Seminar (dr. santosh) medicine practical approach to acid base disordersSantosh Narayankar
This document provides an overview of acid-base disorders, including their importance, physiology, regulation, primary disorders, compensation, and evaluation. It defines key terms like pH, buffers, and discusses the respiratory and renal systems' roles in regulation. The four primary disorders are described as being metabolic or respiratory based on the initial disturbance. Mixed disorders and expected compensation patterns are also covered. Examples of acid-base disorders in patients are provided to demonstrate application of the concepts.
This document discusses acid-base disturbances, including simple vs mixed disturbances, and how to approach and interpret acid-base abnormalities. It covers compensations for various metabolic and respiratory disturbances and how to determine the primary cause. Case examples are provided to demonstrate the approach and interpretation of acid-base status. The key steps are reviewing the history, ABG results including pH, pCO2, HCO3, and serum electrolytes. The appropriateness of compensation and causes such as respiratory, renal, gastrointestinal, or endocrine etiologies are considered.
This document provides an overview of acid-base disorders and their diagnosis and management. It discusses the regulation of acid-base balance and what arterial blood gases can reveal about a patient's condition. It then covers the diagnosis of acid-base disorders including sample handling and analysis. Key concepts around the Henderson-Hasselbalch equation and normal values are explained. The document breaks down simple and expected changes in various acid-base disorders. Case studies are presented and analyzed. Metabolic acidosis, alkalosis, respiratory compensation, and anion gaps are discussed in detail.
This document provides guidance on interpreting arterial blood gas (ABG) results. It discusses evaluating ABG values to determine if a patient has acidosis or alkalosis, and whether the primary problem is respiratory or metabolic. It also covers how to assess for compensatory responses and the effectiveness of oxygenation. Normal and abnormal ABG value ranges are defined. Various acid-base imbalances are described along with their typical causes and presentations. Case examples are also included to demonstrate applying the ABG interpretation process.
This document discusses blood gas analysis and acid-base disorders. It provides details on parameters measured in blood gas analysis like PaO2, PaCO2, HCO3-, and how they are used to evaluate respiratory failure and classify acid-base imbalances. Respiratory failure is classified as type I or II based on PaO2 and PaCO2 levels. Various acid-base disorders like respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis are defined based on changes in pH, PaCO2, and HCO3-. Mixed acid-base disorders involving combinations of respiratory and metabolic components are also described.
PH definition and determinants , how to regulate the Acid/base in our body ,ABG's normal values in atrery and vein , how to obtain an arterial blood sample, the interpretation of ABG's , steps to analuse Acid-base, respiratory acidosis and alkalosis and its causes also about metablic acidosis and alkalosis and the causes and some case studies .
The document provides information on interpreting arterial blood gases (ABGs), including:
- A 6-step process for interpretation involving assessing pH, identifying the primary disorder as respiratory or metabolic, evaluating compensation, calculating anion gap, and considering differential diagnoses.
- Tables listing normal ranges for ABG components like pH, PaCO2, HCO3, and bases for common acid-base disorders.
- Explanations of key components like pH, partial pressure, base excess, bicarbonate, and their relationships in respiratory and metabolic acidosis/alkalosis.
- Causes and mechanisms of respiratory and metabolic acidosis and alkalosis are outlined.
Seminar (dr. santosh) medicine practical approach to acid base disordersSantosh Narayankar
This document provides an overview of acid-base disorders, including their importance, physiology, regulation, primary disorders, compensation, and evaluation. It defines key terms like pH, buffers, and discusses the respiratory and renal systems' roles in regulation. The four primary disorders are described as being metabolic or respiratory based on the initial disturbance. Mixed disorders and expected compensation patterns are also covered. Examples of acid-base disorders in patients are provided to demonstrate application of the concepts.
This document discusses acid-base disturbances, including simple vs mixed disturbances, and how to approach and interpret acid-base abnormalities. It covers compensations for various metabolic and respiratory disturbances and how to determine the primary cause. Case examples are provided to demonstrate the approach and interpretation of acid-base status. The key steps are reviewing the history, ABG results including pH, pCO2, HCO3, and serum electrolytes. The appropriateness of compensation and causes such as respiratory, renal, gastrointestinal, or endocrine etiologies are considered.
This document provides an overview of acid-base disorders and their diagnosis and management. It discusses the regulation of acid-base balance and what arterial blood gases can reveal about a patient's condition. It then covers the diagnosis of acid-base disorders including sample handling and analysis. Key concepts around the Henderson-Hasselbalch equation and normal values are explained. The document breaks down simple and expected changes in various acid-base disorders. Case studies are presented and analyzed. Metabolic acidosis, alkalosis, respiratory compensation, and anion gaps are discussed in detail.
This document provides guidance on interpreting arterial blood gas (ABG) results. It discusses evaluating ABG values to determine if a patient has acidosis or alkalosis, and whether the primary problem is respiratory or metabolic. It also covers how to assess for compensatory responses and the effectiveness of oxygenation. Normal and abnormal ABG value ranges are defined. Various acid-base imbalances are described along with their typical causes and presentations. Case examples are also included to demonstrate applying the ABG interpretation process.
This document discusses blood gas analysis and acid-base disorders. It provides details on parameters measured in blood gas analysis like PaO2, PaCO2, HCO3-, and how they are used to evaluate respiratory failure and classify acid-base imbalances. Respiratory failure is classified as type I or II based on PaO2 and PaCO2 levels. Various acid-base disorders like respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis are defined based on changes in pH, PaCO2, and HCO3-. Mixed acid-base disorders involving combinations of respiratory and metabolic components are also described.
PH definition and determinants , how to regulate the Acid/base in our body ,ABG's normal values in atrery and vein , how to obtain an arterial blood sample, the interpretation of ABG's , steps to analuse Acid-base, respiratory acidosis and alkalosis and its causes also about metablic acidosis and alkalosis and the causes and some case studies .
The document provides information on interpreting arterial blood gases (ABGs), including:
- A 6-step process for interpretation involving assessing pH, identifying the primary disorder as respiratory or metabolic, evaluating compensation, calculating anion gap, and considering differential diagnoses.
- Tables listing normal ranges for ABG components like pH, PaCO2, HCO3, and bases for common acid-base disorders.
- Explanations of key components like pH, partial pressure, base excess, bicarbonate, and their relationships in respiratory and metabolic acidosis/alkalosis.
- Causes and mechanisms of respiratory and metabolic acidosis and alkalosis are outlined.
This patient with type 1 diabetes mellitus (T1DM) presents with diabetic ketoacidosis (DKA) as evidenced by a metabolic acidosis with low bicarbonate and pH, low PCO2 due to compensatory hyperventilation, and elevated blood glucose and ketones. The metabolic acidosis is primarily due to the accumulation of ketone bodies from the breakdown of fat in the absence of insulin. The patient requires emergent treatment including intravenous fluids and insulin.
This document provides an overview of acid-base physiology, including:
- Definitions of acids, bases, and acid-base balance
- The three main systems that maintain pH balance: buffers, respiration, and renal
- The four basic types of acid-base imbalances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis
- Details on specific disorders like respiratory acidosis, metabolic acidosis, and mixed disorders
- Compensatory responses and interpretation of blood gas measurements
- Case studies on mixed disorders involving respiratory and metabolic components
In under 3 sentences, it summarizes key concepts in acid-base physiology and provides examples of interpreting acid-base imbalances.
The document discusses acid-base balance and summarizes key concepts from traditional and modern physical-chemical approaches. It explains that the traditional view focused on hydrogen and bicarbonate ion concentrations, while the Stewart model emphasizes three independent variables: partial pressure of carbon dioxide, non-volatile weak acid concentration, and strong ion difference. The Stewart approach provides a more comprehensive understanding of factors influencing pH.
This document discusses acid-base disorders and their physiology, regulation, and treatment. It begins by introducing acid-base balance and pH in the body. It then covers the chemical buffer systems that help regulate pH, as well as the roles of respiration and the kidneys. It discusses different types of acid-base disorders like metabolic acidosis and alkalosis, respiratory acidosis and alkalosis, and mixed disorders. Interpretation of blood gas analysis and various approaches for analyzing acid-base status are also outlined. Throughout, compensation mechanisms and typical treatment approaches for each disorder are described.
Acid-base disorders occur when pH levels fall outside the normal range of 7.35-7.45. Precise pH regulation is vital for cellular functions and physiological processes. Buffers like bicarbonate help control hydrogen ion concentration. Disorders are classified as metabolic, affecting bicarbonate levels, or respiratory, affecting carbon dioxide levels. The kidneys and lungs work to compensate for changes and return pH to normal ranges through bicarbonate and carbon dioxide regulation. However, compensation cannot fully correct pH without also treating the underlying cause.
The document provides an overview of acid-base physiology and disorders, covering topics such as the carbonic acid buffer system, primary acid-base disorders including their causes and compensatory responses, and approaches for evaluating mixed acid-base disorders. It also reviews instrumentation and practical exercises for analyzing acid-base imbalances.
Diagnosis and treatment of acid base disorders(1)aparna jayara
This document discusses the diagnosis and treatment of acid-base disorders. It begins by explaining the importance of precise pH regulation between 7.35-7.45 for cellular functions. Buffers help control free hydrogen ion concentration. Respiratory regulation controls PaCO2 through lung excretion of volatile acids, while renal regulation maintains plasma HCO3- concentration through kidney processes. Primary acid-base disorders are either metabolic, affecting HCO3-, or respiratory, affecting PaCO2. Expected compensatory responses occur but do not fully correct the primary disorder. Evaluation involves history, exam, basic labs, and arterial blood gas analysis to determine the primary disorder and characterize as acute or chronic.
This document discusses acid-base homeostasis and disorders. It defines normal acid-base parameters and describes the body's response through buffering, lungs, and kidneys. It outlines the approach to evaluating acid-base disorders including initial assessment, acid-base diagnosis using arterial blood gases and electrolytes, identifying compensation, and formulating a diagnosis. Several examples are provided to demonstrate the systematic evaluation and diagnosis of mixed acid-base disorders.
The document discusses metabolic acidosis, defining it as a primary decrease in bicarbonate with a compensatory decrease in PCO2. It notes the causes can include GI or renal bicarbonate loss, lactic acidosis, ketoacidosis from diabetes or alcohol, intoxication from ethylene glycol or methanol, and advanced renal failure. Metabolic acidosis is classified as having a normal or high anion gap, with high anion gap causes including ketoacidosis, lactic acidosis, and certain intoxications.
This document discusses acid-base balance and acid-base imbalances. It begins by explaining that the normal pH range for blood is 7.35-7.45. This balance is maintained primarily by bicarbonate-carbonic acid buffering systems, as well as by lung and kidney function. When the ratio of carbonic acid to bicarbonate falls out of the normal 20:1 range, acid-base imbalances can occur. There are four main types: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. The document provides details on the causes, physiological effects, and compensatory responses for each type of imbalance.
The document provides guidance on evaluating acid-base disorders by assessing whether there is a primary respiratory or metabolic component, determining if there is an anion gap and investigating compensatory responses. It outlines approaches for characterizing different types of acidosis and alkalosis based on pH, pCO2, HCO3 and anion gap measurements and urine anion gap.
The document discusses acid-base balance and acid-base disorders. It describes three main systems that help maintain pH balance - buffers, the respiratory system, and the renal system. It explains how to interpret arterial blood gases by evaluating the pH, pCO2, HCO3, and other values to determine if a patient has respiratory or metabolic acidosis or alkalosis. Compensation by other systems is discussed when one system is imbalanced. Interpreting values and identifying primary vs compensated disorders is key to proper nursing care.
This document provides an overview of acid-base disorders. It defines different types of acid-base disorders based on pH, PCO2, and HCO3 levels. Primary acid-base disorders cause compensatory changes in PCO2 or HCO3 to maintain balance. Respiratory disorders involve changes in PCO2, while metabolic disorders involve changes in HCO3. Compensation occurs rapidly through breathing for metabolic disorders and slowly through the kidneys for respiratory disorders. Formulas are provided to assess acute vs chronic respiratory compensation and expected vs actual pH levels.
This document discusses acid-base balance and summarizes key points about the bicarbonate buffer system and acid-base regulation by the lungs and kidneys. It defines sources of acids in the body, describes the Henderson-Hasselbalch equation and how it relates pH to bicarbonate and carbon dioxide levels. Normal values for an arterial blood gas are provided. The roles of the respiratory and metabolic components in maintaining acid-base balance are explained.
This document discusses acid-base disorders and their physiology, evaluation, and treatment. It defines key terms like pH, acids, bases, and the four primary acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. For each disorder it describes the characteristics, pathophysiology, clinical features, and treatment approach. Primary investigations discussed include serum electrolytes, bicarbonate, PCO2, and anion gap to help evaluate the underlying cause and guide management.
This document 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 discusses acid-base disorders and presents three patient case studies. It provides the normal ranges for pH, pCO2, and HCO3 and outlines the six steps for acid-base analysis. The six steps are used to analyze each case study: a patient with metabolic acidosis and respiratory alkalosis, a patient with metabolic acidosis and metabolic alkalosis, and a patient with metabolic and respiratory acidosis. Causes are provided for different types of acid-base disturbances.
The document summarizes acid-base balance and disturbances. It states that the lungs and kidneys work together to maintain acid-base balance. The kidneys regulate bicarbonate levels to buffer acids produced from metabolism. Disturbances can cause metabolic or respiratory acidosis/alkalosis. Causes, signs, and treatments are provided for various conditions like dehydration, electrolyte imbalances.
The document discusses the four main buffering mechanisms that the body uses to regulate acid-base balance: bicarbonate buffering system, intracellular buffering system, respiratory compensation, and renal compensation. It provides details on how each system works to compensate for metabolic acidosis and alkalosis as well as respiratory acidosis and alkalosis. The bicarbonate buffering system involves carbon dioxide combining with water to form carbonic acid, which dissociates into hydrogen ions and bicarbonate ions. Respiratory compensation increases or decreases breathing rate to alter plasma pH, while renal compensation increases bicarbonate production and acid excretion to restore balance.
This patient with type 1 diabetes mellitus (T1DM) presents with diabetic ketoacidosis (DKA) as evidenced by a metabolic acidosis with low bicarbonate and pH, low PCO2 due to compensatory hyperventilation, and elevated blood glucose and ketones. The metabolic acidosis is primarily due to the accumulation of ketone bodies from the breakdown of fat in the absence of insulin. The patient requires emergent treatment including intravenous fluids and insulin.
This document provides an overview of acid-base physiology, including:
- Definitions of acids, bases, and acid-base balance
- The three main systems that maintain pH balance: buffers, respiration, and renal
- The four basic types of acid-base imbalances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis
- Details on specific disorders like respiratory acidosis, metabolic acidosis, and mixed disorders
- Compensatory responses and interpretation of blood gas measurements
- Case studies on mixed disorders involving respiratory and metabolic components
In under 3 sentences, it summarizes key concepts in acid-base physiology and provides examples of interpreting acid-base imbalances.
The document discusses acid-base balance and summarizes key concepts from traditional and modern physical-chemical approaches. It explains that the traditional view focused on hydrogen and bicarbonate ion concentrations, while the Stewart model emphasizes three independent variables: partial pressure of carbon dioxide, non-volatile weak acid concentration, and strong ion difference. The Stewart approach provides a more comprehensive understanding of factors influencing pH.
This document discusses acid-base disorders and their physiology, regulation, and treatment. It begins by introducing acid-base balance and pH in the body. It then covers the chemical buffer systems that help regulate pH, as well as the roles of respiration and the kidneys. It discusses different types of acid-base disorders like metabolic acidosis and alkalosis, respiratory acidosis and alkalosis, and mixed disorders. Interpretation of blood gas analysis and various approaches for analyzing acid-base status are also outlined. Throughout, compensation mechanisms and typical treatment approaches for each disorder are described.
Acid-base disorders occur when pH levels fall outside the normal range of 7.35-7.45. Precise pH regulation is vital for cellular functions and physiological processes. Buffers like bicarbonate help control hydrogen ion concentration. Disorders are classified as metabolic, affecting bicarbonate levels, or respiratory, affecting carbon dioxide levels. The kidneys and lungs work to compensate for changes and return pH to normal ranges through bicarbonate and carbon dioxide regulation. However, compensation cannot fully correct pH without also treating the underlying cause.
The document provides an overview of acid-base physiology and disorders, covering topics such as the carbonic acid buffer system, primary acid-base disorders including their causes and compensatory responses, and approaches for evaluating mixed acid-base disorders. It also reviews instrumentation and practical exercises for analyzing acid-base imbalances.
Diagnosis and treatment of acid base disorders(1)aparna jayara
This document discusses the diagnosis and treatment of acid-base disorders. It begins by explaining the importance of precise pH regulation between 7.35-7.45 for cellular functions. Buffers help control free hydrogen ion concentration. Respiratory regulation controls PaCO2 through lung excretion of volatile acids, while renal regulation maintains plasma HCO3- concentration through kidney processes. Primary acid-base disorders are either metabolic, affecting HCO3-, or respiratory, affecting PaCO2. Expected compensatory responses occur but do not fully correct the primary disorder. Evaluation involves history, exam, basic labs, and arterial blood gas analysis to determine the primary disorder and characterize as acute or chronic.
This document discusses acid-base homeostasis and disorders. It defines normal acid-base parameters and describes the body's response through buffering, lungs, and kidneys. It outlines the approach to evaluating acid-base disorders including initial assessment, acid-base diagnosis using arterial blood gases and electrolytes, identifying compensation, and formulating a diagnosis. Several examples are provided to demonstrate the systematic evaluation and diagnosis of mixed acid-base disorders.
The document discusses metabolic acidosis, defining it as a primary decrease in bicarbonate with a compensatory decrease in PCO2. It notes the causes can include GI or renal bicarbonate loss, lactic acidosis, ketoacidosis from diabetes or alcohol, intoxication from ethylene glycol or methanol, and advanced renal failure. Metabolic acidosis is classified as having a normal or high anion gap, with high anion gap causes including ketoacidosis, lactic acidosis, and certain intoxications.
This document discusses acid-base balance and acid-base imbalances. It begins by explaining that the normal pH range for blood is 7.35-7.45. This balance is maintained primarily by bicarbonate-carbonic acid buffering systems, as well as by lung and kidney function. When the ratio of carbonic acid to bicarbonate falls out of the normal 20:1 range, acid-base imbalances can occur. There are four main types: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. The document provides details on the causes, physiological effects, and compensatory responses for each type of imbalance.
The document provides guidance on evaluating acid-base disorders by assessing whether there is a primary respiratory or metabolic component, determining if there is an anion gap and investigating compensatory responses. It outlines approaches for characterizing different types of acidosis and alkalosis based on pH, pCO2, HCO3 and anion gap measurements and urine anion gap.
The document discusses acid-base balance and acid-base disorders. It describes three main systems that help maintain pH balance - buffers, the respiratory system, and the renal system. It explains how to interpret arterial blood gases by evaluating the pH, pCO2, HCO3, and other values to determine if a patient has respiratory or metabolic acidosis or alkalosis. Compensation by other systems is discussed when one system is imbalanced. Interpreting values and identifying primary vs compensated disorders is key to proper nursing care.
This document provides an overview of acid-base disorders. It defines different types of acid-base disorders based on pH, PCO2, and HCO3 levels. Primary acid-base disorders cause compensatory changes in PCO2 or HCO3 to maintain balance. Respiratory disorders involve changes in PCO2, while metabolic disorders involve changes in HCO3. Compensation occurs rapidly through breathing for metabolic disorders and slowly through the kidneys for respiratory disorders. Formulas are provided to assess acute vs chronic respiratory compensation and expected vs actual pH levels.
This document discusses acid-base balance and summarizes key points about the bicarbonate buffer system and acid-base regulation by the lungs and kidneys. It defines sources of acids in the body, describes the Henderson-Hasselbalch equation and how it relates pH to bicarbonate and carbon dioxide levels. Normal values for an arterial blood gas are provided. The roles of the respiratory and metabolic components in maintaining acid-base balance are explained.
This document discusses acid-base disorders and their physiology, evaluation, and treatment. It defines key terms like pH, acids, bases, and the four primary acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. For each disorder it describes the characteristics, pathophysiology, clinical features, and treatment approach. Primary investigations discussed include serum electrolytes, bicarbonate, PCO2, and anion gap to help evaluate the underlying cause and guide management.
This document 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 discusses acid-base disorders and presents three patient case studies. It provides the normal ranges for pH, pCO2, and HCO3 and outlines the six steps for acid-base analysis. The six steps are used to analyze each case study: a patient with metabolic acidosis and respiratory alkalosis, a patient with metabolic acidosis and metabolic alkalosis, and a patient with metabolic and respiratory acidosis. Causes are provided for different types of acid-base disturbances.
The document summarizes acid-base balance and disturbances. It states that the lungs and kidneys work together to maintain acid-base balance. The kidneys regulate bicarbonate levels to buffer acids produced from metabolism. Disturbances can cause metabolic or respiratory acidosis/alkalosis. Causes, signs, and treatments are provided for various conditions like dehydration, electrolyte imbalances.
The document discusses the four main buffering mechanisms that the body uses to regulate acid-base balance: bicarbonate buffering system, intracellular buffering system, respiratory compensation, and renal compensation. It provides details on how each system works to compensate for metabolic acidosis and alkalosis as well as respiratory acidosis and alkalosis. The bicarbonate buffering system involves carbon dioxide combining with water to form carbonic acid, which dissociates into hydrogen ions and bicarbonate ions. Respiratory compensation increases or decreases breathing rate to alter plasma pH, while renal compensation increases bicarbonate production and acid excretion to restore balance.
1. The patient has metabolic acidosis with a high anion gap and corrected anion gap, suggesting unmeasured anions like lactic acid.
2. Using the Stewart approach, the patient's strong ion difference (SID) is low, further indicating metabolic acidosis from unmeasured anions.
3. The base deficit gap is also high, quantifying the amount of unmeasured anions as lactate based on the blood level.
4. In summary, the patient has metabolic acidosis driven by lactic acidosis in the setting of septic shock and acute liver failure. Evaluation using different acid-base approaches consistently points to the same diagnosis.
Water is essential for life and makes up about 60% of the human body. It participates in metabolic reactions, transports solutes, regulates temperature, and is distributed between intracellular and extracellular compartments. Electrolytes like sodium, potassium, calcium, and magnesium are balanced in body fluids to maintain water balance. The kidneys, along with hormones like aldosterone and ADH, precisely regulate water and electrolyte balance by controlling water retention, excretion of waste products, and acid-base balance through buffers and respiratory and renal mechanisms.
This document discusses acids and bases in the body. It defines acids as hydrogen containing substances that dissociate to release H+ ions and bases as substances that accept H+ ions. The key physiological acids and bases are discussed including bicarbonate, phosphate, and proteins. The three main mechanisms that regulate blood pH - buffers, respiration, and the kidneys - are summarized. Respiration controls carbonic acid levels while the kidneys regulate bicarbonate reabsorption and acid excretion to maintain pH. Acid-base imbalances can cause metabolic acidosis or alkalosis and respiratory acidosis or alkalosis depending on primary disorder.
This document provides a summary of acid-base physiology, including:
1) Homeostatic mechanisms that regulate acid-base balance, including chemical buffers, respiratory regulation, and renal regulation.
2) Definitions of acids, bases, and the pH scale. Acidosis and alkalosis can arise from excess or deficits of volatile or fixed acids.
3) Key concepts in acid-base regulation including the Henderson-Hasselbalch equation and analyzing arterial blood gases.
This document discusses the normal mechanisms that maintain acid-base balance in the body. It describes how the body uses buffer systems, respiration, and the kidneys to regulate pH and compensate for acid-base imbalances. The buffer systems work quickly to neutralize acids and bases. Respiration then acts to remove carbon dioxide and adjust pH over minutes. Finally, the kidneys excrete or reabsorb acids and bases over longer periods through secretion of hydrogen ions, reabsorption of bicarbonate, and production of new bicarbonate. Together these coordinated systems tightly control pH within a narrow range necessary for normal human function and survival.
This document discusses acid-base balance and disorders. It covers 3 key mechanisms to maintain blood pH: 1) blood buffers, 2) respiratory regulation, and 3) renal regulation. The blood's bicarbonate buffer system uses carbonic acid, while tissues also use phosphate and protein buffers. Respiration controls pH by regulating CO2 exhalation. The kidneys compensate for acid-base imbalances over hours by regulating bicarbonate reabsorption and acid excretion. Acid-base disorders include respiratory and metabolic acidosis and alkalosis.
The document discusses arterial blood gas analysis and interpretation. It provides guidelines for deciding when to intubate based on clinical assessment rather than strict ABG value cutoffs. It also presents two scenarios to determine which case would warrant immediate ventilatory support. The key is that the decision to intubate should be based primarily on clinical factors, not just ABG values alone.
The document 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.
Basics In Arterial Blood Gas Interpretationgueste36950a
This document provides guidelines for interpreting arterial blood gas results, including:
1. It describes how to summarize the acid-base and oxygenation status based on pH, PCO2, HCO3, PO2, and other values.
2. It outlines the steps to determine if a disturbance is respiratory or metabolic in nature, and whether it is acute or chronic.
3. Causes and compensation mechanisms for various acid-base imbalances like respiratory acidosis/alkalosis and metabolic acidosis/alkalosis are reviewed.
This document discusses acid-base balance and disorders. It begins by defining acids and bases, and describing the normal physiology of acid-base balance. It then discusses the four main types of acid-base disorders: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. For each disorder it describes the primary disturbance (pH or HCO3-) and the secondary compensatory response. The document goes on to provide details on the causes, mechanisms, and clinical assessments of different metabolic and respiratory acid-base disorders.
This document provides detailed information about arterial blood gases (ABGs), including:
- The main components of an ABG (pH, PCO2, HCO3) and their normal values.
- How to interpret abnormal ABG readings, distinguishing between compensated and uncompensated disturbances, and identifying the primary acid-base disorder.
- Examples of mixed acid-base disorders and clinical causes of metabolic and respiratory acid-base disorders.
- Practice questions to assess the ability to interpret ABG results.
This document provides information about arterial blood gases (ABGs), including:
- The main components of an ABG are pH, PCO2, and HCO3, which measure acid-base balance.
- Normal and abnormal ABG values are defined. Abnormal readings can indicate respiratory or metabolic acidosis or alkalosis.
- Mixed acid-base disorders are also discussed, which occur when both respiratory and metabolic components are involved.
- Several examples of ABG interpretations are provided to demonstrate analyzing the components to determine the underlying acid-base disturbance.
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.
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.
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.
1. The document discusses acid-base imbalances and how to interpret arterial blood gases (ABGs).
2. It outlines the steps to analyze ABGs which include determining if there is acidemia or alkalemia, identifying if the disturbance is respiratory or metabolic, and assessing compensation.
3. Causes of different acid-base imbalances are provided such as respiratory acidosis resulting from airway obstruction or increased carbon dioxide production, and metabolic acidosis occurring in conditions like diabetic ketoacidosis or lactic acidosis.
This document provides guidance on interpreting arterial blood gases (ABGs). It begins with 11 sample ABG results and asks the reader to identify the primary acid-base disorder in each case. The document then provides detailed explanations for interpreting ABGs and diagnosing mixed acid-base disorders. Key points include calculating the anion gap and excess anion gap to identify concurrent metabolic acidosis or alkalosis complicating the primary disorder suggested by pH, PCO2 and HCO3 levels. The goal is to methodically analyze ABG results to determine the underlying physiologic disturbance(s).
The normal ranges for arterial blood gas values
Approach to arterial blood gas interpretation
Arterial blood gas abnormalities in special circumstances
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 provides an overview of blood gas interpretation and acid-base physiology:
1) It discusses factors that can affect blood gas results like improper sampling technique and gives normal ranges for pH, PCO2, and HCO3.
2) Key concepts in acid-base physiology like the Henderson-Hasselbalch equation, bicarbonate buffering system, and renal regulation of bicarbonate are summarized.
3) The document outlines the pathophysiology and clinical effects of various acid-base disturbances like respiratory acidosis and metabolic alkalosis.
This document discusses acid-base disorders and provides definitions, regulatory mechanisms, causes, and approaches to diagnosis. It defines acids, bases, and pH. The body tightly regulates blood pH between 7.35-7.45 through buffer systems, respiratory control of carbon dioxide levels, and renal regulation of bicarbonate. Causes of acid-base disorders include things like ketoacidosis, renal failure, diarrhea, and respiratory depression. Diagnosis involves determining if the primary disturbance is acidosis or alkalosis, whether it is respiratory or metabolic in nature, and assessing compensation through formulas like the anion gap and Winters formula.
The document discusses acid-base balance in the body. It begins by explaining that acid-base balance refers to the mechanisms that keep body fluids close to a neutral pH between 7.35-7.45. This is regulated by buffer systems like bicarbonate and processes like respiration and renal function. Deviations outside this range can affect membrane and protein function. The major buffer system is the carbonic acid-bicarbonate system regulated by the lungs and kidneys to determine plasma pH. Respiratory and renal systems also help regulate pH through expelling carbon dioxide and secreting/reabsorbing bicarbonate and ions. Imbalances can cause metabolic acidosis, respiratory acidosis, metabolic alkalosis
This document discusses acid-base imbalance and metabolic acidosis. It defines metabolic acidosis as a pH imbalance where the body has too much acid due to metabolism and not enough bicarbonate to neutralize acid effects. Metabolic acidosis is characterized by reduced serum bicarbonate, decreased arterial carbon dioxide partial pressure, and reduced blood pH below 7.35. The document outlines the pathophysiology of metabolic acidosis and discusses compensation mechanisms, arterial blood gas components, and case examples of acid-base imbalances.
This document provides an overview of acid-base imbalances. It defines acid-base balance and pH, and describes the three buffering systems that help maintain homeostasis: respiratory, blood, and renal. It outlines the main types of acid-base disorders including respiratory (changes in PCO2) and metabolic (changes in HCO3). Rules for interpreting arterial blood gases are provided, including how to identify primary vs compensatory abnormalities. Compensatory responses and interpreting mixed disorders are also summarized.
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
This document provides information on arterial blood gas analysis including acid-base terminology, clinical terminology criteria, the anion gap, prediction of compensatory changes, primary acid-base disorders, mixed acid-base disorders, examples of acid-base disorders, and causes of various disorders. Key points include definitions of acidemia, acidosis, alkalemia, and alkalosis. Normal values for pH, PaCO2, and HCO3 are provided. Respiratory and metabolic acidosis and alkalosis are described along with expected compensatory changes.
The document provides information on interpreting arterial blood gases (ABGs), including:
- A 6-step process for interpretation involving assessing pH, identifying the primary disorder as respiratory or metabolic, evaluating compensation, calculating anion gap, and considering ratio of anion gap to bicarbonate change.
- Tables listing normal ABG values and expected compensation patterns for different acid-base disorders.
- Explanations of key ABG components like pH, partial pressures, bicarbonate, and base excess and how they relate to acid-base status.
- Causes and characteristics of respiratory and metabolic acidosis and alkalosis.
Abg.2 Arterial blood gas analysis and example interpretationsamirelansary
This document provides an overview of different approaches to analyzing arterial blood gases (ABG), including the Copenhagen, Boston, and Stewart approaches. It discusses key parameters measured in an ABG such as pH, PaCO2, PaO2, HCO3, and oxygen saturation. The document also summarizes the steps involved in interpreting an ABG, including classifying acid-base disturbances as respiratory or metabolic, assessing compensation, and considering the anion gap in cases of metabolic acidosis.
Mycoplasmas are the smallest free-living organisms that lack cell walls. They colonize humans and can cause diseases. The two medically important genera that infect humans are Mycoplasma and Ureaplasma. Mycoplasma pneumoniae is a major cause of atypical pneumonia while Ureaplasma urealyticum and Mycoplasma hominis can cause nongonococcal urethritis. Mycoplasmas are difficult to culture and require complex media with sterols. They are treated with antibiotics like tetracycline and erythromycin.
1. Spirochetes are spiral-shaped, motile bacteria that include pathogens causing syphilis, Lyme disease, and leptospirosis.
2. Treponema pallidum causes syphilis, which has primary, secondary, and tertiary stages and can be transmitted congenitally. Darkfield microscopy and serological tests are used for diagnosis.
3. Other human pathogenic spirochetes include Borrelia burgdorferi, which causes Lyme disease transmitted through tick bites, and Leptospira interrogans, which causes leptospirosis transmitted through contact with infected animal urine.
Here are brief descriptions of the three forms of anthrax and the mechanism of anthrax toxin:
1. The three forms of anthrax are cutaneous (skin), inhalation (lungs), and gastrointestinal (ingestion).
2. Anthrax toxin is composed of three proteins - protective antigen (PA), lethal factor (LF), and edema factor (EF). PA binds to receptors on cells and helps internalize LF and EF. LF is a metalloprotease that cleaves MAPKK, disrupting cell signaling. EF is an adenylate cyclase that increases cyclic AMP levels, impairing immune function. Together they cause edema, tissue necrosis, and sepsis.
Zoonoses are infectious diseases that can be transmitted between animals and humans. A majority (61%) of known human pathogens are zoonotic. Significant zoonotic pandemics in history include the Black Death plague pandemic in the 14th century spread by Mongol invaders, and the 1918 Spanish flu pandemic. Today, zoonotic diseases pose a threat through increased human-animal contact and potential use in biological terrorism. Bacillus anthracis, the cause of anthrax, is a large, spore-forming, gram-positive rod-shaped bacterium. Its virulence depends on its polysaccharide capsule and lethal and edema toxins. Anthrax is typically transmitted through contact with infected animals or their products and
This document provides information on Corynebacterium diphtheriae, which causes diphtheria. It describes the morphology, cultivation, biochemical characteristics, pathogenicity, clinical manifestations, diagnosis, treatment and prevention of diphtheria. C. diphtheriae produces an exotoxin that inhibits protein synthesis and causes pseudomembrane formation in the throat and other areas. Laboratory diagnosis involves microscopy, culture and toxin production testing. Immunization with diphtheria, tetanus and pertussis vaccine (DTP) provides active immunity against the disease.
Mycobacterium is the only genus in the family Mycobacteriaceae. It is classified into four groups: M. tuberculosis complex, non-tuberculous mycobacteria group I, non-tuberculous mycobacteria group II, and rapidly growing non-tuberculous mycobacteria. M. tuberculosis is the pathogen that causes tuberculosis in humans. It is transmitted through the air and infects the lungs, causing symptoms like cough, fever, and weight loss. Inside the body, it is engulfed by macrophages but can survive and multiply, triggering the formation of granulomas.
Clostridium tetani is an obligate anaerobic, gram-positive bacterium that causes the disease tetanus. It forms terminal spores that give it a distinctive drumstick appearance. Though found worldwide in soil, C. tetani enters the body through wounds and causes tetanus by producing a potent neurotoxin. It is a major cause of mortality in developing countries, with neonatal tetanus accounting for about half of worldwide cases and having a mortality rate of 85%.
This document provides information on Campylobacter and Helicobacter, which are Gram-negative, microaerophilic bacteria. Campylobacter causes foodborne illness in humans and is transmitted through contaminated poultry or water. Its main virulence factors include flagella for motility and adhesins for attachment. Helicobacter pylori colonizes the stomach and is associated with gastritis, ulcers, and gastric cancer. It produces urease and adheres tightly to gastric epithelial cells using flagella and adhesins. Both bacteria are transmitted orally between humans or from animal reservoirs and cause disease by invading and damaging intestinal or gastric mucosa.
This document discusses Vibrio cholerae, the bacteria that causes cholera. It provides details on the history, pathogenesis, clinical manifestations, diagnosis, and immunity aspects of cholera. Some key points include:
- V. cholerae causes the severe, acute diarrheal disease cholera and is transmitted through contaminated food or water.
- There have been several global pandemics of cholera since the 1800s. The causative agent was discovered by Pacini and Koch in the 1800s.
- V. cholerae secretes a toxin that increases cyclic AMP levels in intestinal cells, causing a massive outpouring of fluid in the stool. Colonization factors like pili and flagella
1. Enterobacteriaceae are a family of Gram-negative, non-spore forming rods that are normal flora of the gastrointestinal tract. They include many important pathogens like Escherichia, Salmonella, Shigella.
2. They are facultative anaerobes that ferment glucose and reduce nitrates. Identification is based on lactose fermentation and reactions on selective media.
3. Shigella causes bacillary dysentery. It is non-motile and invades the colonic epithelium, causing severe diarrhea, fever and tenesmus. Virulence factors include invasion plasmid antigens.
This document summarizes Gram positive cocci, focusing on Staphylococcus and Streptococcus. Staphylococcus is classified based on coagulase production. It is a facultative anaerobe that can cause skin infections and food poisoning through toxins like enterotoxins. Streptococcus is classified by hemolytic activity and cell wall antigens. It attaches to host cells using M protein and hyaluronidase. It produces invasive enzymes and exotoxins like pyrogenic toxins that allow it to spread. Both bacteria cause disease through various virulence factors including toxins, enzymes, and structural components.
This document discusses drug resistance and nosocomial infections. It begins by describing the discovery of antibiotics by Alexander Fleming in 1928 and how antibiotics work by either killing bacteria or preventing their growth. While antibiotics were initially a "miracle cure", overuse and misuse has led to the development of drug-resistant bacteria. Resistance can arise through genetic mutations that make bacteria less susceptible to antibiotics or through horizontal gene transfer between bacteria. The document examines several antibiotic targets and mechanisms of resistance, such as beta-lactamase enzymes providing resistance to penicillins and altered cell walls conferring vancomycin resistance. It stresses the importance of properly using and prescribing antibiotics to slow the development and spread of drug-resistant bacteria.
There are two methods of artificial immunity: active immunization and passive immunization. Active immunization involves administering antigens to induce an immune response in the recipient. Passive immunization involves transferring antibodies from an immune individual. Vaccines provide active immunization by exposing the immune system to antigens from pathogens in order to stimulate antibody production and develop immunological memory without causing illness. DNA vaccines are a type of vaccine that attempt to make vaccines more effective, cheaper and safer by using recombinant gene technology.
1. Proper specimen collection is essential for accurate laboratory diagnosis of bacterial infections, as the wrong sample, delay in transport, or contamination can limit test usefulness.
2. Common examination methods for diagnosing bacterial infections include morphological analysis, isolation and culture of pathogens, biochemical reactions, antibiotic susceptibility testing, and detection of antigens or nucleic acids.
3. Antibiotic susceptibility testing determines the sensitivity of isolated bacteria to different antibiotics, which helps clinicians select the proper treatment. Methods include minimum inhibitory concentration and disk diffusion tests.
1. Innate immunity provides the first line of defense against pathogens and includes anatomical barriers, inflammation, phagocytosis, and antimicrobial proteins/peptides.
2. Adaptive immunity develops over time upon exposure to specific pathogens and provides enhanced protection through antibody production and immunological memory.
3. The major categories of innate immunity defenses are anatomical barriers, inflammation, phagocytosis, microbial antagonism by normal flora, and antimicrobial substances in tissues. Adaptive immunity involves B cells, T cells, and production of antibodies.
This document discusses bacterial pathogenesis and infection. It covers several key topics:
1) Normal flora are microorganisms that normally live in or on the human body without causing disease. Opportunistic pathogens are normal flora that can cause disease under certain conditions if the host's immunity is compromised.
2) Bacterial infection is determined by factors of both the bacterium and host. The number and virulence of bacteria as well as the host's innate and acquired immunity impact whether infection occurs.
3) Bacterial pathogenicity is influenced by virulence factors like toxins, invasiveness, and the portal of entry. Virulence refers to an organism's ability to cause disease and is determined by its inv
Bacterial heredity and variation can occur through several mechanisms. Genetic variation arises from mutations in bacterial chromosomes and genetic elements like plasmids, bacteriophages, and transposable elements. Gene transfer and recombination can also introduce variation as bacteria can undergo transformation, conjugation, and transduction to exchange genetic material. This allows bacteria to evolve new traits like antibiotic resistance or changes in virulence over multiple generations.
This document discusses biosafety and the safe handling of biological materials. It defines key terms like sterilization, disinfection, and biosafety. Biosafety aims to ensure safe handling, transport, and disposal of biological materials. Biological risks are classified by levels of containment needed, from BSL-1 to BSL-4. Personal protective equipment and disposal of hazardous waste are important biosafety protocols. Biosafety also addresses bioterrorism threats and ways to prevent the spread of dangerous pathogens.
1. The document discusses the field of medical microbiology, including the definition as the study of microorganisms too small to see with the naked eye, such as viruses, bacteria, and fungi.
2. It describes the key research techniques in medical microbiology including microtechnique, aseptic technique, culture technique, and staining technique.
3. The status and developments of medical microbiology are summarized, such as the discovery of new pathogens like HIV and hepatitis viruses, and the direction of further research into pathogenic mechanisms and new treatments.
Bacteria require certain environmental conditions to grow and multiply, including temperature, pH, oxygen, water, and nutrients. Bacterial metabolism allows bacteria to obtain energy and synthesize cellular components through catabolic and anabolic processes. The products of bacterial anabolism like toxins, enzymes, antibiotics, and pigments have medical significance related to pathogenicity, treatment of disease, and identification of bacteria.
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
"Learn about all the ways Walmart supports nonprofit organizations.
You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
Executive Directors Chat Leveraging AI for Diversity, Equity, and InclusionTechSoup
Let’s explore the intersection of technology and equity in the final session of our DEI series. Discover how AI tools, like ChatGPT, can be used to support and enhance your nonprofit's DEI initiatives. Participants will gain insights into practical AI applications and get tips for leveraging technology to advance their DEI goals.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
How to Build a Module in Odoo 17 Using the Scaffold MethodCeline George
Odoo provides an option for creating a module by using a single line command. By using this command the user can make a whole structure of a module. It is very easy for a beginner to make a module. There is no need to make each file manually. This slide will show how to create a module using the scaffold method.
Natural birth techniques - Mrs.Akanksha Trivedi Rama University
03 acid basedisturbance_ptii
1. Dept. of PathologyDept. of Pathology
Medical CollegeMedical College
Hunan Normal UniversityHunan Normal University
(( 湖南 范大学医学院病理学教研室师湖南 范大学医学院病理学教研室师 )) 1
Chapter 3Chapter 3
Acid-Base Balance andAcid-Base Balance and
ImbalanceImbalance
(酸 平衡紊乱)碱(酸 平衡紊乱)碱
3. §1. Concept :
Decrease of pH induced by primary increase in PaCO2
(or plasma H2
CO3
).
§2. Causes :
Hypoventilation (inside) :
Air way obstructed
Paralysis of respiratory muscle
Fibrosis of the lungs
Insufficient ventilation (outside)
Excessive inspiration of CO2 (e.g, mine workers)
Respiratory acidosis
4. §3. Compensation :
1) Acute respiratory acidosis:
Often decompensated because kidneys play their roles in
compensation slowly.
2) Chronic respiratory acidosis:
The secondary HCO3
-
↑ shows after 3 ~ 5 days.
Respiratory acidosis
Lungs and bicarbonate buffer system can’t play their roles in
compensation.
Mainly depends upon non-bicarbonate systems and the
kidneys.
7. §4. Changes of blood gas parameters :
Respiratory acidosis
pH ↓
PaCO2
↑↑
HCO3
-
↑
AB ↑
SB ↑
BB ↑
BE ↑ (positive value increased)
(in the case of simple RAc)
8. §5. Effects on organism :
Respiratory acidosis
1) Cardiovascular system :
Similar to MAc
Cardiac arrhythmias
Negative inotropic action
Blood vessel dilatation
2) Nervous system : quite prominent
Pulmonary encephalopathy :
PaCO2
↑ CO2
retention (>80 mmHg, narcosis)
9. 1) Correction of underlying disorders :
Improve ventilation
2) Correction of acidosis :
Tris (THAM) should be used with caution after ventilation
improved. (Instead of NaHCO3)
Tris+ H2CO3→TrisH+
+ HCO3
-
§6. Principles of prevention and treatment
:
Respiratory acidosis
11. §1. Concept :
Increase of pH induced by primary increase in plasma HCO3
-
.
§2. Causes :
Acids too little
Bases too much
Metabolic alkalosis
12. H+
Loss ↑ from the stomach : bad vomiting and/or
gastric suction
H+
Loss ↑ from the
kidneys
Long term use of diuretics:
primary or secondary
hyperaldosteronism
Cushing Syndrome
(↑ cortisol →↑ glucocorticoid
[similar to ADS])
Hypokalemia: H+
exchanged into cells
ADS↑:
1) Acids
too little
Metabolic alkalosis
Ammonia (NH3) poisoning during hepatic failure
NH3 + H+
→ NH4
+
13. 2) Bases
too much
Excessive intake of alkaline drugs
(e.g., NaHCO3)
Excessive intake of stored blood
(rich in sodium citrate)
Loss of a lot of fluid
Compensatory HCO3
-
↑:
Hyperaldosteronism → ↑ ADS →
reabsorption of Na+
and HCO3
-
Compensation after chronic respiratory
acidosis (e.g., mechanical ventilation)
Metabolic alkalosis
14. §3. Classification :
1) Saline-responsive alkalosis :
The replacement of saline (0.9%NaCl) is effective.
Cl-
helps excrete HCO3
-
Seen in vomiting, gastric suction and use of the diuretics.
(causing loss of H+
)
2) Saline-resistant alkalosis :
The replacement of saline is not effective.
Seen in ADS↑, Cushing syndrome.
Causative diseases need to be treated first.
Metabolic alkalosis
15. §3. Compensation :
1) Buffer systems :
Plasma buffer systems
Cells
May cause hypokalemia
H+
↓ Hypokalemia
K +
H+
Metabolic alkalosis
16. 2) Regulation by the kidneys:
↓ excretion of H+
/NH4
+
↓ HCO3
-
reabsorption
Alkaline urine
3) Regulation by the lungs - main mechanism :
H+
↓→(-) breathing PaCO2
↑ (secondary)
Metabolic alkalosis
Na+
Capillary Epithelial Cell Tubule
H2O + CO2
H+
Na+
H2CO3
HCO3
-
H+
17. 3.1 Pyloric obstruction patient : pH 7.49 , HCO3
-
36 , PaCO2
48 ;
Predict PaCO2
= 40 + 0.7(36-24)±5 = 43.4 ~ 53.4
Measured PaCO2
= 48, within predicted, simple MAl
Equation : predict PaCO2
= 40 + 0.7 HCO△ 3
-
±5
Example
Judgement :
If measured PaCO2 insofar as predict PaCO2 , simple MAl
If measured > predict maximum, CO2 retention, MAl + RAc
If measured < predict minimum, CO2 too less, MAl + RAl
Metabolic alkalosis
19. §4. Changes of blood gas parameters :
pH ↑
HCO3
-
↑↑
PaCO2
↑
AB ↑
SB ↑
BB ↑
BE ↑ (positive value increased)
Metabolic alkalosis
(in the case of simple MAl)
20. §5. Effects on organism :
1) Central nervous system (CNS) : excitatory, such as
restlessness, mental derangement, delirium and disorder of
consciousness.
Mechanism :↓ γ-GABA (inhibitory neurotransmitter)
2) Neuromuscular excitability : The patient may
manifest tendon hyperreflexia and convulsion.
Mechanism : Plasma free Ca2+
↓ in alkalosis
Glutamate decarboxylase
↑ pH
Glu GABA
Metabolic alkalosis
21. 4) Hypokalemia (arrhythmia) :
5) Urine: usually alkali
But in hypokalemia-alkalosis:
paradoxical acidic urine
Metabolic alkalosis
3) Hypoxia :
pH ↑→ affinity of O2 to Hb ↑ (ODC left shift)
22. §6. Principles of prevention and treatment :
1) Saline-responsive MAl
Saline (NaCl or KCl) infusion
2) Saline-resistant MAl
Carbonic anhydrase (CA) inhibitor
- Acetazolamide (diamox)
- Inhibits generation and secretion of H+
ADS inhibitor
- Spironolactone [ 螺内脂 ]
- Inhibits reabsorption of Na+
and H2CO3
+
Metabolic alkalosis
24. §1. Concept :
Increase of pH induced by primary decrease in PaCO2
(or plasma
H2CO3).
§2. Causes : Hyperventilation is the fundamental
mechanism of respiratory alkalosis.
1) Excitement of respiratory center
Fever, hysteria.
2) Hypoxia
3) Lung diseases
ARDS, interstitial pneumonia.
4) Misuse of mechanical ventilator
Respiratory alkalosis
26. 2) Chronic respiratory alkalosis :
Kidneys are main organs in compensation.
−↓ excretion of H+
−↓ reabsorption of HCO3
-
§3. Compensation :
1) Acute respiratory alkalosis :
Buffers in plasma and cells.
Often decompensated because the lungs and kidneys fail
to play their roles in compensation.
Respiratory alkalosis
27. 4.1 Hysteria patient : pH 7.42 , HCO3
-
19 , PaCO2
29 ;Predict HCO3
-
= 24 + 0.5(40 - 29)±2.5 = 16 ~ 21
Measured HCO3
-
= 19, within predicted, simple RAl
Equation : predict HCO3
-
= 24 + 0.5 PaCO△ 2
±2.5
Example
Judgement :
If measured HCO3
-
insofar as predict HCO3
-
, simple RAl
If measured > predict maximum, HCO3
-
retention, RAl + MAl
If measured < predict minimum, HCO3
-
too less, RAl + MAc
Respiratory alkalosis
29. §4. Changes of blood gas parameters
:
pH ↑
HCO3
-
↓
AB↓
SB↓
BB↓
BE ↓ (negative value increased)
Respiratory alkalosis
(in the case of simple RAl)
PaCO2
↓↓
30. 1) central nervous system :
PaCO2
↓ ( hypocapnia )→ cerebrovascular
contraction → blood content in brain↓ →
disturbances in CNS, such as vertigo (dizzy),
unconsciousness, coma.
§5. Effects on organism :
2) Increased neuromuscular excitability
(↓GABA)
such as convulsion, etc.
3)Hypokalemia
Respiratory alkalosis
31. §6. Principles of prevention and treatment :
1) Treatment of primary diseases;
2) Prevention of mechanical hyperventilation
(ataractic used);
3) Inspiration of oxygen containing 5% CO2.
Respiratory alkalosis
32. Guidelines for the Diagnosis of Acid-Base Disturbances
1. According to the changes of pH, an acidosis or alkalosis can be
determined.
2. According to the case history (or/and H-H equation), primary
disorders of HCO3
–
or PaCO2 can be determined.
3. According to the primary disorders, a respiratory or metabolic
disturbance can be determined.
If a primary HCO3
-
↑or ↓, a metabolic alkalosis or acidosis can be
determined.
If a primary PaCO2 ↑or ↓, a respiratory acidosis or alkalosis can be
determined.
4. According to AG↑ , the types of metabolic acidosis can be
determined.
5. According to compensation equations, simple or mixed acid-base
33. Changes of Blood Gas ParametersChanges of Blood Gas Parameters
pHpH PaCOPaCO22
--
HHCOCO33
--
ABAB SBSB BBBB BEBE
AcidosisAcidosis
MetabolicMetabolic ↓↓ ↓↓ ↓↓↓↓ ↓↓ ↓↓ ↓↓ ↓↓
RespiratoryRespiratory ↓↓ ↑↑↑↑ ↑↑ ↑↑ ↑↑ ↑↑ ↑↑
AlkalosisAlkalosis
MetabolicMetabolic ↑↑ ↑↑ ↑↑↑↑ ↑↑ ↑↑ ↑↑ ↑↑
RespiratoryRespiratory ↑↑ ↓↓↓↓ ↓↓ ↓↓ ↓↓ ↓↓ ↓↓
Metabolic: changes of pH and others at the same direction;
Respiratory: changes of pH and other at the opposite direction.
34. Example :
A 45-year-old women was admitted to the local hospital with nausea,
vomiting, anorexia. She has suffered a 5-year history of hypertension
and a 3-year history of albuminuria. Doctor told her kidneys damaged
one year ago. Now edema and hypertension has been checked out. Her
laboratory results were as follows: pH 7.30 , PaCO2 20
mmHg , HCO3
–
9 mmol/ L , Na+
127 mmol/L , K+
6.7 mmol/L , Cl-
88
mmol/L , BUN 1.5g/L [0.09 – 0.2] 。
1 , Is there acid-base disorders?
2 , Why does PaCO2 decrease too ?
3 , Why her AG ↑ ?
[acids not eliminated from damaged kidneys]
4 , Is there any other acid-base disorders except metabolic
acidosis ?
Equation : predict PaCO2
= 1.5×[HCO3
-
] + 8±2
Disorders are big problems in clinic.
http://v.qihuang99.com/player/1777.html?1777-0-2
Workers at mine with insufficient ventilation (鼓风机障碍) leading to too much CO2 inspiration。
Because of the impairment of the respiratory function, the lungs and HCO3-/H2CO3 can’t function well.
Compensation limit : HCO3-↑ = 45 mmol/L
HCO3- accounts for half of BB.
AB &gt; SB (Because PaCO2 increases, AB &gt; SB).
Pulmonary encephalopathy: first excitement and then inhibitory (when PaCO2 exceeds 80).
Narcosis:麻醉;昏迷状态
In Rac, HCO3- (BE) already increased, better not to give alkali.
Tris (tris(hydroxymethyl)aminomethane, THAM) is an organic compound with the formula (HOCH2)3CNH2. Tris is extensively used in biochemistry and molecular biology.[1] In biochemistry, Tris is widely used as a component of buffer solutions, such as in TAE and TBE buffer, especially for solutions of nucleic acids. It contains a primary amine and thus undergoes the reactions associated with typical amines, e.g. condensations with aldehydes.
Tris (usually known as THAM in this context) is used as alternative to sodium bicarbonate in the treatment of metabolic acidosis.[8][9]
Alkaline drugs such as morphine (one of the at least 50 alkaloids).
HCO3-↑ can be buffered by weak acids in plasma.
Regulation by the lungs are the main mechanisms for metabolic acid-base imbalances; whereas regulation by the kidneys are the main mechanisms for respiratory ones.
Inhibition of the activities of CA will cause decreased excretion of H+; Inhibition of the activities of glutaminase will decrease the excretion of NH4+.
Compensation limit by the lungs to increase PaCO2 = 55 mmHg.
Pyloric obstruction leads to vomiting.
The only difference with respiratory acidosis is pH.
AB &gt; SB
Ca++ binds to plasma protein under alkalosis.
Spironolactone inhibits the effects of mineralocorticoids, namely, aldosterone, by displacing them from mineralocorticoid receptors (MR) in the cortical collecting duct of renal nephrons.
Mechaisms of NaCl treatment of MAl:
1) Increasing extracellular fluid to eliminate concentrated alkalosisl;
2) Circulating blood ↑→ excretion of HCO3- from urine ↑
Reflective stimulation such as hypoxia, fever, pain, also causes respiratory alkalosis.
Hypoxemia is hypoxia in the blood.
Compensation limit: HCO3- = 15 mmol/L
The only difference with metabolic acidosis is pH.
AB &lt; SB
BE negative value increase is because of compensation.
The patient have suffered from metabolic acidosis according to her history and HCO3 - ↓
1.5 x 9 + 8 +/- 2 = 19.5 – 23.5
血尿素氮(BUN, blood urea nitrogen )的正常值为:3.2-7.1mmol/L(90-200mg/L)