This document discusses blood gas analysis and its clinical interpretation. It begins by outlining common errors in blood gas sampling and discusses the components of a blood gas analysis. It then provides steps for analyzing blood gas results, including calculating the anion gap and delta gap to identify specific acid-base disorders. Examples are provided to demonstrate how to use these steps and calculations to interpret blood gas results and determine if findings indicate a respiratory or metabolic disorder and if compensation is appropriate. Causes of anion gap and non-anion gap metabolic acidosis are also reviewed.
This document provides information on interpreting blood gas analysis (ABG). It discusses common errors in ABG sampling and outlines steps to analyze ABG results. Key points include checking if the pH indicates acidosis or alkalosis, identifying the primary disorder, assessing compensation, and calculating the anion and delta gaps to detect mixed disorders. Non-gap causes of acidosis are distinguished using urine anion gap. The document also covers expected changes in respiratory and metabolic acid-base disorders and differentials for specific conditions.
This document outlines the key components and steps in analyzing arterial blood gases (ABGs). It discusses:
1) The main components measured in an ABG - pH, pCO2, pO2, HCO3.
2) A 7-step process for ABG analysis including determining if there is acidemia/alkalemia, the primary acid-base disorder, appropriate compensation, and calculating anion/delta gaps.
3) Causes and expected changes in metabolic and respiratory acidosis/alkalosis.
4) Examples of ABG cases and working through the full analysis, including identifying acute respiratory acidosis in one case and acute respiratory alkalosis in another.
A blood gas analysis showed a pH of 7.27, pCO2 of 58 mmHg, and HCO3- of 26 mmol/L in a patient receiving 5L of oxygen. This represents a primary respiratory acidosis with appropriate chronic compensation, as the pH and pCO2 are low and HCO3- is elevated, consistent with long-standing respiratory acidosis. The anion gap and albumin are normal. This patient is experiencing chronic respiratory acidosis.
The document discusses arterial blood gas (ABG) analysis. It provides 3 key points:
1. ABG analysis aids in establishing diagnoses and assessing the severity of respiratory failure by measuring oxygenation, ventilation, and acid-base balance.
2. The normal values for pH, PCO2, PO2, HCO3, and other components are outlined.
3. A step-wise approach to interpreting an ABG report is described, including assessing whether it indicates a respiratory or metabolic disorder, whether compensation is adequate, and evaluating other acid-base parameters like anion gap.
This document provides information on interpreting arterial blood gas results. It discusses sampling procedures and precautions for ABG tests. The six-step approach to ABG interpretation is outlined, covering assessing acid-base and oxygenation status. Key points include determining if the ABG is authentic, identifying if the primary disturbance is respiratory or metabolic, and assessing compensation. Causes of respiratory acidosis, respiratory alkalosis, and metabolic alkalosis are briefly summarized.
This document outlines the steps for analyzing arterial blood gases (ABGs) and acid-base disorders: 1) Determine if the pH is acidic or alkaline, 2) Identify the primary disorder (respiratory or metabolic), 3) Assess compensation, 4) Determine if compensation is acute or chronic, 5) Calculate the anion gap, 6) If elevated, calculate the delta gap, 7) Consider differentials based on clinical context and lab results. Examples are provided to demonstrate applying the steps to analyze specific acid-base disorders like metabolic acidosis or alkalosis.
This document summarizes a seminar on interpreting arterial blood gas results. It discusses conditions that can invalidate ABG results like delayed analysis or excessive heparin. It also covers assessing a patient's acid-base and oxygenation status from an ABG. For acid-base status, it describes the four primary acid-base disorders and how the respiratory and renal systems compensate. It provides a stepwise approach to ABG interpretation and discusses respiratory alkalosis in particular.
This document provides information on interpreting blood gas analysis (ABG). It discusses common errors in ABG sampling and outlines steps to analyze ABG results. Key points include checking if the pH indicates acidosis or alkalosis, identifying the primary disorder, assessing compensation, and calculating the anion and delta gaps to detect mixed disorders. Non-gap causes of acidosis are distinguished using urine anion gap. The document also covers expected changes in respiratory and metabolic acid-base disorders and differentials for specific conditions.
This document outlines the key components and steps in analyzing arterial blood gases (ABGs). It discusses:
1) The main components measured in an ABG - pH, pCO2, pO2, HCO3.
2) A 7-step process for ABG analysis including determining if there is acidemia/alkalemia, the primary acid-base disorder, appropriate compensation, and calculating anion/delta gaps.
3) Causes and expected changes in metabolic and respiratory acidosis/alkalosis.
4) Examples of ABG cases and working through the full analysis, including identifying acute respiratory acidosis in one case and acute respiratory alkalosis in another.
A blood gas analysis showed a pH of 7.27, pCO2 of 58 mmHg, and HCO3- of 26 mmol/L in a patient receiving 5L of oxygen. This represents a primary respiratory acidosis with appropriate chronic compensation, as the pH and pCO2 are low and HCO3- is elevated, consistent with long-standing respiratory acidosis. The anion gap and albumin are normal. This patient is experiencing chronic respiratory acidosis.
The document discusses arterial blood gas (ABG) analysis. It provides 3 key points:
1. ABG analysis aids in establishing diagnoses and assessing the severity of respiratory failure by measuring oxygenation, ventilation, and acid-base balance.
2. The normal values for pH, PCO2, PO2, HCO3, and other components are outlined.
3. A step-wise approach to interpreting an ABG report is described, including assessing whether it indicates a respiratory or metabolic disorder, whether compensation is adequate, and evaluating other acid-base parameters like anion gap.
This document provides information on interpreting arterial blood gas results. It discusses sampling procedures and precautions for ABG tests. The six-step approach to ABG interpretation is outlined, covering assessing acid-base and oxygenation status. Key points include determining if the ABG is authentic, identifying if the primary disturbance is respiratory or metabolic, and assessing compensation. Causes of respiratory acidosis, respiratory alkalosis, and metabolic alkalosis are briefly summarized.
This document outlines the steps for analyzing arterial blood gases (ABGs) and acid-base disorders: 1) Determine if the pH is acidic or alkaline, 2) Identify the primary disorder (respiratory or metabolic), 3) Assess compensation, 4) Determine if compensation is acute or chronic, 5) Calculate the anion gap, 6) If elevated, calculate the delta gap, 7) Consider differentials based on clinical context and lab results. Examples are provided to demonstrate applying the steps to analyze specific acid-base disorders like metabolic acidosis or alkalosis.
This document summarizes a seminar on interpreting arterial blood gas results. It discusses conditions that can invalidate ABG results like delayed analysis or excessive heparin. It also covers assessing a patient's acid-base and oxygenation status from an ABG. For acid-base status, it describes the four primary acid-base disorders and how the respiratory and renal systems compensate. It provides a stepwise approach to ABG interpretation and discusses respiratory alkalosis in particular.
The document discusses arterial blood gas (ABG) analysis. It provides information on the uses and contraindications of ABG tests, as well as the procedure, normal values, and interpretation of ABG results. It discusses oxygenation, acid-base balance, definitions, regulation of acid-base balance, and a step-wise approach to interpreting ABG reports. Key points include how ABG analysis can help establish diagnoses and guide treatment for conditions like respiratory failure, and the importance of factors like temperature, oxygen levels, and timing when withdrawing and analyzing ABG samples.
This document provides an overview of arterial blood gas interpretation. It discusses the objectives, procedure and precautions for ABG sampling. It covers the interpretation of oxygenation status including how to determine PaO2 and the PaO2/FiO2 ratio. For acid-base status, it explains the bicarbonate buffer system, respiratory and renal regulation and how to assess primary acid-base disorders. A 6-step approach to ABG interpretation is presented covering evaluating authenticity, determining acidemia/alkalemia, respiratory vs. metabolic causes, compensation and using the anion gap to identify high anion gap metabolic acidosis.
This document 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.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and oxygen saturation. It outlines a 4 step method for ABG interpretation including identifying the primary disturbance, determining if it is respiratory or metabolic, and assessing for compensation. Several case examples are provided to demonstrate application of this analytical approach.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and provides steps for analyzing primary vs compensatory abnormalities. Several case examples are presented and analyzed to demonstrate the application of ABG interpretation.
1. The patient has a mixed disorder of metabolic acidosis with respiratory compensation and high anion gap metabolic acidosis.
2. The primary disorder is metabolic acidosis as pH and HCO3 are decreased while PCO2 is normal.
3. The anion gap is elevated indicating a high anion gap metabolic acidosis likely due to an unknown toxin given the clinical context.
1) The document discusses approaches to analyzing blood gases and acid-base disorders. It provides details on how the kidney regulates acid-base balance through bicarbonate reabsorption and secretion of hydrogen ions. Formulas for calculating compensation and identifying dominant acid-base disorders are presented.
2) Mechanisms of bicarbonate and hydrogen ion transport across renal tubular cells are illustrated through diagrams. Equations for calculating expected compensation in common acid-base imbalances are given to help identify the primary disorder.
3) Methods for evaluating systemic acid-base disorders are outlined, including using arterial blood gas results and serum electrolytes to identify
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
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
A pregnant woman presented with worsening nausea, vomiting and dehydration over 10 days. On examination, she was dehydrated with shallow breathing. Her arterial blood gas showed a pH of 7.45, PCO2 of 30 mmHg, HCO3 of 26 mEq/L, indicating a metabolic alkalosis due to vomiting and loss of hydrochloric acid leading to hypokalemia and hypochloremia. Compensation occurred through respiratory depression lowering PCO2.
This document provides information about arterial blood gases (ABGs), including what parameters are measured in an ABG, which artery is commonly used for sampling, cautions when obtaining an ABG, and conditions that can invalidate or modify ABG results. It also outlines the six step approach to evaluating acid-base disorders based on an ABG result, including identifying if the primary disturbance is respiratory or metabolic, ruling out combined disorders, checking the anion gap in metabolic acidosis, and calculating the delta anion gap. An illustrative case is provided where the ABG results indicate a mixed metabolic acidosis and respiratory acidosis based on application of the six step approach.
This document provides an overview of arterial blood gas interpretation. It discusses the objectives, procedure and precautions for ABG sampling. It covers the interpretation of oxygenation status including how to determine PaO2 and the PaO2/FiO2 ratio. For acid-base status, it discusses the bicarbonate buffer system, respiratory and renal regulation, and how to assess primary acid-base disorders. It provides a 6 step approach to ABG interpretation including determining if there is acidemia/alkalemia, if the primary disturbance is respiratory or metabolic, and if metabolic whether the anion gap is normal or high.
blood gas analysis in neonates - Dr Lingaraj MulageLingarajMulage1
This document discusses the interpretation of blood gases in infants and newborns. It provides information on indications for blood gas analysis, terminology used in blood gas analysis like pH, PaO2, PaCO2, and normal blood gas values. It also outlines the steps to interpret arterial blood gases, including evaluating if pH, CO2, and HCO3 are normal and whether the values correlate. Several case studies are presented and interpreted to demonstrate analyzing acid-base imbalances. Formulas for compensating acid-base disturbances are also shown.
This document discusses acid-base disorders and interpretation of arterial blood gases (ABGs). It defines acidosis and alkalosis, and describes respiratory and metabolic causes. Simple and mixed acid-base disorders are explained. Compensation by the lungs and kidneys in response to primary disorders is discussed. A stepwise approach to ABG interpretation is provided, including determining the primary disorder, checking for compensation, calculating the anion gap, and identifying specific etiologies. Characteristics of simple acid-base disturbances and combined disorders are summarized.
This document discusses acid-base regulation and disturbances. It defines metabolic and respiratory acidosis and alkalosis, and describes their causes, symptoms, and treatments. Mixed acid-base disturbances occur when two or more simple disorders take place simultaneously. The Henderson-Hasselbalch equation and anion gap are explained for evaluating acid-base imbalances. Blood gas analysis and considering clinical factors are important for diagnosis.
This document provides an overview of arterial blood gas (ABG) interpretation. It discusses ABG sampling procedures and indications, oxygenation and acid-base status evaluation, and a step-wise approach to ABG interpretation. It also presents examples of clinical cases and discusses metabolic and respiratory acid-base disorders and their compensatory responses.
Interpretation of arterial blood gases:Traditional versus Modern Gamal Agmy
This document discusses the interpretation of arterial blood gases and acid-base disorders. It begins by outlining the Handerson-Hasselbalch equation and normal blood gas values. It then defines respiratory failure and describes the four types based on PaO2 and PaCO2 levels. The document details how to evaluate oxygen status, ventilation, and acid-base disorders from a blood gas analysis. It provides examples of metabolic and respiratory acidosis and alkalosis, explaining compensation mechanisms. Mixed disorders and a step-wise approach to interpretation are also outlined. Three sample problems are worked through as examples.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
The document discusses arterial blood gas (ABG) analysis. It provides information on the uses and contraindications of ABG tests, as well as the procedure, normal values, and interpretation of ABG results. It discusses oxygenation, acid-base balance, definitions, regulation of acid-base balance, and a step-wise approach to interpreting ABG reports. Key points include how ABG analysis can help establish diagnoses and guide treatment for conditions like respiratory failure, and the importance of factors like temperature, oxygen levels, and timing when withdrawing and analyzing ABG samples.
This document provides an overview of arterial blood gas interpretation. It discusses the objectives, procedure and precautions for ABG sampling. It covers the interpretation of oxygenation status including how to determine PaO2 and the PaO2/FiO2 ratio. For acid-base status, it explains the bicarbonate buffer system, respiratory and renal regulation and how to assess primary acid-base disorders. A 6-step approach to ABG interpretation is presented covering evaluating authenticity, determining acidemia/alkalemia, respiratory vs. metabolic causes, compensation and using the anion gap to identify high anion gap metabolic acidosis.
This document 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.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and oxygen saturation. It outlines a 4 step method for ABG interpretation including identifying the primary disturbance, determining if it is respiratory or metabolic, and assessing for compensation. Several case examples are provided to demonstrate application of this analytical approach.
This document provides an overview of arterial blood gas analysis and interpretation. It discusses the key components of an ABG report including pH, PaCO2, PaO2, HCO3 and provides steps for analyzing primary vs compensatory abnormalities. Several case examples are presented and analyzed to demonstrate the application of ABG interpretation.
1. The patient has a mixed disorder of metabolic acidosis with respiratory compensation and high anion gap metabolic acidosis.
2. The primary disorder is metabolic acidosis as pH and HCO3 are decreased while PCO2 is normal.
3. The anion gap is elevated indicating a high anion gap metabolic acidosis likely due to an unknown toxin given the clinical context.
1) The document discusses approaches to analyzing blood gases and acid-base disorders. It provides details on how the kidney regulates acid-base balance through bicarbonate reabsorption and secretion of hydrogen ions. Formulas for calculating compensation and identifying dominant acid-base disorders are presented.
2) Mechanisms of bicarbonate and hydrogen ion transport across renal tubular cells are illustrated through diagrams. Equations for calculating expected compensation in common acid-base imbalances are given to help identify the primary disorder.
3) Methods for evaluating systemic acid-base disorders are outlined, including using arterial blood gas results and serum electrolytes to identify
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
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
A pregnant woman presented with worsening nausea, vomiting and dehydration over 10 days. On examination, she was dehydrated with shallow breathing. Her arterial blood gas showed a pH of 7.45, PCO2 of 30 mmHg, HCO3 of 26 mEq/L, indicating a metabolic alkalosis due to vomiting and loss of hydrochloric acid leading to hypokalemia and hypochloremia. Compensation occurred through respiratory depression lowering PCO2.
This document provides information about arterial blood gases (ABGs), including what parameters are measured in an ABG, which artery is commonly used for sampling, cautions when obtaining an ABG, and conditions that can invalidate or modify ABG results. It also outlines the six step approach to evaluating acid-base disorders based on an ABG result, including identifying if the primary disturbance is respiratory or metabolic, ruling out combined disorders, checking the anion gap in metabolic acidosis, and calculating the delta anion gap. An illustrative case is provided where the ABG results indicate a mixed metabolic acidosis and respiratory acidosis based on application of the six step approach.
This document provides an overview of arterial blood gas interpretation. It discusses the objectives, procedure and precautions for ABG sampling. It covers the interpretation of oxygenation status including how to determine PaO2 and the PaO2/FiO2 ratio. For acid-base status, it discusses the bicarbonate buffer system, respiratory and renal regulation, and how to assess primary acid-base disorders. It provides a 6 step approach to ABG interpretation including determining if there is acidemia/alkalemia, if the primary disturbance is respiratory or metabolic, and if metabolic whether the anion gap is normal or high.
blood gas analysis in neonates - Dr Lingaraj MulageLingarajMulage1
This document discusses the interpretation of blood gases in infants and newborns. It provides information on indications for blood gas analysis, terminology used in blood gas analysis like pH, PaO2, PaCO2, and normal blood gas values. It also outlines the steps to interpret arterial blood gases, including evaluating if pH, CO2, and HCO3 are normal and whether the values correlate. Several case studies are presented and interpreted to demonstrate analyzing acid-base imbalances. Formulas for compensating acid-base disturbances are also shown.
This document discusses acid-base disorders and interpretation of arterial blood gases (ABGs). It defines acidosis and alkalosis, and describes respiratory and metabolic causes. Simple and mixed acid-base disorders are explained. Compensation by the lungs and kidneys in response to primary disorders is discussed. A stepwise approach to ABG interpretation is provided, including determining the primary disorder, checking for compensation, calculating the anion gap, and identifying specific etiologies. Characteristics of simple acid-base disturbances and combined disorders are summarized.
This document discusses acid-base regulation and disturbances. It defines metabolic and respiratory acidosis and alkalosis, and describes their causes, symptoms, and treatments. Mixed acid-base disturbances occur when two or more simple disorders take place simultaneously. The Henderson-Hasselbalch equation and anion gap are explained for evaluating acid-base imbalances. Blood gas analysis and considering clinical factors are important for diagnosis.
This document provides an overview of arterial blood gas (ABG) interpretation. It discusses ABG sampling procedures and indications, oxygenation and acid-base status evaluation, and a step-wise approach to ABG interpretation. It also presents examples of clinical cases and discusses metabolic and respiratory acid-base disorders and their compensatory responses.
Interpretation of arterial blood gases:Traditional versus Modern Gamal Agmy
This document discusses the interpretation of arterial blood gases and acid-base disorders. It begins by outlining the Handerson-Hasselbalch equation and normal blood gas values. It then defines respiratory failure and describes the four types based on PaO2 and PaCO2 levels. The document details how to evaluate oxygen status, ventilation, and acid-base disorders from a blood gas analysis. It provides examples of metabolic and respiratory acidosis and alkalosis, explaining compensation mechanisms. Mixed disorders and a step-wise approach to interpretation are also outlined. Three sample problems are worked through as examples.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
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Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
1. Blood Gas Analysis and it’s
Clinical Interpretation
Dr R.S.Gangwar
MD, PDCC, FIPM
Assistant Professor
Geriatric ICU,DGMH
2. Outline
1. Common Errors During ABG Sampling
2. Components of ABG
3. Discuss simple steps in analyzing ABGs
4. Calculate the anion gap
5. Calculate the delta gap
6. Differentials for specific acid-base disorders
3. Delayed Analysis
Consumptiom of O2 & Production of CO2
continues after blood drawn
Iced Sample maintains values for 1-2 hours
Uniced sample quickly becomes invalid within 15-
20 minutes
PaCO2 3-10 mmHg/hour
PaO2
pH d/t lactic acidosis generated by glycolysis
in R.B.C.
4. Parameter 37 C (Change
every 10 min)
4 C (Change
every 10 min)
pH 0.01 0.001
PCO2 1 mm Hg 0.1 mm Hg
PO2 0.1 vol % 0.01 vol %
Temp Effect On Change of ABG Values
5. FEVER OR HYPOTHERMIA
1. Most ABG analyzers report data at N body temp
2. If severe hyper/hypothermia, values of pH &
PCO2 at 37 C can be significantly diff from pt’s
actual values
3. Changes in PO2 values with temp also predictable
Hansen JE, Clinics in Chest Med 10(2), 1989 227-237
If Pt.’s temp < 37C
Substract 5 mmHg Po2, 2 mmHg Pco2 and Add
0.012 pH per 1C decrease of temperature
6. AIR BUBBLES
:
1. PO2 150 mmHg & PCO2 0 mm Hg in air bubble(R.A.)
2. Mixing with sample, lead to PaO2 & PaCO2
To avoid air bubble, sample drawn very slowly and
preferabily in glass syringe
Steady State:
Sampling should done during steady state after change in
oxygen therepy or ventilator parameter
Steady state is achieved usually within 3-10 minutes
7. Leucocytosis :
pH and Po2 ; and Pco2
0.1 ml of O2 consumed/dL of blood in 10
min in pts with N TLC
Marked increase in pts with very high
TLC/plt counts – hence imm chilling/analysis
essential
EXCESSIVE HEPARIN
Dilutional effect on results HCO3
- & PaCO2
Only .05 ml heperin required for 1 ml blood.
So syringe be emptied of heparin after flushing or only dead
space volume is sufficient or dry heperin should be used
8. TYPE OF SYRINGE
1. pH & PCO2 values unaffected
2. PO2 values drop more rapidly in plastic syringes (ONLY
if PO2 > 400 mm Hg)
Differences usually not of clinical significance so plastic
syringes can be and continue to be used
Risk of alteration of results with:
1. size of syringe/needle
2. vol of sample
HYPERVENTILATION OR BREATH HOLDING
May lead to erroneous lab results
9. COMPONENTS OF THE ABG
pH: Measurement of acidity or alkalinity, based on the hydrogen
(H+). 7.35 – 7.45
Pao2 :The partial pressure oxygen that is dissolved in arterial
blood. 80-100 mm Hg.
PCO2: The amount of carbon dioxide dissolved in arterial blood.
35– 45 mmHg
HCO3 : The calculated value of the amount of bicarbonate in the
blood. 22 – 26 mmol/L
SaO2:The arterial oxygen saturation.
>95%
pH,PaO2 ,PaCO2 , Lactate and electrolytes are measured Variables
HCO3 (Measured or calculated)
10. Contd…
Buffer Base:
It is total quantity of buffers in blood including both
volatile(Hco3) and nonvolatile (as Hgb,albumin,Po4)
Base Excess/Base Deficit:
Amount of strong acid or base needed to restore
plasma pH to 7.40 at a PaCO2 of 40 mm Hg,at
37*C.
Calculated from pH, PaCO2 and HCT
Negative BE also referred to as Base Deficit
True reflection of non respiratory (metabolic) acid
base status
Normal value: -2 to +2mEq/L
11. CENTRAL EQUATION OF ACID-BASE
PHYSIOLOGY
Henderson Hasselbach Equation:
where [ H+] is related to pH by
To maintain a constant pH, PCO2/HCO3- ratio should be
constant
When one component of the PCO2/[HCO3- ]ratio is altered,
the compensatory response alters the other component in the
same direction to keep the PCO2/[HCO3- ] ratio constant
[H+] in nEq/L = 24 x (PCO2 / [HCO3 -] )
[ H+] in nEq/L = 10 (9-pH)
12. Compensatory response or regulation of
pH
By 3 mechanisms:
Chemical buffers:
React instantly to compensate for the addition or
subtraction of H+ ions
CO2 elimination:
Controlled by the respiratory system
Change in pH result in change in PCO2 within minutes
HCO3- elimination:
Controlled by the kidneys
Change in pH result in change in HCO3-
It takes hours to days and full compensation occurs in 2-
5 days
13. Normal Values
Variable Normal Normal
Range(2SD)
pH 7.40 7.35 - 7.45
pCO2 40 35-45
Bicarbonate 24 22-26
Anion gap 12 10-14
Albumin 4 4
14. Steps for ABG analysis
1. What is the pH? Acidemia or Alkalemia?
2. What is the primary disorder present?
3. Is there appropriate compensation?
4. Is the compensation acute or chronic?
5. Is there an anion gap?
6. If there is a AG check the delta gap?
7. What is the differential for the clinical processes?
15. Step 1:
Look at the pH: is the blood acidemic or alkalemic?
EXAMPLE :
65yo M with CKD presenting with nausea, diarrhea and
acute respiratory distress
ABG :ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
ACIDMEIA OR ALKALEMIA ????
16. EXAMPLE ONE
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/
Cr 5.1
Answer PH = 7.23 , HCO3 7
Acidemia
17. Step 2: What is the primary disorder?
What disorder is
present?
pH pCO2 HCO3
Respiratory
Acidosis
pH low high high
Metabolic Acidosis pH low low low
Respiratory
Alkalosis
pH high low low
Metabolic Alkalosis pH high high high
18. Contd….
Metabolic Conditions are suggested if
pH changes in the same direction as pCO2 or pH is
abnormal but pCO2 remains unchanged
Respiratory Conditions are suggested if:
pH changes in the opp direction as pCO2 or pH is abnormal
but HCO3- remains unchanged
19. EXAMPLE
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
PH is low , CO2 is Low
PH and PCO2 are going in same directions then its most
likely primary metabolic
21. Step 3-4: Is there appropriate
compensation? Is it chronic or acute?
Respiratory Acidosis
Acute (Uncompensated): for every 10 increase in pCO2 -> HCO3
increases by 1 and there is a decrease of 0.08 in pH
Chronic (Compensated): for every 10 increase in pCO2 -> HCO3
increases by 4 and there is a decrease of 0.03 in pH
Respiratory Alkalosis
Acute (Uncompensated): for every 10 decrease in pCO2 -> HCO3
decreases by 2 and there is a increase of 0.08 in PH
Chronic (Compensated): for every 10 decrease in pCO2 -> HCO3
decreases by 5 and there is a increase of 0.03 in PH
1 4
2 5
10
Partial Compensated: Change
in pH will be between 0.03 to
0.08 for every 10 mmHg
change in PCO2
22. Step 3-4: Is there appropriate
compensation?
Metabolic Acidosis
Winter’s formula: Expected pCO2 = 1.5[HCO3] + 8 ± 2
OR
pCO2 = 1.2 ( HCO3)
If serum pCO2 > expected pCO2 -> additional respiratory
acidosis and vice versa
Metabolic Alkalosis
Expected PCO2 = 0.7 × HCO3 + (21 ± 2)
OR
pCO2 = 0.7 ( HCO3)
If serum pCO2 < expected pCO2 - additional respiratory
alkalosis and vice versa
23. EXAMPLE
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
Winter’s formula : 17= 1.5 (7) +8 ±2 = 18.5(16.5 –
20.5)
So correct compensation so there is only one
disorder Primary metabolic
24. Step 5: Calculate the anion gap
AG used to assess acid-base status esp in D/D of
met acidosis
AG & HCO3
- used to assess mixed acid-base
disorders
AG based on principle of electroneutrality:
Total Serum Cations = Total Serum Anions
Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4
+ Protein + Organic Acids)
Na + UC = HCO3 + Cl + UA
Na – (HCO3 + Cl) = UA – UC
Na – (HCO3 + Cl) = AG
Normal =12 ± 2
25. Contd…
AG corrected = AG + 2.5[4 – albumin]
If there is an anion Gap then calculate the
Delta/delta gap (step 6) to determine
additional hidden nongap metabolic acidosis
or metabolic alkalosis
If there is no anion gap then start analyzing
for non-anion gap acidosis
26. EXAMPLE
Calculate Anion gap
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin
2.
AG = Na – Cl – HCO3 (normal 12 ± 2)
123 – 97 – 7 = 19
AG corrected = AG + 2.5[4 – albumin]
= 19 + 2.5 [4 – 2]
= 19 + 5 = 24
27. Step 6: Calculate Delta Gap
Delta gap = (actual AG – 12) + HCO3
Adjusted HCO3 should be 24 (+_ 6) {18-30}
If delta gap > 30 -> additional metabolic alkalosis
If delta gap < 18 -> additional non-gap metabolic
acidosis
If delta gap 18 – 30 -> no additional metabolic
disorders
28. EXAMPLE : Delta Gap
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin
4.
Delta gap = (actual AG – 12) + HCO3
(19-12) +7 = 14
Delta gap < 18 -> additional non-gap
metabolic acidosis
So Metabolic acidosis anion and non anion
gap
30. EXAMPLE: WHY ANION GAP?
65yo M with CKD presenting with nausea, diarrhea and
acute respiratory distress
ABG :ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
So for our patient for anion gap portion its due to
BUN of 119 UREMIA
But would still check lactic acid
31. Nongap metabolic acidosis
For non-gap metabolic acidosis, calculate the urine anion
gap
URINARY AG
Total Urine Cations = Total Urine Anions
Na + K + (NH4 and other UC) = Cl + UA
(Na + K) + UC = Cl + UA
(Na + K) – Cl = UA – UC
(Na + K) – Cl = AG
Distinguish GI from renal causes of loss of HCO3 by estimating
Urinary NH4+ .
Hence a -ve UAG (av -20 meq/L) seen in GI, while +ve value (av
+23 meq/L) seen in renal problem.
UAG = UNA + UK – UCL
Kaehny WD. Manual of Nephrology 2000; 48-62
32. EXAMPLE : NON ANION GAP ACIDOSIS
65yo M with CKD presenting with nausea, diarrhea and
acute respiratory distress
ABG :ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 14
AG = 123 – 97-14 = 12
Most likely due to the diarrhea
33. Causes of nongap metabolic acidosis - DURHAM
Diarrhea, ileostomy, colostomy, enteric fistulas
Ureteral diversions or pancreatic fistulas
RTA type I or IV, early renal failure
Hyperailmentation, hydrochloric acid administration
Acetazolamide, Addison’s
Miscellaneous – post-hypocapnia, toulene, sevelamer, cholestyramine ingestion
34. Metabolic alkalosis
Calculate the urinary chloride to differentiate saline
responsive vs saline resistant
Must be off diuretics in order to interpret urine chloride
Saline responsive UCL<25 Saline-resistant UCL >25
Vomiting If hypertensive: Cushings, Conn’s, RAS,
renal failure with alkali administartion
NG suction If not hypertensive: severe hypokalemia,
hypomagnesemia, Bartter’s, Gittelman’s,
licorice ingestion
Over-diuresis Exogenous corticosteroid administration
Post-hypercapnia
35. Respiratory Alkalosis
Causes of Respiratory Alkalosis
Anxiety, pain, fever
Hypoxia, CHF
Lung disease with or without hypoxia – pulmonary embolus, reactive
airway, pneumonia
CNS diseases
Drug use – salicylates, catecholamines, progesterone
Pregnancy
Sepsis, hypotension
Hepatic encephalopathy, liver failure
Mechanical ventilation
Hypothyroidism
High altitude
36. Case1.
7.27/58/60 on 5L, HCO3
- 26, anion gap is
12, albumin is 4.0
1. pH= Acidemia (pH < 7.4)
2.CO2= Acid (CO2>40)
Opposite direction so Primary disturbance =
Respiratory Acidosis
3 &4: Compensation : Acute or chronic? ACUTE
CO2 has increased by (58-40)=18
If chronic the pH will decrease 0.05 (0.003 x 18 = 0.054)
pH would be 7.35
If acute the pH will decrease 0.14 (0.008 x 18 = 0.144)
pH would be 7.26.
37. Contd.
5: Anion gap –N/A
6: There is an acute respiratory acidosis, is there
a metabolic problem too?
ΔHCO3
- = 1 mEq/L↑/10mmHg↑pCO2
The pCO2 is up by 18 so it is expected that the HCO3
-
will go up by 1.8. Expected HCO3
- is 25.8, compared to
the actual HCO3
- of 26, so there is no additional
metabolic disturbance.
Dx-ACUTE RESPIRATORY ACIDOSIS
38. Case.2
7.54/24/99 on room air, HCO3
- 20, anion
gap is 12, albumin is 4.0.
1: pH= Alkalemia (pH > 7.4)
2.CO2= Base (CO2<40)
pH & pCO2 change in opposite Direction So
Primary disturbance = Respiratory Alkalosis
3 &4: Compensation ? acute or chronic? ACUTE
ΔCO2 =40-24=16
If chronic the pH will increase 0.05 (0.003 x 16 = 0.048)
pH would be 7.45
If acute the pH will increase 0.13(0.008 x 16 = 0.128)
pH would be 7.53
39. Contd…
5:Anion gap – N/A
6: There is an acute respiratory alkalosis, is there
a metabolic problem too?
ΔHCO3
- = 2 mEq/L↓/10mmHg↓pCO2
The pCO2 is down by 16 so it is expected that the
HCO3
- will go down by 3.2. Expected HCO3
- is 20.8,
compared to the actual HCO3
- of 20, so there is no
additional metabolic disturbance.
Dx-ACUTE RESPIRATORY ALKALOSIS
40. Case-3
7.58/55/80 on room air, HCO3
- 46, anion gap is
12, albumin is 4.0. Ucl -20
1: pH= Alkalemia(pH > 7.4)
2:CO2= Acid (CO2>40)
Same direction so Primary disturbance = Metabolic
Alkalosis
3&4: Compensation:
∆ pCO2=0.7 x ∆ HCO3
-
The HCO3
- is up by 22.CO2 will increase by 0.7x22 = 15.4.
Expected CO2 is 55.4, compared to the actual CO2 of 55,
therefore there is no additional respiratory disturbance.
41. contd
5: No anion gap is present; and no adjustment
needs to be made for albumin. Metabolic
Alkalosis
Urinary chloride is 20 meq/l (< 25 meq/l)so
chloride responsive, have to treat with Normal
saline.
Dx-METABOLIC ALKALOSIS
42. Case-4
7.46/20/80 on room air, HCO3
- 16, anion
gap = 12, albumin = 4.0
1: pH = Alkalemia (pH > 7.4)
2:CO2 = Base (CO2<40)
So Primary disturbance = Respiratory Alkalosis
3 &4: Compensation? acute or chronic? Chronic
ΔCO2 =40-20= 20.
If chronic the pH will increase 0.06 (0.003 x 20 = 0.06)
pH would be 7.46.
If acute the pH will increase 0.16 (0.008 x 20 = 0.16) pH
would be 7.56.
43. Contd….
5: Anion gap – N/A
6: There is a chronic respiratory alkalosis, is there
a metabolic problem also?
Chronic: ΔHCO3
- = 4 mEq/L↓/10mmHg↓pCO2
The pCO2 is down by 20 so it is expected that the
HCO3
- will go down by 8. Expected HCO3
- is 16, therefore
there is no additional metabolic disorder.
Dx-CHRONIC RESPIRATORY ALKALOSIS
44. Case-5
7.19/35/60 on 7L, HCO3
- 9, anion gap = 18,
albumin = 4.0
1: pH = Acidemia (pH < 7.4)
2:CO2= Base (CO2<40)
So Primary disturbance: Metabolic Acidosis
3&4: Compensation ?
∆ pCO2=1.2 x ∆ HCO3
-
CO2 will decrease by 1.2 (∆HCO3
-) 1.2 (24-9) 18. 40 – 18=
22 Actual CO2 is higher than expected Respiratory Acidosis
5: Anion Gap = 18 (alb normal so no correction necessary)
45. Contd…..
6: Delta Gap:
Delta gap = (actual AG – 12) + HCO3
= (18-12) + 9
= 6 + 9 = 15 which is<18 Non-AG Met Acidosis
Dx-ANION GAP METABOLIC ACIDOSIS with NON-ANION GAP
METABOLIC ACIDOSIS with RESPIRATORY ACIDOSIS
46. Case-6
7.54/80/65 on 2L, HCO3
- 54, anion gap
12,albumin = 4.0 , Ucl 40 meq/l
1: pH = Alkalemia (pH > 7.4)
2:CO2= Acid (CO2>40)
So Primary disturbance: Metabolic Alkalosis
3&4: Compensation?
∆ pCO2=0.7 x ∆ HCO3
-
CO2 will increase by 0.7 (∆HCO3
-) 0.7 (54-24) 2140
+ 21 = 61 Actual CO2 is higher than expected
Respiratory Acidosis
47. Contd….
5: Anion Gap = 12 (alb normal so no correction
necessary)
Urinary chloride is 40 meq/l (> 25 meq/l)so
chloride resistant. So treatment would be disease
specific and repletion of potassium
Dx-METABOLIC ALKALOSIS with RESPIRATORY
ACIDOSIS
48. Case-7
7.6/30/83 on room air, HCO3
- 28, anion gap = 12, albumin =
4.0
1: pH = Alkalemia (pH > 7.4)
2:CO2= Base (CO2<40)
SoPrimary Disturbance: Metabolic Alkalosis
3&4: Compensation ?
∆ pCO2=0.7 x ∆ HCO3
-
CO2 will increase by 0.7 (∆HCO3
-) 0.7 (28-24) 2.8 40 + 2.8 = 42.8
Actual CO2 is lower than expected Respiratory Alkalosis
Anion Gap = 12 (alb normal so no correction necessary)
See urinary chloride for further Dx.
Dx-METABOLIC ALKALOSIS with RESPIRATORY ALKALOSIS
49. Case-8
A 50 yo male present with sudden onset of SOB with
following ABG 7.25/46/78 on 2L, HCO3
- 20, anion gap = 10,
albumin = 4.0
1: pH = Acidemia (pH < 7.4)
2:CO2= Acid (CO2>40)
So Primary disturbance: Respiratory Acidosis
3 &4: If respiratory disturbance is it acute or chronic?
ACUTE
∆ CO2 = 46-40= 6
If chronic the pH will decrease 0.02 (0.003 x 6 = 0.018)
pH would be 7.38
If acute the pH will decrease 0.05 (0.008 x 6 = 0.048)
pH would be 7.35.
50. Contd…
Anion Gap = 10 (alb normal so no correction necessary)
6: There is an acute respiratory acidosis, is there a metabolic
problem too?
∆ HCO3
- = 1 mEq/L↑/10mmHg↑pCO2
The HCO3
- will go up 1mEq/L for every 10mmHg the pCO2goes up
above 40
The pCO2 is up by 6 so it is expected that the HCO3
- will go up by 0.6.
Expected HCO3
- is 24.6, compared to the actual HCO3
- of 20. Since the
HCO3
- is lower than expected Non-Anion Gap Metabolic Acidosis
(which we suspected).
Dx-RESPIRATORY ACIDOSIS with NON-ANION GAP
METABOLIC ACIDOSIS
51. Case-9
7.15/22/75 on room air, HCO3
- 9, anion gap = 10, albumin =
2.0
1: pH = Acidemia (pH < 7.4)
2:CO2= Base (CO2<40)
So Primary disturbance: Metabolic Acidosis
3&4:∆ Compensation ?
pCO2=1.2 x ∆ HCO3
-
Expected pCO2 = 1.2 x ∆ HCO3
- 1.2 (24 -9) 1.2 (15)
18. The expected pCO2is 22mmHg. The actual pCO2 is
22, which is expected, so there is no concomitant
disorder.
52. Contd….
5: Anion Gap = 10
AGc = 10 + 2.5(4-2) = 15 Anion Gap Metabolic
Acidosis
6: Delta Gap:
Delta gap = (actual AG – 12) + HCO3
= (15-12) + 9
= 3+ 9 = 12 which is<18 Non-AG Met
Acidosis
Dx-ANION GAP METABOLIC ACIDOSIS with NON-ANION
GAP METABOLIC ACIDOSIS
Editor's Notes
Consumptiom of O2 & Production of CO2 continues after blood drawn into syringe
Iced Sample maintains values for 1-2 hours
Uniced sample quickly becomes invalid
No consensus regarding reporting of ABG values esp pH & PCO2 after doing ‘temp correction’
? Interpret values measured at 37 C:
Most clinicians do not remember normal values of pH & PCO2 at temp other than 37C
In pts with hypo/hyperthermia, body temp usually changes with time (per se/effect of rewarming/cooling strategies) – hence if all calculations done at 37 C easier to compare
Values other than pH & PCO2 do not change with temp
? Use Nomogram to convert values at 37C to pt’s temp
Some analysers calculate values at both 37C and pt’s temp automatically if entered
Pt’s temp should be mentioned while sending sample & lab should mention whether values being given in report at 37 C/pts actual temp
25% lower values if 1ml sample taken in 10 ml syringe (0.25 ml heparin in needle)
Syringes must be > 50% full with blood sample
Min friction of barrel with syringe wall
Usually no need to ‘pull back’ barrel – less chance of air bubbles entering syringe
Small air bubbles adhere to sides of plastic syringes – difficult to expel
Though glass syringes preferred,
Std HCO3-: HCO3- levels measured in lab after equilibration of blood PCO2 to 40 mm Hg ( routine measurement of other serum electrolytes)
Actual HCO3-: HCO3- levels calculated from pH & PCO2 directly
Reflection of non respiratory (metabolic) acid-base status.
Does not quantify degree of abnormality of buffer base/actual buffering capacity of blood.
Memorize these values .
Just read off slides.
Just read the steps off the slides. Quick overview .
Determine if you have acidemia or alkalemia based on the PH
Here we determine primary disorder is it respiratory or metabolic
Check to see if there is appropriate compensation for the primary disorder in order to figure if its simple or mixed disorder
Then analyze if this is an acute event or chronic
Always look to see if there is an anion gap
Due the other calculation depending on the underlying primary source . Such as if AG acidosis check to see if there is also a Delta gap to see if there is also non-anion gap present
And lastly then come up with a DDX
Just go over the table
Then point out the arrows :A quick trick is to determine respiratory versus metabolic is : If PH and PCO2 are going in the opposite direction : then its respiratory, If PH and PCO2 are going in same directions then its metabolic.
- Be careful with the mixed disorders using the trick.
You need to memorize these and know it by heart . Then quickly go over the changes
Then summarize : The easiest one is that for acute situations for every change of 10 in the PCO2 there is should be a change of 0.08 in PH and in chronic situation there should be a change of 0.03 .
If there is a different change then know that there is most likely a mixed disorder
In ac resp alkalosis, imm response to fall in CO2 (& H2CO3) release of H+ by blood and tissue buffers react with HCO3- fall in HCO3- (usually not less than 18) and fall in pH
Cellular uptake of HCO3- in exchange for Cl-
Steady state in 15 min - persists for 6 hrs
After 6 hrs kidneys increase excretion of HCO3- (usually not less than 12-14)
Steady state reached in 11/2 to 3 days.
Timing of onset of hypocapnia usually not known except for pts on MV. Hence progression to subac and ch resp alkalosis indistinct in clinical practice
Imm response to rise in CO2 (& H2CO3) blood and tissue buffers take up H+ ions, H2CO3 dissociates and HCO3- increases with rise in pH.
Steady state reached in 10 min & lasts for 8 hours.
PCO2 of CSF changes rapidly to match PaCO2.
Hypercapnia that persists > few hours induces an increase in CSF HCO3- that reaches max by 24 hr and partly restores the CSF pH.
After 8 hrs, kidneys generate HCO3-
Steady state reached in 3-5 d
Metabolic acidosis is the disorder you will mostly encounter in the hospital.
You must memorize Winter’s formula
Winter’s formula calculates the expected pCO2 in the setting of metabolic acidosis.
If the serum pCO2 > expected pCO2 then there is additional respiratory acidosis in which the etiology needs to also be determined.
Always calculate the AG . (fyi most BMP ordered calculate the gap for you but need to memorize the formula)
Don’t forget to look at albumin and adjust the calculated gap. If albumin is less than 4 then add 2.5 to your gap for every decrease of 1
Delta/Delta gap needs to be calculated to see if there is other underlying acidosis/alkolosis that are present
Must memorize how to calculate the delta gap
Just read off the slide
Go over the table
One thing to watch out for is Toluene (initially high gap, subsequent excretion of metabolites normalizes gap)
Calculate osmol gap to determine if osmotically active ingestions (methanol, paraldehyde) are the cause of the gap metabolic acidosis. Other ingestions are toluene, isopropyl alcohol.
- Go over the table
- Most common cause in the hospital is IV fluids and Diarrhea
For metabolic alkalosis , check urine cholride (must be off diuretics)
Urine chloride < 10 implies responsivenss to saline : extracelluar fluid volume depletion
Urine chloride >10 implies resistance to sailne : severe poatssium depletion , mineralcorticoid excees syndrome Etc
Read the chart then summarize
Can divide into three categories
1. systemic : (sepsis , asa , liver failure , endocrine , chf)
2. Central causes (respiratory center, ischmia , CNS tumor )
3. Lungs (pna, asthma , PE )
(Diabeticic ketoacidosis)
(secondary tochronic kidney disease or type IV Renal Tubular Acidosis (RTA 4)secondary to diabetic nephropathy),\
This problem is very complicated. Since the diabetic ketoacidosis is the presenting problem, it is therefore the primary disturbance. Presumably the CKD or RTA is a chronic issue that has been present for some time and is therefore, secondary
(secondary to a strep pneumoniaepneumonia – which probably triggered the DKA)
(secondary to contraction alkalosis from the furosemide)
(secondary to COPD)
(secondary to vomiting)
(secondary to pregnancy)
(This makes sense given the history of sudden onset of shortness of breath. Since the pH is lower than expected and the HCO3- is low, there is clearly a secondary metabolic acidosis. See below for clarification.)
(secondary to pulmonary edema)
(secondary to chronic kidney disease)
secondary to lactic acidosis from ischemic bowel)
(secondary to a Type IV Renal Tubular Acidosis from her Diabetes Mellitus)