Unit 4 Acid-Base Homeostasis

Total Page：16

File Type：pdf, Size：1020Kb

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. Fluid and electrolytes b. Renal disease c. Total parenteral nutrition d. Pulmonary disease.

Copy Link

Recommended publications

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.
[Show full text]
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.
[Show full text]
CHEM 301 Assignment #3
CHEM 301 Assignment #3 Provide solutions to the following questions in a neat and well organized manner. Clearly state assumptions and reference sources for any constants used. Due date: November 18th 1. Methane and carbon dioxide are produced under anaerobic conditions by the fermentation of organic matter, approximated by the following equation 2 {CH2O} CH4 + CO2 As gas bubbles are evolved at the sediment interface at 5 m depth and remain in contact with water at the sediment surface long enough so that equilibrium is attained. The total pressure at this depth is 148 kPa. If the pH is 8.20, calculate the total carbonate concentration in the interstitial water at 25oC. How would you expect your answer to change if these gas bubbles were present at 500 m depth? Strategy: The total pressure inside the gas bubble must be equal to the total pressure on the outside of the gas bubble (or else it would either explode or collapse). Furthermore, the total pressure inside that gas bubble is equal to the sum of the partial pressures of CH4 and CO2. We can then use the partial pressure of CO2 inside the gas bubble and the corresponding Henry’s law constant to calculate the concentration of aqueous CO2 at equilibrium. Given the pH of the solution and the expressions for Ka1 and Ka2, we can determine the concentration of HCO3- and 2- CO3 . (see textbook pgs 241-242; Chap 11, Q9) Solution: The total carbonate concentration is given by; 2- - 2- [CO3 ]T = [CO2(aq)] + [HCO3 ] + [CO3 ] From the pH speciation diagram (Fig.
[Show full text]
Arterial Blood Gases: Acid-Base Balance
EDUCATIONAL COMMENTARY – ARTERIAL BLOOD GASES: ACID-BASE BALANCE Educational commentary is provided through our affiliation with the American Society for Clinical Pathology (ASCP). To obtain FREE CME/CMLE credits click on Earn CE Credits under Continuing Education on the left side of the screen. **Florida licensees, please note: This exercise will appear in CE Broker under the specialty of Blood Gas Analysis. LEARNING OUTCOMES On completion of this exercise, the participant should be able to • identify the important buffering systems in the human body. • explain the Henderson-Hasselbalch equation and its relationship to the bicarbonate/carbonic acid buffer system. • explain the different acid-base disorders, causes associated with them, and compensatory measures. • evaluate acid-base status using patient pH and pCO2 and bicarbonate levels. Introduction Arterial blood gas values are an important tool for assessing oxygenation and ventilation, evaluating acid- base status, and monitoring the effectiveness of therapy. The human body produces a daily net excess of acid through normal metabolic processes: cellular metabolism produces carbonic, sulfuric, and phosphoric acids. Under normal conditions, the body buffers accumulated hydrogen ions (H+) through a variety of buffering systems, the respiratory center, and kidneys to maintain a plasma pH of between 7.35 and 7.45. This tight maintenance of blood pH is essential: even slight changes in pH can alter the functioning of enzymes, the cellular uptake and use of metabolites, and the uptake and release of oxygen. Although diagnoses are made by physicians, laboratory professionals must be able to interpret arterial blood gas values to judge the validity of the laboratory results they report.
[Show full text]
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.
[Show full text]
Relationship Between PCO 2 and Unfavorable Outcome in Infants With
nature publishing group Articles Clinical Investigation Relationship between PCO2 and unfavorable outcome in infants with moderate-to-severe hypoxic ischemic encephalopathy Krithika Lingappan1, Jeffrey R. Kaiser2, Chandra Srinivasan3, Alistair J. Gunn4; on behalf of the CoolCap Study Group BACKGROUND: Abnormal PCO2 is common in infants with term infants with HIE, both minimum and cumulative expo- hypoxic ischemic encephalopathy (HIE). The objective was to sure to hypocapnia in the first 12 h of the trial were associated determine whether hypocapnia was independently associated with death or adverse neurodevelopmental outcome (13). The with unfavorable outcome (death or severe neurodevelopmen- dose–response relationship between PCO2 and outcome for tal disability at 18 mo) in infants with moderate-to-severe HIE. infants with moderate-to-severe HIE is unknown. METHODS: This was a post hoc analysis of the CoolCap Study The risk of developing hypocapnia or hypercapnia may be in which infants were randomized to head cooling or standard affected by severity of brain injury, intensity and duration of care. Blood gases were measured at prespecified times after newborn resuscitation, timing after the primary injury, and/or randomization. PCO2 and follow-up data were available for 196 response to metabolic acidosis. Thus, in this secondary analy- of 234 infants. Analyses were performed to investigate the rela- sis of the CoolCap Study (14), we sought to confirm the obser- tionship between hypocapnia in the first 72 h after randomiza- vation that
[Show full text]
The Basics of Ventilator Management Overview How We Breath
3/23/2019 The Basics of Ventilator Management What are we really trying to do here Peter Lutz, MD Pulmonary and Critical Care Medicine Pulmonary Associates, Mobile, Al Overview • Approach to the physiology of the lung and physiological goals of mechanical Ventilation • Different Modes of Mechanical Ventilation and when they are indicated • Ventilator complications • Ventilator Weaning • Some basic trouble shooting How we breath http://people.eku.edu/ritchisong/301notes6.htm 1 3/23/2019 How a Mechanical Ventilator works • The First Ventilator- the Iron Lung – Worked by creating negative atmospheric pressure around the lung, simulating the negative pressure of inspiration How a Mechanical Ventilator works • The Modern Ventilator – The invention of the demand oxygen valve for WWII pilots if the basis for the modern ventilator https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcRI5v-veZULMbt92bfDmUUW32SrC6ywX1vSzY1xr40aHMdsCVyg6g How a Mechanical Ventilator works • The Modern Ventilator – How it works Inspiratory Limb Flow Sensor Ventilator Pressure Sensor Expiratory Limb 2 3/23/2019 So what are the goals of Mechanical Ventilation • What are we trying to control – Oxygenation • Amount of oxygen we are getting into the blood – Ventilation • The movement of air into and out of the lungs, mainly effects the pH and level of CO 2 in the blood stream Lab Oxygenation Ventilation Pulse Ox Saturation >88-90% Arterial Blood Gas(ABG) Po 2(75-100 mmHg) pCO 2(40mmHg) pH(~7.4) Oxygenation How do we effect Oxygenation • Fraction of Inspired Oxygen (FIO 2) – Percentage of the gas mixture given to the patient that is Oxygen • Room air is 21% • On the vent ranges from 30-100% • So if the patient’s blood oxygen levels are low, we can just increase the amount of oxygen we give them 3 3/23/2019 How do we effect Oxygenation • Positive End Expiratory Pressure (PEEP) – positive pressure that will remains in the airways at the end of the respiratory cycle (end of exhalation) that is greater than the atmospheric pressure in mechanically ventilated patients.
[Show full text]
Lecture-1 Keto Acidosis, Bovine Ketosis, Ovine Pregnancy Toxemia
Lecture-1 Keto acidosis Ketoacidosis is a metabolic acidosis due to an excessive blood concentration of ketone bodies (acetone, acetoacetate and beta-hydroxybutyrate). Ketone bodies are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. The abnormal accumulation of ketones in the body occurs due to excessive breakdown of fats in deficiency or inadequate use of carbohydrates. It is characterized by ketonuria, loss of potassium in the urine, and a fruity odor of acetone on the breath. Untreated, ketosis may progress to ketoacidosis, coma, and death. This condition is seen in starvation, occasionally in pregnancy if the intake of protein and carbohydrates is inadequate, and most frequently in diabetes mellitus. Different Types of Ketoacidosis Diabetes Keto Acidosis (DKA): Due to lack of insulin glucose uptake and metabolism by cells is decrased.Fatty acid catabolism increased in resulting in excess production of ketone bodies. Starvation Ketosis: Starvation leads to hypoglycemia as there is little or no absorption of glucose from intestine and also due to depletion of liver glycogen. In Fatty acid oxidation leads to excess ketone body. Bovine Ketosis Introduction Bovine ketosis occurs in the high producing dairy cows during the early stages of lactation, when the milk production is generally the highest. Abnormally high levels of the ketone bodies, acetone, acetoacetic and beta-hydroxy butyric acid and also iso- propanol appear in blood, urine and in milk. The alterations are accompanied by loss of appetite , weight loss, decrease in milk production and nervous disturbances. Hypoglycemia (starvation) is a common finding in bovine ketosis and in ovine pregnancy toxemia.
[Show full text]
Diabetic Ketoalkalosis in Children and Adults
Original Article Diabetic Ketoalkalosis in Children and Adults Emily A. Huggins, MD, Shawn A. Chillag, MD, Ali A. Rizvi, MD, Robert R. Moran, PhD, and Martin W. Durkin, MD, MPH and DR are calculated because the pH and bicarbonate may be near Objectives: Diabetic ketoacidosis (DKA) with metabolic alkalosis normal or even elevated. In addition to having interesting biochemical (diabetic ketoalkalosis [DKALK]) in adults has been described in the features as a complex acid-base disorder, DKALK can pose diagnostic literature, but not in the pediatric population. The discordance in the and/or therapeutic challenges. change in the anion gap (AG) and the bicarbonate is depicted by an Key Words: delta ratio, diabetic ketoacidosis, diabetic ketoalkalosis, elevated delta ratio (DR; rise in AG/drop in bicarbonate), which is metabolic alkalosis normally approximately 1. The primary aim of this study was to de- termine whether DKALK occurs in the pediatric population, as has been seen previously in the adult population. The secondary aim was iabetic ketoacidosis (DKA), a common and serious dis- to determine the factors that may be associated with DKALK. Dorder that almost always results in hospitalization, is de- Methods: A retrospective analysis of adult and pediatric cases with a ﬁned by the presence of hyperglycemia, reduced pH, metabolic 1 primary or secondary discharge diagnosis of DKA between May 2008 and acidosis, elevated anion gap (AG), and serum or urine ketones. August 2010 at a large urban hospital was performed. DKALK was as- In some situations, a metabolic alkalosis coexists with DKA sumedtobepresentiftheDRwas91.2 or in cases of elevated bicarbonate.
[Show full text]
Acid-Base Physiology & Anesthesia
ACID-BASE PHYSIOLOGY & ANESTHESIA Lyon Lee DVM PhD DACVA Introductions • Abnormal acid-base changes are a result of a disease process. They are not the disease. • Abnormal acid base disorder predicts the outcome of the case but often is not a direct cause of the mortality, but rather is an epiphenomenon. • Disorders of acid base balance result from disorders of primary regulating organs (lungs or kidneys etc), exogenous drugs or fluids that change the ability to maintain normal acid base balance. • An acid is a hydrogen ion or proton donor, and a substance which causes a rise in H+ concentration on being added to water. • A base is a hydrogen ion or proton acceptor, and a substance which causes a rise in OH- concentration when added to water. • Strength of acids or bases refers to their ability to donate and accept H+ ions respectively. • When hydrochloric acid is dissolved in water all or almost all of the H in the acid is released as H+. • When lactic acid is dissolved in water a considerable quantity remains as lactic acid molecules. • Lactic acid is, therefore, said to be a weaker acid than hydrochloric acid, but the lactate ion possess a stronger conjugate base than hydrochlorate. • The stronger the acid, the weaker its conjugate base, that is, the less ability of the base to accept H+, therefore termed, ‘strong acid’ • Carbonic acid ionizes less than lactic acid and so is weaker than lactic acid, therefore termed, ‘weak acid’. • Thus lactic acid might be referred to as weak when considered in relation to hydrochloric acid but strong when compared to carbonic acid.
[Show full text]
Diabetic Ketoacidosis: Evaluation and Treatment DYANNE P
Diabetic Ketoacidosis: Evaluation and Treatment DYANNE P. WESTERBERG, DO, Cooper Medical School of Rowan University, Camden, New Jersey Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitro- gen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocar- diography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in chil- dren. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symp- toms to prevent it.
[Show full text]
BLOOD GAS ANALYSIS Deorari , AIIMS 2008
Deorari , AIIMS 2008 BLOOD GAS ANALYSIS Deorari , AIIMS 2008 Contents 1. Introduction, indications and sources of errors 2. Terminology and normal arterial blood gases 3. Understanding the print outs 4. Details about (i) pH (ii) Oxygenation, oxygen saturation, oxygen content, alveolar gas equation, indices of oxygenation (iii) Carbon dioxide transport, Pco2 total CO2 content, and bicarbonate levels (iv) Base excess and buffer base 5. Simple and mixed disorders 6. Compensation mechanisms 7. Anion Gap 8. Approach to arterial blood gases and exercises 9. Arterial blood gases decision tree 10. Practical tips for sampling for ABG. 2 Deorari , AIIMS 2008 Abbreviations ABE Actual base excess ABG Arterial blood gas AaDO2 Alveolar to arterial oxygen gradient Baro/PB Barometric pressure BB Buffer base BE Base excess BEecf Base excess in extracellular fluid BPD Bronchopulmonary dysplasia CH+ Concentration of hydrogen ion CO2 Carbon dioxide ECMO Extra corporeal membrane oxygenation FiO2 Fraction of inspired oxygen HCO3 Bicarbonate H2CO3 Carbonic acid MAP Mean airway pressure O2CT Oxygen content of blood PaCO2 Partial pressure of carbon dioxide in arterial blood PaO2 Partial pressure of oxygen in arterial blood pAO2 Partial pressure of oxygen in alveoli pH2O Water vapour pressure PPHN Persistent pulmonary hypertension in newborn RBC Red blood corpuscles 3 Deorari , AIIMS 2008 RQ Respiratory quotient Sat Saturation SBE Standard base excess - St HCO 3/SBC Standard bicarbonate TCO2 Total carbon dioxide content of blood THbA Total haemoglobin concentration UAC Umbilical artery catheter 4 Deorari , AIIMS 2008 The terminology of arterial blood gas (ABG) is complex and confusing. It is made worse by the printouts generated by recent microprocessors.
[Show full text]