DOCSLIB.ORG

Respiratory Or Metabolic Objectives Respiratory Acidosis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Respiratory or Metabolic Acidosis or Alkalosis Objectives • Discuss causes of respiratory and metabolic acid base disturbances. • Identifyyp pH values, CO2 values and HCO3 values in acid base imbalances. • Identify the acid base imbalance based on clinical conditions. • Define supportive treatment of acid base disturbance. Respiratory acidosis. 20 3 1 Causes Respiratory Acidosis • Any condition that impairs pulmonary ventilation and the removal of CO2. Leads to an increase in CO2 circulating in the blood.. – respiratory depression – respiratory arrest – Medications (narcotics) – cardiac arrest – neuromuscular impairment – chest wall injury - flail chest, pneumothorax – pulmonary - obstruction, COPD, asthma, pulmonary edema S/S Respiratory Acidosis • SOB, chronic cough, or wheezing • Confusion, irritability, or lethargy Respiratory Acidosis • Treatment – Improve ventilation • assist ventilation •addseminister oxygen(hypoxemia leads to acidosis) – Consider causes and initiate treatment • Bronchodilators • narcan 2 Respiratory acidosis. 20 3 Metabolic acidosis. 20 3 Metabolic Acidosis • Four common forms of metabolic acidosis – Lactic acidosis – Diabetic ketoacidosis – Renal failure – Diarrhea – Ingestion of toxins 3 S/S Metabolic Acidosis • Confusion, lethargy, stupor or coma • Kussmaul’s respiration, deep, rapid respiration • Dysrhythmia’s Lactic Acidosis • Lactic acid is produced when a large number of cells are inadequately perfused with oxygen, anaerobic metabolism. – The end product of anaerobic metabolism is lactic acid. • Causes of Lactic Acidosis – Seizure – ischemia to large muscles or organs – circulatory failure – shock S/S Lactic acidosis • Cardiovascular compromise: – Cyanosis, cold extremities, tachycardia, hypotension • Dehydration – Thirsty, dry oral mucosa, warm, dry skin • Hyperventilation • Lethargy, stupor or coma • Abdominal pain, vomiting 4 Lactic Acidosis • Treatment – reestablish tissue perfusion and cardiac output – ventilation – rehydration to support circulation – sodium bicarbonate administration if the patient is in cardiac arrest Diabetic Ketoacidosis (DKA) • Usually a complication of diabetes. • Insulin is needed for cells to metabolize glucose for immediate use, or store it in the liver for future use. • When the cells don’t have glucose available the cells use fatty acids for energy. • When the fatty acids breakdown they produce ketones, a strong acid. • The acidosis results when a patient fails to take adequate insulin or when the need for insulin increases(infection, trauma). Diabetic Ketoacidosis • The respiratory system will respond by increasing rate and depth of ventilation. (Kussmaul) Increasing the amount of CO2 being blown off in an attempt to bring the pH within normal range. • Treatment – Administration of normal saline for volume replacement – Administration of insulin 5 Renal Failure • The kidneys help maintain acid base balance by reabsorbing bicarbonate or excreting hydrogen ions. Renal failure affects the kidneys ability to function. – Acidosis can result because the kidneys are unable to excrete the excess H+ ions that are produced by normal metabolism and ammonia is not being excreted. – The bicarb buffer system is disrupted because the kidneys are not dumping HCO3 back into the blood stream. Ingestion of Toxins • Causes of metabolic acidosis – Ingestion of: Ethylene glycol(antifreeze), methanol(windshield washer fluid), salicylate(aspirin) • Treatment – GI evacuation – Hemodialysis –Diuresis – Hydration to promote excretion – Antidote therapy Metabolic acidosis. 20 3 6 Respiratory alkalosis. 1 S/S Respiratory Alkalosis • Muscle twitching, tingling and numbness of the fingers • Nervousness, irritability , agitation • Convulsions, coma Respiratory Alkalosis • Treatment – place patient on low concentration oxygen – provide calming measures – treat underlying problem 7 Metabolic alkalosis. Metabolic Alkalosis (rare) •Causes – Ingestion of large amounts of absorbable base sodium bicarbonate or calcium carbt(tid)bonate(antacids) – Excessive IV administration of alkali(NaHCO3) – Diuretic use(excrete too much Hydrogen ion) – Vomiting(gastric acid lost) – only initially as vomiting becomes severe dehydration develops and you see acidosis. Metabolic Alkalosis • Treatment – aimed at correcting the underlying condition – if volume depleted rehydrate 8 Arterial Blood Gas (ABG’s) • Blood gases measure the pH, O2, CO2 (acid) and HCO3 (base) content of the blood. • The test is used to evaluate respiratory diseases and conditions that affect the lungs. • The test also gives information on how well the kidneys are functioning. ABG’s • Normal Values at sea level: – PaO2 – 75-100mmhg – PaCO2 – 35-45mmhg – pH – 7.35-7.45 – HCO3 – 22-26meq/L Acid - Base If you have a CO2 of 55 What do you expect your pH to be? 9 Correct answer pH<7.35 What is the state of acid base balance? Correct answer Acidosis Is your patient in respiratory arrest or hyperventilating? Correct answer: Arrest Is this metabolic or respiratory acidosis? 10 Correct answer: Respiratory acidosis Acid - Base If you have a pH <7.35, what do you expect your CO2 to be? Correct answer: CO2 >45mmhg What is the state of acid base balance? 11 Correct answer: Acidosis Your patient is a diabetic, is this metabolic or respiratory acidosis? Correct answer: Metabolic acidosis Acid - Base You arrive to find your patient leaning forward breathing rapid c/o cramping and pain in fingers, and hands. What do you expect her pH to be? 12 Correct answer: pH >7.45 Is your patient in respiratory or metabolic alkalosis? Correct answer: Respiratory Why is she in respiratory alkalosis? Correct answer: Blowing off too much CO2 13 Acid - Base Your patient is in cardiac arrest. What do you expect the pH to be? Correct answer: pH <7.35 What is the acid base state of this patient? Correct answer: Acidosis Why is this patient acidotic? 14 Correct answer: Anaerobic metabolism with increased production of acids and no circulation for buffer systems to do their work, maintaining homeostasis. Is this patient in metabolic or respiratory acidosis? Correct answer: Metabolic and respiratory acidosis, because there is no circulation and no ventilation H2O HCO3 H2CO3 CO2 H+ O2 Cl O2 H+ CO2+H20 H2CO3 H+HCO3 H CO CO 2 3 Cl 2 H CO 2 3 H2O HCO 3 H2CO3 HCO3 + H2O H O2 Cl CO2 Angie Brindowski, RN, EMT P, MCEMS 15.
Recommended publications
  • Diabetic Ketoacidosis and Hyperosmolar BMJ: First Published As 10.1136/Bmj.L1114 on 29 May 2019

    Diabetic Ketoacidosis and Hyperosmolar BMJ: First Published As 10.1136/Bmj.L1114 on 29 May 2019

    STATE OF THE ART REVIEW Diabetic ketoacidosis and hyperosmolar BMJ: first published as 10.1136/bmj.l1114 on 29 May 2019. Downloaded from hyperglycemic syndrome: review of acute decompensated diabetes in adult patients Esra Karslioglu French,1 Amy C Donihi,2 Mary T Korytkowski1 1Division of Endocrinology and Metabolism, Department of ABSTRACT Medicine, University of Pittsburgh, Pittsburgh, PA, USA Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome (HHS) are life threatening 2University of Pittsburgh School of complications that occur in patients with diabetes. In addition to timely identification of the Pharmacy, Pittsburgh, PA, USA Correspondence to: M Korytkowski precipitating cause, the first step in acute management of these disorders includes aggressive [email protected] administration of intravenous fluids with appropriate replacement of electrolytes (primarily Cite this as: BMJ 2019;365:l1114 doi: 10.1136/bmj.l1114 potassium). In patients with diabetic ketoacidosis, this is always followed by administration Series explanation: State of the of insulin, usually via an intravenous insulin infusion that is continued until resolution of Art Reviews are commissioned on the basis of their relevance to ketonemia, but potentially via the subcutaneous route in mild cases. Careful monitoring academics and specialists in the US and internationally. For this reason by experienced physicians is needed during treatment for diabetic ketoacidosis and HHS. they are written predominantly by Common pitfalls in management include premature termination of intravenous insulin US authors therapy and insufficient timing or dosing of subcutaneous insulin before discontinuation of intravenous insulin. This review covers recommendations for acute management of diabetic ketoacidosis and HHS, the complications associated with these disorders, and methods for http://www.bmj.com/ preventing recurrence.
  • The History of Carbon Monoxide Intoxication

    The History of Carbon Monoxide Intoxication

    medicina Review The History of Carbon Monoxide Intoxication Ioannis-Fivos Megas 1 , Justus P. Beier 2 and Gerrit Grieb 1,2,* 1 Department of Plastic Surgery and Hand Surgery, Gemeinschaftskrankenhaus Havelhoehe, Kladower Damm 221, 14089 Berlin, Germany; fi[email protected] 2 Burn Center, Department of Plastic Surgery and Hand Surgery, University Hospital RWTH Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany; [email protected] * Correspondence: [email protected] Abstract: Intoxication with carbon monoxide in organisms needing oxygen has probably existed on Earth as long as fire and its smoke. What was observed in antiquity and the Middle Ages, and usually ended fatally, was first successfully treated in the last century. Since then, diagnostics and treatments have undergone exciting developments, in particular specific treatments such as hyperbaric oxygen therapy. In this review, different historic aspects of the etiology, diagnosis and treatment of carbon monoxide intoxication are described and discussed. Keywords: carbon monoxide; CO intoxication; COHb; inhalation injury 1. Introduction and Overview Intoxication with carbon monoxide in organisms needing oxygen for survival has probably existed on Earth as long as fire and its smoke. Whenever the respiratory tract of living beings comes into contact with the smoke from a flame, CO intoxication and/or in- Citation: Megas, I.-F.; Beier, J.P.; halation injury may take place. Although the therapeutic potential of carbon monoxide has Grieb, G. The History of Carbon also been increasingly studied in recent history [1], the toxic effects historically dominate a Monoxide Intoxication. Medicina 2021, 57, 400. https://doi.org/10.3390/ much longer period of time. medicina57050400 As a colorless, odorless and tasteless gas, CO is produced by the incomplete combus- tion of hydrocarbons and poses an invisible danger.
  • Acid-Base Abnormalities in Dogs with Diabetic Ketoacidosis: a Prospective Study of 60 Cases

    Acid-Base Abnormalities in Dogs with Diabetic Ketoacidosis: a Prospective Study of 60 Cases

    325 Acid-base abnormalities in dogs with diabetic ketoacidosis: a prospective study of 60 cases Distúrbios ácido-base em cães com cetoacidose diabética: estudo prospectivo de 60 casos Ricardo DUARTE1; Denise Maria Nunes SIMÕES1; Khadine Kazue KANAYAMA1; Márcia Mery KOGIKA1 1School of Veterinary Medicine and Animal Science, University of São Paulo, São Paulo-SP, Brazil Abstract Diabetic ketoacidosis (DKA) is considered a typical high anion gap metabolic acidosis due to the retention of ketoanions. The objective of this study was to describe the acid-base disturbances of dogs with DKA and further characterize them, according to their frequency, adequacy of the secondary physiologic response, and occurrence of mixed disturbances. Sixty dogs with DKA were enrolled in the study. Arterial blood pH and gas tensions, plasma electrolytes, serum b-hydroxybutyrate (b-OHB), glucose, albumin and urea concentrations were determined for all dogs included in the study. All dogs were evaluated individually and systematically by the traditional approach to the diagnosis of acid- base disorders. Most of the dogs had a high anion gap acidosis, with appropriated respiratory response (n = 18; 30%) or concurrent respiratory alkalosis (n = 14; 23%). Hyperchloremic acidosis with moderated to marked increases in b-OHB was observed in 18 dogs (30%) and 7 of these patients had concurrent respiratory alkalosis. Hyperchloremic acidosis with mild increase in b-OHB was observed in 6 dogs (10%). Four dogs (7%) had a high anion gap acidosis with mild increase in b-OHB and respiratory alkalosis. Most of dogs with DKA had a high anion gap acidosis, but mixed acid-base disorders were common, chiefly high anion gap acidosis and concurrent respiratory alkalosis, and hyperchloremic acidosis with moderated to marked increases in serum b-OHB.
  • Pathophysiology of Acid Base Balance: the Theory Practice Relationship

    Pathophysiology of Acid Base Balance: the Theory Practice Relationship

    Intensive and Critical Care Nursing (2008) 24, 28—40 ORIGINAL ARTICLE Pathophysiology of acid base balance: The theory practice relationship Sharon L. Edwards ∗ Buckinghamshire Chilterns University College, Chalfont Campus, Newland Park, Gorelands Lane, Chalfont St. Giles, Buckinghamshire HP8 4AD, United Kingdom Accepted 13 May 2007 KEYWORDS Summary There are many disorders/diseases that lead to changes in acid base Acid base balance; balance. These conditions are not rare or uncommon in clinical practice, but every- Arterial blood gases; day occurrences on the ward or in critical care. Conditions such as asthma, chronic Acidosis; obstructive pulmonary disease (bronchitis or emphasaemia), diabetic ketoacidosis, Alkalosis renal disease or failure, any type of shock (sepsis, anaphylaxsis, neurogenic, cardio- genic, hypovolaemia), stress or anxiety which can lead to hyperventilation, and some drugs (sedatives, opoids) leading to reduced ventilation. In addition, some symptoms of disease can cause vomiting and diarrhoea, which effects acid base balance. It is imperative that critical care nurses are aware of changes that occur in relation to altered physiology, leading to an understanding of the changes in patients’ condition that are observed, and why the administration of some immediate therapies such as oxygen is imperative. © 2007 Elsevier Ltd. All rights reserved. Introduction the essential concepts of acid base physiology is necessary so that quick and correct diagnosis can The implications for practice with regards to be determined and appropriate treatment imple- acid base physiology are separated into respi- mented. ratory acidosis and alkalosis, metabolic acidosis The homeostatic imbalances of acid base are and alkalosis, observed in patients with differing examined as the body attempts to maintain pH bal- aetiologies.
  • Cardiac Dysfunction and Lactic Acidosis During Hyperdynamic and Hypovolemic Shock

    Cardiac Dysfunction and Lactic Acidosis During Hyperdynamic and Hypovolemic Shock

    è - \-o(J THESIS FOR TIIE DEGREE OF DOCTOR OF MEDICINE CARDIAC DYSFUNCTION AND LACTIC ACIDOSIS DURING HYPERDYNAMIC AND HYPOVOLEMIC SHOCK DAVID JAMES COOPER DEPARTMENT OF ANAESTIIESIA AND INTENSIVE CARE FACULTY OF MEDICINE UNIVERSITY OF ADELAIDE Submitted: October,1995 Submitted in revised form: November, 1996 2 J TABLE OF CONTENTS Page 5 CH 1(1.1) Abstract (1.2) Signed statement (1.3) Authors contribution to each publication (1.4) Acknowledgments (1.5) Publications arising 9 CH2Introduction (2.1) Shock and lactic acidosis (2.2) Cardiac dysfunction and therapies during lactic acidosis (2.3) Cardiac dysfunction during hyperdynamic shock (2.4) Cardiac dysfunction during hypovolemic shock (2.5) Cardiac dysfunction during ionised hypocalcaemia l7 CH3 Methods (3. 1) Left ventricular function assessment - introduction (3.2) Left ventricular function assessment in an animal model 3.2.I Introduction 3.2.2 Anaesthesia 3.2.3 Instrumentation 3.2.4 Systolic left ventricular contractility 3.2.5 Left ventricular diastolic mechanics 3.2.6 Yentricular function curves 3.2.1 Limitations of the animal model (3.3) Left ventricular function assessment in human volunteers 3.3.7 Left ventricular end-systolic pressure measurement 3.3.2 Left ventricular dimension measurement 3.3.3 Rate corrected velocity of circumferential fibre shortening (v"¡.) 3.3.4. Left ventricular end-systolic meridional wall stress (o"r) 4 33 CH 4 Cardiac dysfunction during lactic acidosis (4.1) Introduction 4.7.1 Case report (4.2) Human studies 4.2.1 Bicarbonate in critically ill patients
  • Persistent Lactic Acidosis - Think Beyond Sepsis Emily Pallister1* and Thogulava Kannan2

    Persistent Lactic Acidosis - Think Beyond Sepsis Emily Pallister1* and Thogulava Kannan2

    ISSN: 2377-4630 Pallister and Kannan. Int J Anesthetic Anesthesiol 2019, 6:094 DOI: 10.23937/2377-4630/1410094 Volume 6 | Issue 3 International Journal of Open Access Anesthetics and Anesthesiology CASE REPORT Persistent Lactic Acidosis - Think beyond Sepsis Emily Pallister1* and Thogulava Kannan2 1 Check for ST5 Anaesthetics, University Hospitals of Coventry and Warwickshire, UK updates 2Consultant Anaesthetist, George Eliot Hospital, Nuneaton, UK *Corresponding author: Emily Pallister, ST5 Anaesthetics, University Hospitals of Coventry and Warwickshire, Coventry, UK Introduction • Differential diagnoses for hyperlactatemia beyond sepsis. A 79-year-old patient with type 2 diabetes mellitus was admitted to the Intensive Care Unit for manage- • Remember to check ketones in patients taking ment of Acute Kidney Injury refractory to fluid resusci- Metformin who present with renal impairment. tation. She had felt unwell for three days with poor oral • Recovery can be protracted despite haemofiltration. intake. Admission bloods showed severe lactic acidosis and Acute Kidney Injury (AKI). • Suspect digoxin toxicity in patients on warfarin with acute kidney injury, who develop cardiac manifes- The patient was initially managed with fluid resus- tations. citation in A&E, but there was no improvement in her acid/base balance or AKI. The Intensive Care team were Case Description asked to review the patient and she was subsequently The patient presented to the Emergency Depart- admitted to ICU for planned haemofiltration. ment with a 3 day history of feeling unwell with poor This case presented multiple complex concurrent oral intake. On examination, her heart rate was 48 with issues. Despite haemofiltration, acidosis persisted for blood pressure 139/32.
  • Evaluation and Treatment of Alkalosis in Children

    Evaluation and Treatment of Alkalosis in Children

    Review Article 51 Evaluation and Treatment of Alkalosis in Children Matjaž Kopač1 1 Division of Pediatrics, Department of Nephrology, University Address for correspondence Matjaž Kopač, MD, DSc, Division of Medical Centre Ljubljana, Ljubljana, Slovenia Pediatrics, Department of Nephrology, University Medical Centre Ljubljana, Bohoričeva 20, 1000 Ljubljana, Slovenia J Pediatr Intensive Care 2019;8:51–56. (e-mail: [email protected]). Abstract Alkalosisisadisorderofacid–base balance defined by elevated pH of the arterial blood. Metabolic alkalosis is characterized by primary elevation of the serum bicarbonate. Due to several mechanisms, it is often associated with hypochloremia and hypokalemia and can only persist in the presence of factors causing and maintaining alkalosis. Keywords Respiratory alkalosis is a consequence of dysfunction of respiratory system’s control ► alkalosis center. There are no pathognomonic symptoms. History is important in the evaluation ► children of alkalosis and usually reveals the cause. It is important to evaluate volemia during ► chloride physical examination. Treatment must be causal and prognosis depends on a cause. Introduction hydrogen ion concentration and an alkalosis is a pathologic Alkalosis is a disorder of acid–base balance defined by process that causes a decrease in the hydrogen ion concentra- elevated pH of the arterial blood. According to the origin, it tion. Therefore, acidemia and alkalemia indicate the pH can be metabolic or respiratory. Metabolic alkalosis is char- abnormality while acidosis and alkalosis indicate the patho- acterized by primary elevation of the serum bicarbonate that logic process that is taking place.3 can result from several mechanisms. It is the most common Regulation of hydrogen ion balance is basically similar to form of acid–base balance disorders.
  • ./0) (Mm...)Conte H

    ./0) (Mm...)Conte H

    BRITISH 511 Auc,.Auo. 25,25, 19621962 CARBON-MONOXIDE POISONIN6 MEDICAL JOURNAL Br Med J: first published as 10.1136/bmj.2.5303.511 on 25 August 1962. Downloaded from Case Reports HYPERVENTILATION IN Case 1.-A woman aged 61 was found with her head in CARBON-MONOXIDE POISONING a gas-oven. On admission to hospital she was deeply unconscious, with a generalized increase of muscle tone. BY pulse rate 140 a minute, and blood-pressure 110/70 mm. Hg. G. L. LEATHART, M.D., M.R.C.P. There was marked hyperventilation suggesting the possibility of coincident aspirin poisoning. A stomach wash-out, how- Nuflield Department of Industrial Health, the Medical ever, revealed no tablets, and a sample of urine collected School, King's College, Newcastle upon Tyne a few hours later contained no detectable salicylate. In 24 hours she had recovered fully and was transferred to a The recent revival of interest in the use of 5% or 7% mental hospital. carbogen in the treatment of carbon-monoxide poisoning Case 2.-An accountant aged 40 was working late in his has prompted the description of four unusual cases in office and was seen to be well at 9.15 p.m. At 8.45 a.m. which gross hyperventilation occurred. The investiga- the following morning he was found in the office with the tion of these cases was not very thorough, but such cases gas turned on but unlit. He was deeply unconscious with are seen so seldom that it is felt that even this incomplete strikingly deep and rapid respiration suggesting a condition report may be of value in stimulating further research.
  • Oral Rehydration of Adult Cattle Using Isotonic Solution of Sugar, Sodium Chloride and Potassium Chloride

    Oral Rehydration of Adult Cattle Using Isotonic Solution of Sugar, Sodium Chloride and Potassium Chloride

    Haryana Vet. (Dec., 2019) 58(2), 166-169 Research Article ABSTRACT Fig 2: Transmission electron photomicrograph of monocyte of dog Present study comprised of 72 crossbred cows (group I= 60 endometritic and group II=12 healthy) at 30±2days postpartum. The showing heterochromatin (a), euchromatin (b), cytoplasmic process (c), polymorphonuclear neutrophils (PMN) cell coun Vacuole and nuclear membrane. Uranyl acetate and lead citrate × 25500 Figure 1: Cyclic conditions for PCR profiling for detection of Salmonella genes ASSOCIATION OF SEMEN TRAITS IN CONSECUTIVE EJACULATES WITH FSH-β GENE POLYMORPHISM IN HOLSTEIN-FRIESIAN CROSSBRED BULLS FROM INDIA VIJAY KADAM, ABH trus synchronizathod that synchronizes ovulations is Corresponding author: [email protected] Fig. 1. Histogram depicting frequency distribution of animal named briefly as “Ovsynch” (Pursley et al., 1995). The right score of respondents Clinical Article study was aimed to evaluate the efficacy of different methods of estrus sync Fig. 1. Semilogarithmic plot of plasma concentration time profile of amoxicillin and cloxacillin following single dose (10 mg/kg) i.v. and i.m. administration in sheep (n=4) Haryana Vet. (Dec., 2019) 58(2), 166-169 Research Article 2003) which might lead to increased chances of urolith the time for the urinary tract to restore patency (Parrah, Haryana Vet. (March, 2020) 59(SI), 93-95 Short Communication Research Article formation. The increased hospital incidence can also be 2009) in conjugation with supportive treatments like COMPARATIVE EFFICACY OF SYNCHRONIZATION PROTOCOLS FOR IMPROVING attributed to the proximity of the clinic as well. According to peritoneal lavage, urinary acidifiers and urinary ORAL REHYDRATION OF ADULT CATTLE USING ISOTONIC SOLUTION OF SUGAR, FERTILITY IN POSTPARTUM CROSSBRED DAIRY COWS data published by Department ff Soil Science, Haryana, antiseptics.
  • TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam

    TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam

    TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam Slide 1: Hello, my name is Brenda Suh-Lailam. I am an Assistant Director of Clinical Chemistry and Mass Spectrometry at Ann & Robert H. Lurie Children’s Hospital of Chicago, and an Assistant Professor of Pathology at Northwestern Feinberg School of Medicine. Welcome to this Pearl of Laboratory Medicine on “Acid-Base Disorders.” Slide 2: During metabolism, the body produces hydrogen ions which affect metabolic processes if concentration is not regulated. To maintain pH within physiologic limits, there are several buffer systems that help regulate hydrogen ion concentration. For example, bicarbonate, plasma proteins, and hemoglobin buffer systems. The bicarbonate buffer system is the major buffer system in the blood. Slide 3: In the bicarbonate buffer system, bicarbonate, which is the metabolic component, is controlled by the kidneys. Carbon dioxide is the respiratory component and is controlled by the lungs. Changes in the respiratory and metabolic components, as depicted here, can lead to a decrease in pH termed acidosis, or an increase in pH termed alkalosis. Slide 4: Because the bicarbonate buffer system is the major buffer system of blood, estimation of pH using the Henderson-Hasselbalch equation is usually performed, expressed as a ratio of bicarbonate and carbon dioxide. Where pKa is the pH at which the concentration of protonated and unprotonated species are equal, and 0.0307 is the solubility coefficient of carbon dioxide. Four variables are present in this equation; knowing three variables allows for calculation of the fourth. Since pKa is a constant, and pH and carbon dioxide are measured during blood gas analysis, bicarbonate can, therefore, be determined using this equation.
  • Ethylene Glycol Ingestion Reviewer: Adam Pomerlau, MD Authors: Jeff Holmes, MD / Tammi Schaeffer, DO

    Ethylene Glycol Ingestion Reviewer: Adam Pomerlau, MD Authors: Jeff Holmes, MD / Tammi Schaeffer, DO

    Pediatric Ethylene Glycol Ingestion Reviewer: Adam Pomerlau, MD Authors: Jeff Holmes, MD / Tammi Schaeffer, DO Target Audience: Emergency Medicine Residents, Medical Students Primary Learning Objectives: 1. Recognize signs and symptoms of ethylene glycol toxicity 2. Order appropriate laboratory and radiology studies in ethylene glycol toxicity 3. Recognize and interpret blood gas, anion gap, and osmolal gap in setting of TA ingestion 4. Differentiate the symptoms and signs of ethylene glycol toxicity from those associated with other toxic alcohols e.g. ethanol, methanol, and isopropyl alcohol Secondary Learning Objectives: detailed technical/behavioral goals, didactic points 1. Perform a mental status evaluation of the altered patient 2. Formulate independent differential diagnosis in setting of leading information from RN 3. Describe the role of bicarbonate for severe acidosis Critical actions checklist: 1. Obtain appropriate diagnostics 2. Protect the patient’s airway 3. Start intravenous fluid resuscitation 4. Initiate serum alkalinization 5. Initiate alcohol dehydrogenase blockade 6. Consult Poison Center/Toxicology 7. Get Nephrology Consultation for hemodialysis Environment: 1. Room Set Up – ED acute care area a. Manikin Set Up – Mid or high fidelity simulator, simulated sweat if available b. Airway equipment, Sodium Bicarbonate, Nasogastric tube, Activated charcoal, IV fluid, norepinephrine, Simulated naloxone, Simulate RSI medications (etomidate, succinylcholine) 2. Distractors – ED noise For Examiner Only CASE SUMMARY SYNOPSIS OF HISTORY/ Scenario Background The setting is an urban emergency department. This is the case of a 2.5-year-old male toddler who presents to the ED with an accidental ingestion of ethylene glycol. The child was home as the father was watching him. The father was changing the oil on his car.
  • Unit 4 Acid-Base Homeostasis

    Unit 4 Acid-Base Homeostasis

    Vanderbilt University Medical Center Emergency General Surgery Service Surgical Residency Rotation and Curriculum UNIT 4 ACID-BASE HOMEOSTASIS UNIT OBJECTIVES: 1. Demonstrate an understanding of the biochemistry and physiology of acid-base homeostasis. 2. Demonstrate the ability to diagnose and effectively treat complex disorders of acid-base balance. COMPETENCY-BASED KNOWLEDGE OBJECTIVES: 1. Explain hydrogen ion biochemistry and physiology to include: a. The Henderson-Hasselbalch equation (1) Ventilatory component (pCO2) (2) Renal component (HCO3-) 2. Classify metabolic acidosis, including "anion gap" and hyperchloremic acidosis. 3. Identify specific causes of metabolic acidosis. 4. Given values for pH, pCO2, and HCO3-, distinguish between metabolic acidosis, respiratory acidosis, metabolic alkalosis, respiratory alkalosis, and mixed abnormalities; derive a differential diagnosis for each. 5. Predict the importance of primary diseases and their complications to the evaluation of patient risk for: a. Shock b. Bowel obstruction c. Sepsis 6. Analyze the acid-base problem and its cause in specific clinical situations, and determine an appropriate course of therapy for the following conditions: a. "Medical" problems such as: (1) Diabetic ketoacidosis (2) Lactic acidosis (3) Renal tubular acidosis (4) Renal insufficiency (5) Respiratory failure b. "Surgical" problems such as: (1) Gastric outlet obstruction (2) Fistulas (3) Shock COMPETENCY-BASED PERFORMANCE OBJECTIVES: 1. Diagnose and treat acid-base disturbances of all types. 2. Diagnose and treat complex and combined problems in acid-base disturbances as a component of overall care. 3. Manage complex situations in the intensive care unit where acid-base Vanderbilt University Medical Center Emergency General Surgery Service Surgical Residency Rotation and Curriculum abnormalities coexist with other metabolic derangements, including: a.