps are to check the pH and determine if the patient is acidemic or alkalemic, identify the primary respiratory or metabolic disorder based on pH and pCO2/HCO3 levels, assess compensation and determine if it is acute or chronic, calculate the anion gap and delta gap if indicated, and consider differentials based on clinical context and lab results. Causes of common acid-base disorders like respiratory acidosis, metabolic acidosis, respiratory alkalosis, and metabolic alkalosis are also reviewed.
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.
Interpretation of the Arterial Blood Gas analysisVishal Golay
The document discusses the basics of acid-base balance, the role of kidneys in homeostasis, and a step-wise approach to diagnosing acid-base disorders from arterial blood gas results including evaluating pH, PCO2, HCO3, and other electrolytes and looking at changes from normal values. It also covers proper sampling techniques for arterial blood gases and interpreting various values calculated from the measured results.
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 strategies for optimizing preoxygenation prior to endotracheal intubation. It notes that conventional preoxygenation techniques provide safe intubation for most ED patients but that a subset may still desaturate. To safely intubate this higher risk group, the document recommends optimizing preoxygenation through techniques like non-invasive ventilation, apneic oxygenation through nasal cannula, positioning patients in a head-up position, and breaking the sequence of rapid sequence intubation administration. The goal is to prevent deoxygenation and extend the safe apneic period for patients undergoing endotracheal intubation.
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.
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 perioperative fluid therapy. It covers topics such as total body water, fluid compartments, preoperative fluid status evaluation, intravenous fluids including crystalloids like normal saline and lactated ringer's solution and colloids like albumin, gelatin and hydroxyethyl starches. It provides guidelines on calculating fluid requirements including maintenance fluids, deficits, third spacing losses and blood loss replacement. The document emphasizes using crystalloids over colloids for resuscitation and limiting colloid volumes due to lack of evidence for their continued use in acute illness.
This document outlines the steps for analyzing arterial blood gases (ABGs) and determining the underlying acid-base disorder. The key steps are to check the pH and determine if the patient is acidemic or alkalemic, identify the primary respiratory or metabolic disorder based on pH and pCO2/HCO3 levels, assess compensation and determine if it is acute or chronic, calculate the anion gap and delta gap if indicated, and consider differentials based on clinical context and lab results. Causes of common acid-base disorders like respiratory acidosis, metabolic acidosis, respiratory alkalosis, and metabolic alkalosis are also reviewed.
The document summarizes the anatomy and blood supply of the liver and how anesthetic drugs can affect liver function. It describes the lobes, ligaments, vascularization including the portal triad, and histology of the liver. It then discusses factors that can increase or decrease hepatic blood flow and the effects of various anesthetic drugs on liver function and blood flow, such as halothane potentially causing hepatitis, propofol increasing blood flow, and opioids having little effect if blood flow is maintained.
by the renowned pediatrician, Dr Satish Deopujari,
National Chairperson (Ex)
Intensive Care Chapter I A P
Founder Chairman.....
National conference on pediatric critical care
Professor of pediatrics ( Hon ) JNMC:Wardha
Nagpur : INDIA
The document discusses the history and use of laryngeal mask airways (LMA). It describes how Dr. Brain developed the first LMA prototype in 1981 as a supraglottic device that sits outside the trachea but provides an airway. Over time, different types of LMAs were developed including the classic LMA, ProSeal LMA, reinforced LMA, LMA-Unique, and Supreme LMA. The document outlines the features and proper insertion technique for each LMA and discusses their advantages, such as being less invasive than endotracheal tubes, as well as potential complications if not properly placed.
Dr. Y. Krishna presented on arterial blood gas analysis. Key points include:
- ABG analysis provides pH, PaCO2, PaO2, HCO3, SaO2 and other values to assess acid-base status and ventilation.
- Primary acid-base disorders involve changes in PaCO2 or HCO3, while secondary involve compensatory changes. Acute vs chronic compensation affects HCO3 changes.
- Anion gap is used to determine if metabolic acidosis is due to organic acids or HCO3 loss. Delta gap identifies additional hidden processes.
- Common causes of acid-base imbalances include respiratory disorders like hypoventilation; and metabolic disorders like ketoacidosis
The document discusses thyroid disorders including hyperthyroidism, hypothyroidism, and thyroid storm and their implications for anesthesia such as increased sensitivity to drugs, risks of tachycardia and arrhythmias, and need for careful monitoring of cardiac and respiratory function. It provides guidance on preoperative preparation, intraoperative management, and postoperative care for patients with thyroid disorders undergoing surgery.
Caudal anesthesia involves needle penetration through the sacral hiatus into the sacral canal. In adults, the sacrum is a triangular bone formed from the fusion of five sacral vertebrae. It differs in neonates and infants due to delayed myelination and fusion of vertebrae. The sacral hiatus is wider in children, allowing easier identification and catheter insertion for caudal anesthesia. Regional techniques require lower approaches in pediatrics due to the lower termination of the spinal cord and dural sac.
Thiopentone (also known as thiopental sodium) is a short-acting barbiturate used for inducing anesthesia. It works by enhancing the effects of the neurotransmitter GABA at GABAA receptors in the brain, which increases chloride conductance and inhibits neuronal activity. Thiopentone is administered intravenously as a 2.5% solution for induction of anesthesia in adults and children. Common side effects include respiratory depression, hypotension, and pain or tissue damage if accidentally injected into an artery. Proper dosage depends on factors like age, weight, and medical history. Thiopentone is metabolized in the liver and redistributes rapidly from the brain after administration, which allows for quick awakening.
- Minimum alveolar concentration (MAC) is a measure of the potency of inhaled anesthetic agents, defined as the concentration needed to suppress movement in 50% of patients.
- MAC was developed in 1965 and provides an objective standard for assessing anesthetic depth compared to prior subjective tools.
- Several factors can influence a patient's MAC including age, temperature, medications, and medical conditions.
- The relative potencies of common inhaled anesthetics correlates with the Meyer-Overton rule regarding solubility in lipid membranes.
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.
This document provides information about arterial blood gas (ABG) analysis. It defines an ABG as a blood sample drawn from an artery to assess acid-base balance, oxygenation, and ventilation. ABGs are ordered to diagnose and monitor respiratory failure and changes in acid-base homeostasis. The components of an ABG include pH, PaCO2, PaO2, HCO3, O2 saturation, and base excess. Normal values for these components are provided. The document discusses how to properly collect an ABG sample and handle it to avoid inaccurate results. It also covers acid-base physiology and the four primary acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alk
An arterial blood gas test involves puncturing an artery, usually the radial artery, to draw blood and measure acidity, oxygen and carbon dioxide levels. It can help diagnose conditions, guide treatment, and monitor ventilator management. The test measures pH, pO2, pCO2, HCO3, SaO2 and base excess. Abnormal results can indicate respiratory or metabolic acidosis or alkalosis which have distinct causes, signs, and treatments. Interpreting blood gases involves assessing oxygenation, acid-base status, and whether the disturbance is primarily respiratory or metabolic in nature.
This document provides an overview of arterial blood gas interpretation. It discusses normal values for pH, PaCO2, HCO3, PaO2 and SaO2. It explains acid-base balance and the respiratory and metabolic mechanisms that control pH. A 3-step process is outlined for interpreting ABG results: 1) determine if acidosis or alkalosis based on pH, 2) evaluate the respiratory mechanism using PaCO2, and 3) evaluate the metabolic mechanism using HCO3. Compensation and combined disturbances are also addressed. Case examples are provided to demonstrate interpreting ABG results and diagnosing respiratory vs. metabolic causes of acid-base imbalances.
This document provides information on interpreting blood gas analysis (ABG). It discusses common errors in ABG sampling and outlines steps to analyze ABG results. Key points include checking if the pH indicates acidosis or alkalosis, identifying the primary disorder, assessing compensation, and calculating the anion and delta gaps to detect mixed disorders. Non-gap causes of acidosis are distinguished using urine anion gap. The document also covers expected changes in respiratory and metabolic acid-base disorders and differentials for specific conditions.
HFNC therapy provides high flow oxygen through a nasal cannula. It has several benefits over traditional oxygen delivery methods, including more accurate oxygen delivery, washout of dead space, and generation of positive end-expiratory pressure. HFNC is a well-tolerated therapy that can be used for hypoxemic respiratory failure, pre-intubation, and post-extubation. While promising, further research is still needed to establish clear guidelines for its use.
Malignant hyperthermia is a rare but serious genetic disorder triggered by certain anesthetic gases and succinylcholine. It results from an abnormality in the skeletal muscle calcium regulation that leads to excess calcium accumulation and sustained muscle contraction. Early signs include increased carbon dioxide, tachycardia, and muscle rigidity. Later signs include hyperthermia, abnormal EKG readings, and rhabdomyolysis. Treatment involves discontinuing triggers, administering dantrolene to inhibit calcium release, supporting ventilation and organ function, and treating complications like acidosis and kidney damage. Prompt treatment can reduce mortality from over 15% to under 2%.
The anaesthetic machine (UK English) or anesthesia machine (US English) or Boyle's machine is used by anaesthesiologists, nurse anaesthetists, and anaesthesiologist assistants to support the administration of anaesthesia. The most common type of anaesthetic machine in use in the developed world is the continuous-flow anaesthetic machine, which is designed to provide an accurate and continuous supply of medical gases (such as oxygen and nitrous oxide), mixed with an accurate concentration of anaesthetic vapour (such as isoflurane), and deliver this to the patient at a safe pressure and flow. Modern machines incorporate a ventilator, suction unit, and patient monitoring devices.
Anesthesia Consideration in Pediatric and ObstetricsRifhan Kamaruddin
Pediatric patients have important physiological differences compared to adults that impact anesthesia care. Their respiratory systems have higher minute ventilation, oxygen consumption, and risk of airway closure. Blood volume is higher in neonates compared to older children and adults. The liver and kidneys are immature, increasing risk of hypoglycemia and difficulty excreting drugs. Thermoregulation is less developed, requiring measures to prevent hypothermia. Pre-operative assessment includes medical history, physical exam, and investigations to evaluate risk. Post-operative care focuses on preventing nausea, vomiting and adequately managing pain.
Dr. Milan Kharel presented on inhalational anesthetic agents. He discussed the history of anesthesia including the first agents used like ether and chloroform. He then covered the basic concepts of MAC, vapor pressure, factors affecting uptake and distribution of gases. The ideal characteristics of an anesthetic were noted. Various agents were classified and discussed in detail including nitrous oxide, halothane, enflurane, isoflurane, sevoflurane and desflurane.
This document provides information about arterial blood gas (ABG) analysis, including how to interpret levels of oxygenation, ventilation, and acid-base imbalance from an ABG test. It discusses key measurements like PaO2, PaCO2, oxygen saturation, and bicarbonate levels. It also reviews respiratory physiology concepts like ventilation-perfusion mismatch, shunt fraction, and the oxygen-hemoglobin dissociation curve that are important for understanding ABG results.
The document discusses targeting low levels of PaO2 in patients with ARDS. It notes that while specific PaO2 levels cannot be defined, values between 60-75 mmHg are generally appropriate, and 50-60 mmHg may be tolerated in healthy young patients. Lower values between 40-50 mmHg should not be desirable. The key consideration is the "clinical price" of interventions to increase PaO2, such as increased FiO2 or mean airway pressures. As long as tissue oxygenation is maintained, permissive hypoxemia in ARDS appears to be well tolerated without evidence of tissue hypoxia.
The document summarizes the anatomy and blood supply of the liver and how anesthetic drugs can affect liver function. It describes the lobes, ligaments, vascularization including the portal triad, and histology of the liver. It then discusses factors that can increase or decrease hepatic blood flow and the effects of various anesthetic drugs on liver function and blood flow, such as halothane potentially causing hepatitis, propofol increasing blood flow, and opioids having little effect if blood flow is maintained.
by the renowned pediatrician, Dr Satish Deopujari,
National Chairperson (Ex)
Intensive Care Chapter I A P
Founder Chairman.....
National conference on pediatric critical care
Professor of pediatrics ( Hon ) JNMC:Wardha
Nagpur : INDIA
The document discusses the history and use of laryngeal mask airways (LMA). It describes how Dr. Brain developed the first LMA prototype in 1981 as a supraglottic device that sits outside the trachea but provides an airway. Over time, different types of LMAs were developed including the classic LMA, ProSeal LMA, reinforced LMA, LMA-Unique, and Supreme LMA. The document outlines the features and proper insertion technique for each LMA and discusses their advantages, such as being less invasive than endotracheal tubes, as well as potential complications if not properly placed.
Dr. Y. Krishna presented on arterial blood gas analysis. Key points include:
- ABG analysis provides pH, PaCO2, PaO2, HCO3, SaO2 and other values to assess acid-base status and ventilation.
- Primary acid-base disorders involve changes in PaCO2 or HCO3, while secondary involve compensatory changes. Acute vs chronic compensation affects HCO3 changes.
- Anion gap is used to determine if metabolic acidosis is due to organic acids or HCO3 loss. Delta gap identifies additional hidden processes.
- Common causes of acid-base imbalances include respiratory disorders like hypoventilation; and metabolic disorders like ketoacidosis
The document discusses thyroid disorders including hyperthyroidism, hypothyroidism, and thyroid storm and their implications for anesthesia such as increased sensitivity to drugs, risks of tachycardia and arrhythmias, and need for careful monitoring of cardiac and respiratory function. It provides guidance on preoperative preparation, intraoperative management, and postoperative care for patients with thyroid disorders undergoing surgery.
Caudal anesthesia involves needle penetration through the sacral hiatus into the sacral canal. In adults, the sacrum is a triangular bone formed from the fusion of five sacral vertebrae. It differs in neonates and infants due to delayed myelination and fusion of vertebrae. The sacral hiatus is wider in children, allowing easier identification and catheter insertion for caudal anesthesia. Regional techniques require lower approaches in pediatrics due to the lower termination of the spinal cord and dural sac.
Thiopentone (also known as thiopental sodium) is a short-acting barbiturate used for inducing anesthesia. It works by enhancing the effects of the neurotransmitter GABA at GABAA receptors in the brain, which increases chloride conductance and inhibits neuronal activity. Thiopentone is administered intravenously as a 2.5% solution for induction of anesthesia in adults and children. Common side effects include respiratory depression, hypotension, and pain or tissue damage if accidentally injected into an artery. Proper dosage depends on factors like age, weight, and medical history. Thiopentone is metabolized in the liver and redistributes rapidly from the brain after administration, which allows for quick awakening.
- Minimum alveolar concentration (MAC) is a measure of the potency of inhaled anesthetic agents, defined as the concentration needed to suppress movement in 50% of patients.
- MAC was developed in 1965 and provides an objective standard for assessing anesthetic depth compared to prior subjective tools.
- Several factors can influence a patient's MAC including age, temperature, medications, and medical conditions.
- The relative potencies of common inhaled anesthetics correlates with the Meyer-Overton rule regarding solubility in lipid membranes.
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.
This document provides information about arterial blood gas (ABG) analysis. It defines an ABG as a blood sample drawn from an artery to assess acid-base balance, oxygenation, and ventilation. ABGs are ordered to diagnose and monitor respiratory failure and changes in acid-base homeostasis. The components of an ABG include pH, PaCO2, PaO2, HCO3, O2 saturation, and base excess. Normal values for these components are provided. The document discusses how to properly collect an ABG sample and handle it to avoid inaccurate results. It also covers acid-base physiology and the four primary acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alk
An arterial blood gas test involves puncturing an artery, usually the radial artery, to draw blood and measure acidity, oxygen and carbon dioxide levels. It can help diagnose conditions, guide treatment, and monitor ventilator management. The test measures pH, pO2, pCO2, HCO3, SaO2 and base excess. Abnormal results can indicate respiratory or metabolic acidosis or alkalosis which have distinct causes, signs, and treatments. Interpreting blood gases involves assessing oxygenation, acid-base status, and whether the disturbance is primarily respiratory or metabolic in nature.
This document provides an overview of arterial blood gas interpretation. It discusses normal values for pH, PaCO2, HCO3, PaO2 and SaO2. It explains acid-base balance and the respiratory and metabolic mechanisms that control pH. A 3-step process is outlined for interpreting ABG results: 1) determine if acidosis or alkalosis based on pH, 2) evaluate the respiratory mechanism using PaCO2, and 3) evaluate the metabolic mechanism using HCO3. Compensation and combined disturbances are also addressed. Case examples are provided to demonstrate interpreting ABG results and diagnosing respiratory vs. metabolic causes of acid-base imbalances.
This document provides information on interpreting blood gas analysis (ABG). It discusses common errors in ABG sampling and outlines steps to analyze ABG results. Key points include checking if the pH indicates acidosis or alkalosis, identifying the primary disorder, assessing compensation, and calculating the anion and delta gaps to detect mixed disorders. Non-gap causes of acidosis are distinguished using urine anion gap. The document also covers expected changes in respiratory and metabolic acid-base disorders and differentials for specific conditions.
HFNC therapy provides high flow oxygen through a nasal cannula. It has several benefits over traditional oxygen delivery methods, including more accurate oxygen delivery, washout of dead space, and generation of positive end-expiratory pressure. HFNC is a well-tolerated therapy that can be used for hypoxemic respiratory failure, pre-intubation, and post-extubation. While promising, further research is still needed to establish clear guidelines for its use.
Malignant hyperthermia is a rare but serious genetic disorder triggered by certain anesthetic gases and succinylcholine. It results from an abnormality in the skeletal muscle calcium regulation that leads to excess calcium accumulation and sustained muscle contraction. Early signs include increased carbon dioxide, tachycardia, and muscle rigidity. Later signs include hyperthermia, abnormal EKG readings, and rhabdomyolysis. Treatment involves discontinuing triggers, administering dantrolene to inhibit calcium release, supporting ventilation and organ function, and treating complications like acidosis and kidney damage. Prompt treatment can reduce mortality from over 15% to under 2%.
The anaesthetic machine (UK English) or anesthesia machine (US English) or Boyle's machine is used by anaesthesiologists, nurse anaesthetists, and anaesthesiologist assistants to support the administration of anaesthesia. The most common type of anaesthetic machine in use in the developed world is the continuous-flow anaesthetic machine, which is designed to provide an accurate and continuous supply of medical gases (such as oxygen and nitrous oxide), mixed with an accurate concentration of anaesthetic vapour (such as isoflurane), and deliver this to the patient at a safe pressure and flow. Modern machines incorporate a ventilator, suction unit, and patient monitoring devices.
Anesthesia Consideration in Pediatric and ObstetricsRifhan Kamaruddin
Pediatric patients have important physiological differences compared to adults that impact anesthesia care. Their respiratory systems have higher minute ventilation, oxygen consumption, and risk of airway closure. Blood volume is higher in neonates compared to older children and adults. The liver and kidneys are immature, increasing risk of hypoglycemia and difficulty excreting drugs. Thermoregulation is less developed, requiring measures to prevent hypothermia. Pre-operative assessment includes medical history, physical exam, and investigations to evaluate risk. Post-operative care focuses on preventing nausea, vomiting and adequately managing pain.
Dr. Milan Kharel presented on inhalational anesthetic agents. He discussed the history of anesthesia including the first agents used like ether and chloroform. He then covered the basic concepts of MAC, vapor pressure, factors affecting uptake and distribution of gases. The ideal characteristics of an anesthetic were noted. Various agents were classified and discussed in detail including nitrous oxide, halothane, enflurane, isoflurane, sevoflurane and desflurane.
This document provides information about arterial blood gas (ABG) analysis, including how to interpret levels of oxygenation, ventilation, and acid-base imbalance from an ABG test. It discusses key measurements like PaO2, PaCO2, oxygen saturation, and bicarbonate levels. It also reviews respiratory physiology concepts like ventilation-perfusion mismatch, shunt fraction, and the oxygen-hemoglobin dissociation curve that are important for understanding ABG results.
The document discusses targeting low levels of PaO2 in patients with ARDS. It notes that while specific PaO2 levels cannot be defined, values between 60-75 mmHg are generally appropriate, and 50-60 mmHg may be tolerated in healthy young patients. Lower values between 40-50 mmHg should not be desirable. The key consideration is the "clinical price" of interventions to increase PaO2, such as increased FiO2 or mean airway pressures. As long as tissue oxygenation is maintained, permissive hypoxemia in ARDS appears to be well tolerated without evidence of tissue hypoxia.
Respiratory failure and the acute respiratory distress syndrome (and shock) Jim Lavelle
The document provides an overview of respiratory failure and mechanical ventilation. It discusses the types and pathophysiology of respiratory failure, key ventilator settings, the definition and management of acute respiratory distress syndrome (ARDS), and some basics about shock. The goal is to help understand arterial blood gases, optimize ventilator settings, and improve survival in ARDS patients.
Oxygen therapy aims to correct hypoxemia by maintaining SpO2 around 95% with minimum oxygen. It aims to decrease hypoxemia symptoms and minimize workload from compensatory responses. Oxygen is delivered via cascades from atmosphere to mitochondria. Failure at any point can cause downstream tissue injury. Tissue oxygenation depends on adequate ventilation, gas exchange, and circulation. Supplemental oxygen increases PaO2 and helps correct hypoxemia from respiratory causes like V/Q mismatch or diffusion barrier issues. Oxygen therapy must be properly administered and supervised to provide benefits while avoiding potential adverse effects.
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 discusses taking and interpreting arterial blood gases (ABGs). It covers topics like:
- Anatomy of arteries used for ABG sampling
- Components of an ABG report and their definitions
- Key equations for understanding ABG results, relating to alveolar ventilation, oxygenation, and acid-base balance
- Causes and implications of abnormal ABG values like hypercapnia, hypoxemia, and changes in pH
- Factors that can affect ABG values like temperature, carbon monoxide levels, and hemoglobin concentration
The document provides information on interpreting arterial blood gas results, including normal values and equations. It discusses the key equations that relate to alveolar ventilation, oxygenation, and acid-base balance. These equations include the PaCO2 equation, alveolar gas equation, oxygen content equation, and Henderson-Hasselbalch equation. The document uses these equations to explain physiological processes and interpret blood gas abnormalities such as hypercapnia and hypoxemia.
The document provides an overview of arterial blood gas (ABG) analysis and interpretation. It covers the basics of ABG sampling and testing, indices of gas exchange including oxygen saturation and partial pressures, and indices of acid-base balance like bicarbonate and base excess. The document uses examples to demonstrate calculating and interpreting these values in simple and complex clinical scenarios. It aims to help clinicians understand ABG reports and apply them to clinical practice.
This document provides information about arterial blood gases (ABGs), including how to perform an ABG, normal ranges for ABG values, and how to interpret ABG results. It discusses how to determine if a patient has a respiratory or metabolic acidosis or alkalosis based on ABG values such as pH, pCO2, and HCO3-. It also covers oxygenation status, compensation, mixed acid-base disturbances, and causes of hypoxemia, respiratory acidosis/alkalosis, and metabolic acidosis/alkalosis.
The document discusses acute respiratory failure, which can be either hypercapnic or hypoxemic. It provides details on the causes, pathophysiology, and assessment of different types of respiratory failure including acute respiratory distress syndrome. It also describes a case study of a patient with respiratory failure and discusses their management.
The document discusses the physiological causes of hypoxemia, including hypoventilation, ventilation-perfusion (V/Q) mismatching, and diffusion impairment. Hypoxemia can result from decreased alveolar ventilation leading to higher PaCO2 and lower PAO2, or from V/Q mismatching like shunts or dead space. Disease states like COPD, pulmonary edema, and fibrotic lung disease cause hypoxemia through various combinations of V/Q mismatching and diffusion impairment. Understanding the alveolar gas and ventilation equations is key to determining the root cause and response to hypoxemia in clinical practice.
Oxygen therapy is an integral part of the treatment of critically ill patients. Maintenance of adequate
oxygen delivery to vital organs often requires the administration of supplemental oxygen,
sometimes at high concentrations. Although oxygen therapy is lifesaving, it may be associated
with deleterious effects when administered for prolonged periods at high concentrations.
This document discusses a case of acute respiratory failure in a 300 kg patient who presented with sudden severe hypoxia and unconsciousness. It then provides an overview of acute respiratory failure, distinguishing between hypercapnic and hypoxemic respiratory failure. Various causes of each type are described in detail. The case is specifically focused on acute respiratory distress syndrome (ARDS), explaining its pathogenesis, risk factors, complications, and management including a landmark ARMA clinical trial showing benefit of lower tidal volumes.
Oxygen therapy involves administering oxygen at concentrations greater than room air to treat hypoxemia. The purpose is to increase oxygen saturation in tissues where it is too low due to illness or injury. Oxygen can be delivered via various low or high flow devices like nasal cannulas, masks, tents or venturi masks to maintain adequate oxygen saturation. Close monitoring of oxygen saturation levels via pulse oximetry or arterial blood gases is needed to properly titrate oxygen therapy.
An arterial blood gas test measures pH, oxygen, and carbon dioxide levels in blood from an artery. It provides information about oxygenation, ventilation, and acid-base levels. ABGs are useful for evaluating respiratory failure, severe illnesses that can cause metabolic acidosis like cardiac or liver failure, and conditions in ventilated patients or those undergoing sleep studies. Interpretation of ABG results involves considering pH, carbon dioxide, bicarbonate, and oxygen levels to determine if any acid-base imbalances exist and their underlying cause.
The document discusses arterial blood gas analysis and interpretation. It provides two scenarios to consider for intubation decisions based on clinical presentation and ABG values. It then presents five cases and asks which would warrant immediate ventilatory support. Key points about ABG components, indications for airway/ventilation support, and the approach to ABG interpretation focusing on assessment of ventilation, oxygenation, and acid-base balance are summarized.
------Introduction to Oxygen Therapy.pptAishaAli67229
This document provides an overview of oxygen therapy, including relevant terminology, oxygen transport and monitoring, causes of hypoxemia and hypoxia, administration of oxygen therapy, and clinical situations where oxygen is commonly used. Key points covered include the partial pressure of oxygen in the lungs and blood, how supplemental oxygen increases this pressure gradient and oxygen saturation, and the five major categories where oxygen therapy is generally applied: medical emergencies, pulmonary disease, the perioperative period, the ICU, and home oxygen therapy.
Blood gas analysis evaluates gases in blood and acid-base content to diagnose respiratory, circulatory, and metabolic disorders. It is important for monitoring patients on oxygen therapy or intensive care, and those with blood loss, sepsis, or other conditions. Blood gas analysis measures pH, partial pressures of oxygen and carbon dioxide, and calculates bicarbonate and oxygen saturation. Interpreting the values helps establish diagnoses and treatment plans by indicating acid-base and gas exchange status. Disorders are classified as metabolic or respiratory based on the primary pH change. Compensation responses also provide insights.
The document discusses arterial blood gas analysis, which provides information on oxygenation, ventilation, and acid-base balance. It outlines the key parameters measured in an ABG test and strategies for interpreting the results, including evaluating for respiratory or metabolic causes of acid-base imbalances and hypoxemia. Several case studies are presented to demonstrate interpreting ABG values in the context of patients' clinical presentations.
About the newer drugs in anaesthesia. What are the problems with the existing drugs? Which all drugs failed commercially? And why? Which are the newer drugs in anaesthesia?
1) Awake craniotomy is a technique used for brain tumor excision from eloquent areas of the brain to allow for brain mapping during surgery while the patient is awake.
2) The anesthesiologist's role includes extensive preoperative psychological preparation of the patient, administration of sedation and analgesia during surgery to maintain the patient's comfort and cooperation during brain mapping, and careful titration of medications to avoid complications.
3) There are two main anesthetic approaches for awake craniotomy - monitored anesthesia care with sedation or asleep-awake-asleep general anesthesia. Both have benefits and risks depending on factors like surgery duration and patient characteristics. Careful planning and execution of the anesthetic technique
This document discusses the use of target-controlled infusion (TCI) versus manually controlled infusion (MCI) for neuroanesthesia. It outlines the benefits of TCI, including faster achievement of therapeutic drug concentrations, reduced risk of errors, and easier titration of drugs like propofol and remifentanil for hypnosis and analgesia. However, it notes that current TCI models are limited in options and that MCI is still needed in some cases. It provides details on using and optimizing both TCI and MCI for different patient populations and procedures in neuroanesthesia.
This document provides guidance on safely and appropriately administering total intravenous anesthesia (TIVA). It discusses the differences between TIVA and other techniques, and describes the two main methods for TIVA - manual and target-controlled infusion (TCI). For TCI, it emphasizes the importance of using the correct pharmacokinetic model and carefully entering patient information. It provides tips for setup, monitoring, starting and terminating infusions, and highlights vigilance to avoid complications. The overall message is that understanding and applying TIVA requires a thorough knowledge of anesthesiology principles.
The document summarizes several key physiological changes that occur in the central nervous system with aging. It discusses changes in brain morphology like brain atrophy and widening of sulci. There are reductions in neurons, myelinated axons and neurotransmitter function. Cerebral blood flow decreases along with metabolic demand. Calcium regulation is also impaired with aging impacting neurotransmitter release. The hypothalamic-pituitary-adrenal axis shows changes reducing stress response capacity. Overall the aging brain shows structural, metabolic and functional declines impacting cognition, mood and homeostasis.
This document provides information on preparing for and managing obstetric hemorrhage. Some key points:
- Severe bleeding is a leading cause of maternal death worldwide, with rapid blood loss occurring within 24 hours of delivery in many cases.
- Non-pharmacological measures for postpartum hemorrhage include uterine massage, uterine tamponade, compression sutures, and ligation of internal iliac or uterine arteries. Pharmacological options include oxytocin, ergometrine, carboprost, and tranexamic acid.
- For severe hemorrhage, measures such as hysterectomy, arterial embolization, factor VIIa, or cell salvage may be needed. Initial
This document provides information about gas cylinders used in healthcare. It discusses the parts of cylinders including bodies, valves, and pressure relief devices. It explains how gases are measured in psi and other units of pressure. The document outlines safety rules for handling, storing, and using cylinders including proper labeling and preventing damage. Medical gas pipeline systems are described along with components like terminal units, hoses, and testing procedures to ensure safety.
This document discusses the approach to hypo- and hypernatremia in neurosurgical patients in the perioperative period. It covers several key points:
1. Hyponatremia is common in neurosurgical patients and is associated with high mortality. It can be categorized based on extracellular fluid volume status. SIADH and cerebral salt wasting require different treatments.
2. Hypernatremia results from a loss of free water and can cause central nervous system dysfunction. Rapid correction poses risks like cerebral edema. The approach involves assessing volume status based on labs and symptoms.
3. Diabetes insipidus is a potential complication after pituitary or brain surgeries/injuries. It involves excessive
important points regarding ICU psychosis, role of dexmedetomidine in it's treatment, mortality associated with delirium, symptomatic and definitive management
This document discusses anesthesia considerations for procedures performed outside the operating room. It notes that the number and complexity of such procedures has increased, bringing additional responsibilities for anesthesiologists. Special challenges include limited space, equipment, and support staff unfamiliar with patient management. Proper equipment, monitoring, and planning are important when providing anesthesia or sedation in remote locations. The document discusses various locations like radiology suites, specific procedures like ECT, and choices of anesthetic agents and techniques. Patient safety is the top priority for remote location anesthesia.
This document discusses thromboprophylaxis, or the prevention of deep vein thrombosis (DVT) and pulmonary embolism (PE) in hospitalized patients. It notes that evidence-based guidelines for venous thromboembolism prophylaxis have been available for over 15 years, but are still underused globally. It provides the rationale for thromboprophylaxis, stating that DVT is prevalent in at-risk patients, often clinically silent, and difficult to predict; complications are also difficult to manage. Thromboprophylaxis, it concludes, is highly effective at preventing DVT and PE, and cost-effective.
This document discusses the field of anesthesiology. It provides information on what anesthesiologists do, including administering medications to alter physiology, being rapid problem solvers, and leading medical teams in complex environments like operating rooms. The document highlights some of the skills involved in the specialty like airway management, pharmacology, resuscitation, and regional anesthesia. It also outlines some of the tools used in anesthesiology like inhaled anesthetics, muscle relaxants, and opioids. The field has advanced greatly in recent decades to improve patient safety during medical procedures.
This document provides an overview of pediatric anesthesia. It discusses:
1) The challenges of understanding and treating children due to their soft organs, immature systems, and sensitivity. Pain management requires careful planning.
2) Various anesthesia induction and maintenance techniques for children including inhaled anesthetics, intravenous agents, opioids, muscle relaxants and their reversal.
3) Airway management considerations like different laryngeal mask sizes for children of varying weights and the challenges of needles and intravenous access for children.
4) Fluid maintenance using Holliday-Segar formula and blood replacement guidelines based on child's age. Reversal and extubation procedures are also outlined.
This document discusses trigeminal neuralgia, a neuropathic pain condition that causes severe, sporadic facial pain. It provides information on:
1) The etiology, including neurovascular compression as a common cause.
2) Symptoms like brief, severe facial pain that may be triggered by light touch.
3) Treatment options like carbamazepine, microvascular decompression surgery, and percutaneous radiofrequency thermocoagulation of the gasserian ganglion.
4) Imaging techniques like MRI that can identify compressive vascular structures.
Here are the key issues with the gastrointestinal system after spinal cord injury and brief comments:
- Gastric distention - Increased risk of aspiration
- Gastric emptying delayed - Adversely affect ventilation. Rx: Put NG tube.
- Peptic ulcer disease - One cause is high dose steroids.
- Gastritis, hemorrhage - Rx: PPI, Sucralfate (continued for 4 weeks). Enteral feeding.
- Ileus
This document discusses the issue of fatigue among anesthesiologists and its impacts. It notes that fatigue due to lack of adequate sleep can degrade cognitive function and increase medical errors. Studies have found that over 50% of anesthesiologists report making fatigue-related errors. The document calls for more research into tools and strategies to address fatigue, such as scheduling algorithms, light therapy, melatonin, modafinil, and napping. It argues that more must be done to solve the problem of fatigue in anesthesiology in order to improve patient safety.
1. Primary injuries occur at the moment of trauma from physical forces that deform brain tissue, leading to focal injuries like skull fractures and hemorrhages or diffuse injuries like axonal shearing.
2. Specific primary injuries include skull fractures, intracranial hematomas, brain contusions and lacerations caused by compressive, tensile and shear forces on brain tissue.
3. Epidural hematomas are caused by tears to the middle meningeal artery, potentially causing rapid neurologic decline, while intracerebral hemorrhages result from tears to deep cerebral vessels with extensive cortical contusions.
The document discusses the hypothalamus and pituitary gland. It notes that the hypothalamus secretes hormones that regulate the anterior pituitary, while the posterior pituitary is an extension of the hypothalamus and stores hormones. The anterior pituitary develops from Rathke's pouch and the posterior pituitary develops from the infundibulum. The hypothalamus regulates water balance and vasopressin secretion through the posterior pituitary. Diabetes insipidus occurs when there is a deficiency of vasopressin, and can be central or nephrogenic in origin. Post-operative diabetes insipidus is a common complication of pituitary surgery.
Are you looking for a long-lasting solution to your missing tooth?
Dental implants are the most common type of method for replacing the missing tooth. Unlike dentures or bridges, implants are surgically placed in the jawbone. In layman’s terms, a dental implant is similar to the natural root of the tooth. It offers a stable foundation for the artificial tooth giving it the look, feel, and function similar to the natural tooth.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
How to Control Your Asthma Tips by gokuldas hospital.Gokuldas Hospital
Respiratory issues like asthma are the most sensitive issue that is affecting millions worldwide. It hampers the daily activities leaving the body tired and breathless.
The key to a good grip on asthma is proper knowledge and management strategies. Understanding the patient-specific symptoms and carving out an effective treatment likewise is the best way to keep asthma under control.
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7shruti jagirdar
Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
to be treated is characteristically a disease of aging ( e.g., Alzheimer's disease) or
because the population to be treated is known to include substantial numbers of
geriatric patients (e.g., hypertension).
Discover the benefits of homeopathic medicine for irregular periods with our guide on 5 common remedies. Learn how these natural treatments can help regulate menstrual cycles and improve overall menstrual health.
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“Psychiatry and the Humanities”: An Innovative Course at the University of Mo...Université de Montréal
“Psychiatry and the Humanities”: An Innovative Course at the University of Montreal Expanding the medical model to embrace the humanities. Link: https://www.psychiatrictimes.com/view/-psychiatry-and-the-humanities-an-innovative-course-at-the-university-of-montreal
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)MuskanShingari
Statistics- Statistics is the science of collecting, organizing, presenting, analyzing and interpreting numerical data to assist in making more effective decisions.
A statistics is a measure which is used to estimate the population parameter
Parameters-It is used to describe the properties of an entire population.
Examples-Measures of central tendency Dispersion, Variance, Standard Deviation (SD), Absolute Error, Mean Absolute Error (MAE), Eigen Value
3. Questions that an ABG can answer
How is oxygenation: is there any hypoxia?
Cause? How severe?
How is ventilation: any hypercarbia?
Any Acid Base abnormalities? Compensation?
Mixed?
5. At the end of the day…
Clinical condition
Interpret PaO2 with the knowledge of FiO2, A-a Gradient and
P/F ratio- PvO2 if needed
Interpret PCO2 with the knowledge that, it depends on CO2
production and alveolar ventilation & Dead space ventilation
Primary acid-base disturbances: See the pH, PaCO2 and
SBE
Look for compensation / mixed imbalances
Anion gap for metabolic acidosis
6. Case Scenario 1
A 24 year-old woman is found unconcious by some
bystanders. The medics are called and, upon arrival, find her
with an oxygen saturation of 88% on room air and pinpoint
pupils on exam. She is brought into the ER where a room air
arterial blood gas is performed and reveals:
pH 7.25,
PCO2 60 mmHg
PO2 65 mmHg
HCO3 – 26 mEq/L
Base Excess 1.22
7. Case Scenario:1
Acid-base status:• The patient has a low pH (acidemia)• The
PCO2 is high (respiratory acidosis) and the SBE is normal.
The low pH and high PCO2 imply that the respiratory
acidosis the primary process
PaO2/FiO2= 325 , 550-325= 225=10%
PAO2=713x0.2-1.25x60=68
pAO2-paO2=3 mm of Hg.. Normal, which tells us that her
hypoxemia is entirely due to hypoventilation
8. Sorry.. Foreign ABG
There is no compensation happening
The respiratory acidosis implies that the patient is
hypoventilating. This fact, in combination with the pinpoint
pupils suggests the patient is suffering from an acute narcotic
overdose.
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9. Case Scenario:2
Patient presenting to casualty with tachypnoea, sweating &
agitation. He is disoriented and agitated. ABG in RA:
pH 7.22,
pCO2 24 mmHg
pO2 60 mmHg
HCO3 8 mEq/L
SBE -20,
SpO2 96%,
CXR: R lower lobe pneumonia and creatinine 2.0.
10. Case Scenario:2
How a good interpretation can help a patient?
Patient presenting to casualty with tachypnoea, sweating &
agitation. He is disoriented and agitated. ABG in RA: pH
7.22, pCO2 24, pO2 60, HCO3 8, SBE -20, SpO2 96%, CXR:
R lower lobe pneumonia and creatinine 2.0. Please use the
template to solve this ABG
PAO2 = 713 x 0.2 – 1.25 x 24 = 112
A-a gradient = 52
P/F= 300
Metabolic acidosis
Pneumonia V/Q mismatch
Gas exchange issues + Metabolic acidosis
Hyperventilation-⬆️ WOB
Will he tolerate the extra 20% of VO2 demand by respiratory
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11. Case Scenario:3
55 yr old male came to ER with h/o fall. The trainee took
ABG sample, value are as follows:
pH= 7.36,
PaO2 40 mmHg
PCO2 = 42 mmHg,
SaO2 72%,
SpO2 95%
SBE = -6 mEq/L
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12. Case Scenario:3
pH= 7.36, SBE = -6 mEq/L , PaO2 40, SaO2 72%, PCO2 =
42 mmHg, SpO2 95%
Metabolic acidosis. Compensation? PaCO2=SBE
marked metabolic acidosis with mild respiratory
compensation.
Wrong answer
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13. Don’t satisfy the criteria for OCD
Even stable patients on ventilator can show variability in
PaO2 in the range of 2-37 mm of Hg and in PCO2 in the
range of 1-12 mm of Hg…should be considered as normal
Unnecessary repeating of ABGs will create confusion
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14.
15. Key Step: Oxygenation- any shunt or
dead space ventilation?
V/Q mismatch is the commonest cause
What alters the Ventilation-perfusion match?
Dead space is wasted ventilation
Shunt is wasted perfusion: No rise in SpO2 with
⬆️ in FiO2, Wide A-a O2 gradient, low
PaO2/FiO2
Different diseases have varying proportion of
shunt & dead space ventilation: eg ARDS* &
emphysema*
16. V/Q MISMATCH : The shunt!
Shunt doesn’t affect pCO2 because of the stimulation of
respiration by chemoreceptors
Shunt fraction Consequence
2-3% Normal
10% Tolerated by a healthy person
25-45% Life threatening: Requires
mechanical ventilation, PEEP,
recruitment, positioning, FOB
and suctioning
17. Key Step: Check the validity of PaO2,
look for the gradient & quantify the
shunt if present
Clinical context
Use the Alveolar Gas Equation
Know the alveolar PO2 (PAO2)
Know the arterial PO2 (PaO2)
Find PaO2/FiO2 ratio
Quantification of the shunt fraction
18. pAO2 from Alveolar Gas Equation
PAO2 =[(PB – PH2O) FiO2 ] – (PaCO2 / RQ)
Atmospheric pressure is 760 mm Hg at sea level
PH2O is vapor pressure of water at 37°C and is equal to 47
mmHg
713 x FiO2 – 1.25 x PaCO2
The respiratory quotient or respiratory coefficient (RQ) is the
ratio of CO2 produced divided by the O2 consumed, and its
value is typically 0.8 (RQ = CO2 eliminated / O2 consumed).
R is taken as 1 @FiO2> 0.6
PB – PH2O is known as PiO2 713
Simplified as
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PAO2 = 713 x FiO2 – 1.25 x
PaCO2
19. The Alveolar –Arterial Oxygen Gradient
PAO2-PaO2
The expected paO2 will be 10-15 mm of Hg lower than that in
the alveoli: A-a O2 gradient
10-15 mm in young to middle aged
PaO2= 109- 0.43 [age in years]
It increases with increase in FiO2 [@FiO2 of 1,110!)
If higher than expected for age, shunt fraction is high
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20. The Alveolar –Arterial Oxygen Gradient
Hypoxemic respiratory failure with Normal A-a DO2
Hypoventilation**
High altitude
Fire
Inadvertent use of low O2 containing mixtures during anesthesia
Hypoxemic respiratory failure with widened A-a DO2
Increased shunt fraction
Increased dead space ventilation
Diffusion abnormality
Low cardiac output and increased O2 uptake
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21. PaO2 /FiO2
Normal 500-550
Used to diagnose ARDS (< 200) and ALI (< 300); 300-500 =
acceptable
Obtained value is subtracted from 550
For every difference of 100, the shunt fraction is 5%
Roughly, shunt %: 5005, 30015, 20020
Eg 68/0.4=170 , 550-170=380 20%
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22. Case Scenario 4
Patient breathing room air, has
PaO2 90 mm of Hg,
SpO2 96%, and
PaCO2 110 mm of Hg.
Check the validity
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23. Case Scenario 4
Patient breathing room air, has PaO2 90 mm of Hg, SpO2
96%, and PaCO2 110 mm of Hg. Check the validity (PaO2,
PaCO2 values reliable or not?)
Apply Alveolar Gas Equation
[713x0.2]-[1.2x110]= PAO2 is 18!, but SpO2 is 96. So one
among the value is wrong.
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24. Case Scenario 4
Patient on mechanical ventilation, has PaO2 150 mm of Hg,
FiO2 0.8, and PaCO2 30 mm of Hg. Check the validity and
find the gradient.
Apply Alveolar Gas Equation
[713x0.8]-[1.2x30]= PAO2 is 534. PaO2 is 150. A-a gradient
384
But please remember that the gradient increases with the
FiO2
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25. Case Scenario 5
Patient breathing room air. PaO2 125. PC02 50. Please find
the gradient?
[713x0.2]-[1.2x50]= PAO2 is 86.
PaO2 then cannot be 125
Air bubble?
MESSAGE: Isolated PaO2 value is meaningless without info
about FiO2 and PaCO2- so give enough importance for
’AGE’
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26. Case Scenario 5
Patient breathing room air. PaO2 125. PC02 50.
Please find the gradient?
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27. CaO2- Oxygen Content
Oxygen carried as oxyhemoglobin + dissolved O2
CaO2= [1.39 X Hb (gm/dl) X Saturation] + 0.003 X PaO2
If Hb=15 g/dl, SaO2 99%, 20.4 ml as oxy Hb + 0.3 ml in
plasma20.7
Anemia: will not affect saturation and evoke physiological
adaptations
Abnormal Hbs will decrease saturation and decrease O2
content; will not affect solubility and so PaO2 will be normal
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28. Case Scenario 6
24 years old male patient rescued from a burning house has
dyspnoea- was given O2 6l/min and shows SpO2 of 99%.
ABG: PaO2 125 mm of Hg PaCO2 of 35 mm of Hg.
Is the blood gas normal? Does he need supplemental O2?
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29. Case Scenario 6
24 years old male patient rescued from a burning house has
dyspnoea- was given O2 6l/min and shows SpO2 of 99%.
ABG: PaO2 125 mm of Hg PaCO2 of 35 mm of Hg. Is the
blood gas normal? Does he need supplemental O2?
Co-oximetry to find the amount of Carboxy Hb-SpO2 won’t be
correct
PaO2 will be normal
Give O2
Don’t rely on N PaO2
If metabolic acidosis/ disorientation Mechanical Ventilation
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30. Key Step: Check for Mixed Venous ‘Hypoxia’!
Decreased Cardiac Output (QT) in the presence of constant
O2 consumption (VO2)
Increased VO2 (shivering, fever)
Decrease mixed venous O2 content: CvO2= (1.39xHbx
SvO2)+(0.003xPvO2)
Normal: SvO2= 75% SvO2 ~ SaO2-[VO2/Hb x QT]
PvO2= 40 mm of Hg
In low CO states with continuing O2 extraction, PvO2 will be
low
Sample from a CVC [if no PAC] can identify low CO states
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31. Hypoventilation will cause hypoxia too
1.Hypoventilation shallow breathing atelectasis
reduce FRC
2.Hypoventilation V decrease overall V/Q of the lung
decrease
1+2 = Hypoxia
So hypoventilation = Hypercarbia + Hypoxia
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32. Also note hypoxia can occur even with
normal PaO2
Low Hb- Anemic hypoxia
Decreased O2 delivery- Stagnant hypoxia
Reduced utilization- Histotoxic hypoxia
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33.
34. Key Step: Abnormal production/ alveolar
ventilation/ dead space?
Abnormality in Production OR Washout
37. Increased dead space?
Clues to increased dead space ventilation
Persisently high PCO2 despite high minute ventilation
PCO2-ETCO2 disparity > 5 mmof Hg
Increased dead space
Pulmonary vascular disease
Pulmonary embolism
Hypovolemia
Low cardiac output
COPD
ARDS
Pulmonary fibrosis
40. SBE is a convenient representative
of all the buffer systems
The concept of Standard Base Excess (SBE)
puts all buffers into a single hypothetical system
Bring the pCO2 to 40 to negate the effect of
respiratory system and assume that the blood is
alkaline/acidic now
Base Excess/base deficit is the amount of
acid/alkali required to return the pH of the blood
to 7.4 and hence is the amount of ‘excess
base/acid’
41. Further exposing the SBE
SBE is the SB of ECF and SBa is that of blood
SBE is the perfect parameter as ECF is the
vehicle through which AB changes are
regulated
SBE normal range is +/- 2 mM/L
Other measures shown in the ABG like standard
pH, standard bicarbonate, buffer base, total
CO2 has been given up- no need to learn them
42. So when we arrange it in order, in response
to an acid base change
First defense: Buffering
Second: Respiratory : alteration in arterial pCO2
Third defense: Renal : alteration in HCO3 excretion
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46. Compensation
In respiratory derangements the primary change
is in pCO2. Compensation is by kidneys which
reabsorb more bicarbonate, which increases the
SBE
In metabolic derangements, the primary change
is in SBE and compensatory changes are
provided by the lungs
For eg metabolic acidosis make SBE more
negative and lungs tries to excrete more CO2
(respiratory acid) to compensate this resulting in
a compensatory respiratory alkalosis
47. KEY STEP: ACUTE RESPIRATORY ACID BASE
CHANGES
PaCO2 pH SBE=0
• ACUTE RESPIRATORY ACIDOSIS[
buffering only; 99% in ICF]
PaCO2 pH
• ACUTE RESPIRATORY ALKALOSIS
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48. KEY STEP: CHRONIC RESPIRATORY ACIDOSIS
& ALKALOSIS
compensated by renal handling of bicarbonate; hence SBE
changes
pH return to 2/3 rd of normal
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SBE = 0.4 PaCO2
• Direction of change of SBE is
same as that of direction of
change of PaCO2
49. Respiratory Acidosis :Causes
E.g. if PaCO2 is 60 mm of Hg and cause is chronic
respiratory acidosis, then the expected SBE is 0.4 X 20 = 8
mM/L
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CAUSES
Upper airway obstruction
Status asthmaticus
Pneumonia
Pulmonary edema
CNS depression
Neuro muscular impairment
Ventilatory restriction
50. Respiratory Alkalosis
Normal in mountain dwellers and pregnant women
pH>7.45 PaCO2<35 mm of Hg
Generally a poor prognostic sign, when present in critically ill
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CAUSES
Hypoxemia
Pulmonary embolism, asthma, pulmonary edema
CNS disorders
Hepatic failure
Sepsis
Salicylate toxicity
Anxiety- hyperventilation
51. Case Scenario:7
A patient with a long history of COPD presented to the
casualty with difficulty in breathing. He was conscious,
tachypneic with accessory muscle use. His pH is 7.35; PaO2
is 34 mm of Hg; PaCO2 of 72 mm of Hg, HCO3 37.5 mM/L
and SBE is 14 mM/L. He is given 4L O2 by mask and an
ABG drawn after 15 mins. Now his pH is 7.30, PaO2 is 70
mm of Hg, PaCO2 of 88 mm of Hg and SBE is 14 mM/L.
Analyse these 2 ABGs
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52. Case Scenario:7
A patient with a long history of COPD presented to the
casualty with difficulty in breathing. He was conscious,
tachypneic with accessory muscle use. His pH is 7.35; PaO2
is 34 mm of Hg; PaCO2 of 72 mm of Hg, HCO3 37.5 mM/L
and SBE is 14 mM/L. He is given 4L O2 by mask and an
ABG drawn after 15 mins. Now his pH is 7.30, PaO2 is 70
mm of Hg, PaCO2 of 88 mm of Hg and SBE is 14 mM/L.
Analyse these 2 ABGs
RA: A-a gradient-18; P/F-170
He is conscious!
Near normal pH.
O2 improves PaO2; but PaCO2 increases!
Despite a fall in pH, SBE is remaining same!
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53. Respiratory Acidosis: effects
CBF and ICP
Arrhythmia
Hyperventilation
Hypoxemia
In patients breathing room air, PCO2 > 90 mm of Hg is not
compatible with life
If you acutely reduce CO2: accumulated HCO3 will remain
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54. KEY STEP: METABOLIC ACIDOSIS
Produced by increase in titratable hydrogen ion concentration
Diagnosis: pH low and SBE <-5 mM/L, HCO3 <20 mM/L
Respiratory compensation is immediate and return pH to one
third to half way normal
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PaCO2 = SBE
55. KEY STEP: FINDING THE ANION GAP
When all the commonly measured anions are substracted
from the cations, the result is a positive value of 12±4 mEq/L
Due to unmeasured anions
Corrected AG = Calculated AG + 2.5 [4.5-measured albumin
in g/dl]
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56. WIDE & NORMAL AG GAP ACIDOSIS
If AG > 20 suspect ; if > 25 confirmed
Some conditions generate anions these are neutralized by
bicarbonatebicarbonate falls
AG widens
Some conditions lead to loss of bicarbonate this is
counterbalanced by gain in chloride gain in chloride exactly
matches loss of bicarbonate AG is normal
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59. Case Scenario:8
A young woman suffering from fever 4 days has been
admitted in the ER. She is semi comatose and tachypnoeic.
Cool peripheries with BP of 90/30 mm Hg. SpO2- unreliable
trace. ABG on RA:
pH 7.19,
PaO2 100,
PaCO2 20,
HCO3 8,
SBE -17.7.
Serum electrolytes
Na 140 K 4.5 Cl 100
lactate 10
S creatinine 2.4
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60. Case Scenario:8
A young woman suffering from fever 4 days has been
admitted in the ER. She is semi comatose and tachypnoeic.
Cool peripheries with BP of 90/30 mm Hg. SpO2- unreliable
trace. ABG on RA: pH 7.19, PaO2 100, PaCO2 20, HCO3 8,
SBE -17.7. Serum electrolytes Na 140 K 4.5 Cl 100 lactate
10 S creatinine 2.4
No oxygenation issue
Metabolic acidosis
Lungs compensated it by increasing Mv. Pa CO2 20.
AG is 37 ( accumulated metabolic acids)
Lactate =10 = 10/ 17 is lactate; rest is by accumulation of
metabolites from renal failure
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61. Metabolic Acidosis : effects
Decreased strength of respiratory muscles
Hyperventilation
Myocardial depression
Sympathetic over activity
Decreased arrhythmia threshold
Resistance to catecholamines
Hyperkalemia
Increased metabolic demand [N:5% of VO2; in distress 25%]
Insulin resistance
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62. Metabolic Acidosis and Mechanical ventilation
Respiratory effect is hyper ventilation may not be tolerated
by patients with compromised cardiac or respiratory
reserve mechanical ventilation may be required in such
patients , till underlying metabolic acidosis is addressed
When on ventilator, try to mimic the natural compensation;
but don’t go < 30 mmof Hg of PaCO2
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63. NaHCO3 Therapy
Sodium bicarbonate should probably be administered to
intensive care patients with severe metabolic acidemia (pH ≤
7.20, PaCO2 < 45 mmHg) and moderate to severe acute
renal insufficiency
The administration of sodium bicarbonate could limit the
deleterious cardiovascular, respiratory, and cellular energy
effects of loss of bicarbonate .
Sodium bicarbonate should be administered carefully as it is
associated with a risk of hypokalemia, hypernatremia,
hypocalcemia, rebound alkalemia, and water–sodium
overload
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64. Respiratory Alkalosis : Effects
Increased neuromuscular irritability
Cerebral vasoconstriction
Decreased ICP
Increased cerebral excitability
Inhibition of respiratory drive
Hypokalemia
Respiratory alkalosis + abnormal respiratory muscle
activity? High ventilatory demand cautious decision
making regarding extubation
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65. Case Scenario:9
A 68 year-old man with a history of very severe COPD and
chronic carbon dioxide retention presents to the emergency
room complaining of worsening dyspnea and an increase in
the frequency and purulence of his sputum production over
the past 2 days. His oxygen saturation is 78% on room air.
Before he is placed on supplemental oxygen, a room air
arterial blood gas is drawn and reveals: pH 7.25, PCO2 68,
PO2 48, HCO3 31, SBE 6
Pao2/fio2=240, shunt fraction 15%, PAO2-PaO2=13
SBE=0.4 X paCO2= 11.2, Why only 6?
Acute on chronic respiratory failure with respiratory acidosis
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66. KEY STEP: METABOLIC ALKALOSIS
Produced by decrease in titratable hydrogen ion
concentration
Depress ventilation
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PaCO2 = 0.6 SBE
weaning
67. Metabolic Alkalosis
Generally pCO2 wont go > 55; if > 55, indicates severe
alkalosis OR combined metabolic alkalosis + respiratory
acidosis
Usually [HCO3-] prompt [HCO3-] excretion by kidney;
persistence requires additional process to impair [HCO3-]
excretion
69. Effects of Metabolic Alkalosis:
Reduced cerebral blood flow
Seizures
Tetany
Reduction in coronary blood flow
Predisposistion to refractory arrhythmias
Decreased contractility
Hypoventilation
Hypokalemia , Hypomagnesemia
Reduced ionized calcium
Promote anaerobic glycolysis lactate
Weaning failure, especially if HCO3 is >35
70. Impaired arterial oxygen content
Hypoventilation
Micro atelectasis
V-P mismatch
So assess for the requirement of supplemental
oxygen in metabolic alkalosis
71. Additional points- Metabolic alkalosis
Depresses respiration hypoxemia & hypercarbia
Effects on PaCO2 are seen only when HCO3> 35 Mm/L
Chloride responsive [Urinary Cl- < 15 mEq/L]: Rx is chloride-
volume-potassium repletion
Chloride resistant [Urinary Cl- >25 mEq/L]: Rx is correction of
the cause of mineralocorticoid excess and potassium
depletion and Acetazolamide
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72. You cant exist alone man; who is behind you?
Reduced GFR
Chloride depletion
Potassium depletion
ECF volume depletion
Because kidney has a large capacity to excrete bicarbonate
and return the plasma level to normal
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73. Case Scenario:10
10 years old boy who underwent occipital-C2 fusion for
complex Chiari malformation developed stress
cardiomyopathy on POD 1. After resuscitating the initial
decompensation using milrinone and diuretics, an ABG was
taken with FiO2 0.6: PCV- PC:13,PEEP:8, RR:20 MVe
3.8L/min PaO2 86 mm of Hg, PCO2 44, pH 7.26, SBE: -
7.4. How will you explain the changes? Do you think any
change in the ventilatory management would have been
more appropriate in this patient?
A-a gradient: 373-86=287
P/F: 86/0.6=143; 550-143=407shunt fraction 20%
Acidosis
Metabolic
Expected compensation: △PaCO2=SBE7.4Expected
PCO2-33Present PCO2-44-?
76. References :
Dr Suneel P.R., SCTIMST, Arterial blood gas
before, during and after mechanical ventilation,
Respiratory Care Update 2007
Arterial blood gases made easy, Ian A M
Hennessey, Alan G Japp
Lawrence Martin, All you really need to know to
interpret arterial blood gases, 2 nd edition
Simple as ABG, Ted &Larry’s
A. Hasan, Handbook of Blood Gas/Acid-Base
Interpretation, 2013
Standard Base Excess, T. J. MORGAN,
Australasian anesthesia 2003