DOCSLIB.ORG

BRS Physiology Cases and Problems 2Nd Edition

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
BRS Physiology Cases and Problems 2Nd Edition 1 98 PHYSIOLOGY CASES AND PROBLEMS Case 34 Metabolic Acidosis: Diabetic Ketoacidosis David Mandel, who was diagnosed with type I diabetes mellitus when he was 12 years old (see Case 30), is now a third-year medical student. David's diabetes remained in control throughout middle and high school, college, and the first 2 years of medical school. However, when David started his surgery clerkship, his regular schedule of meals and insulin injections was completely disrupted. One morning, after a very late night in trauma surgery, David completely forgot to take his insulin! At 5 A.M., before rounds, he drank orange juice and ate two doughnuts. At 7 A.M., he drank more juice because he was very thirsty. He mentioned to the student next to him that he felt "strange" and that his heart was racing. At 9 A.M., he excused himself from the operating room because he thought he was going to faint. Later that morning, he was found unconscious in the call room. He was transferred immediately to the emergency department, where the information shown in Table 4-9 was obtained. TABLE 4-9 David's Physical Examination and Laboratory Values Blood pressure 90/40 Pulse rate 130/min Respirations 32/min, deep and rapid Plasma concentration Glucose 560 mg/dL Na. 132 mEq/L (normal, 140 mEq/L) 5.8 mhq/L (normal, 4.5 mEq/L) Cl- 96 mEq/L (normal, 105 mEq/L) HCO3 8 mEq/L (normal, 24 mEq/L) Ketones (normal, none) Arterial blood P02 112 mm Hg (normal, 100 mm Hg) Pco2 20 mm Hg (normal, 40 mm Hg) pH 7.22 (normal, 7.4) Based on the information shown in Table 4-9, it was determined that David was in diabetic ketoacidosis. He was given an intravenous infusion of saline and insulin. Later, after his blood glucose had decreased to 175 mg/dL and his plasma K' had decreased to 4 mEq/L, glucose and were added to the infusion. David stayed in the hospital overnight. By the next morning, his blood glucose, electrolytes, and blood gas values were normal. rOj QUESTIONS 1. What acid-base disorder did David have? What was its etiology? 2. Did David's lungs provide the expected degree of "respiratory compensation"? 3. Why was his breathing rate so rapid and deep? What is this type of breathing called? 4. How did David's failure to take insulin cause his acid-base disorder? RENAL AND ACID-BASE PHYSIOLOGY 199 5. What was David's serum anion gap, and what is its significance? 6. Why was David so thirsty at 7 A.M.? 7. Why was his pulse rate increased? 8. What factors contributed to David's elevated plasma IQ- concentration (hyperkalemia)? Was his K. balance positive, negative, or normal? 9. How did the initial treatment with insulin and saline help to correct David's fluid and electrolyte disturbances? 10. Why were glucose and K. added to the infusion after his plasma glucose and K' levels were corrected to normal? 200 PHYSIOLOGY CASES AND PROBLEMS PrAl ANSWERS AND EXPLANATIONS 1. David's pH, HCO3, and Pc 0, values are consistent with metabolic acidosis: decreased pH, decreased HCO 3-, and decreased Pc02 (Table 4-10). TABLE 4-10 Sutmnaiy of Acid-Base Disorders Respiratory Renal Disorder CO2 + H20 <-> 11+ + HCO3- Compensation Compensation Metabolic ,I, (respiratory Hyperventilation acidosis compensation) Metabolic T (respiratory Hypoventilation alkalosis compensation) Respiratory T excretion acidosis T HCO 3- reabsorption Respiratory .1,11+excretion alkalosis .1, HCO3- reabsorption Heavy arrows indicate primary disturbance. (Reprinted with permission from Costanzo LS: BRS Physiology, 3rd ed. Baltimore, Lippincott Williams & Wilkins, 2003, p 195.) David had metabolic acidosis [diabetic ketoacidosis (DKA)] secondary to overproduction of the ketoacids 13-OH-butyric acid and acetoacetic acid. Metabolic acidosis is usually caused by an increase in the amount of fixed acid in the body, as a result of either ingestion or overpro- duction of acid. The excess fixed acid is buffered by extracellular HCO3 and, as a result, the HCO3 concentration in blood decreases. This decrease in blood HCO3 concentration causes the pH of the blood to decrease (acidemia), as described by the Henderson-Hasselbalch equa- tion (see Case 29): 3 - pH = 6.1 + log HCO co, The acidemia then causes an increase in breathing rate, or hyperventilation, by stimulating peripheral chemoreceptors. As a result, arterial Pc 02 decreases. This decrease in arterial Pco, is the respiratory compensation for metabolic acidosis. Essentially, the lungs are attempting to decrease the denominator (CO 2) of the Henderson-Hasselbalch equation as much as the numerator (HCO3) is decreased, which tends to normalize the ratio of HCO 3 to CO2 and to normalize the pH. 2. The expected degree of respiratory compensation can be calculated from the "renal rules." These rules predict the appropriate compensatory responses for simple acid-base disorders (see Appendix). For example, in simple metabolic acidosis, the renal rules can determine whether the lungs are hyperventilating to the extent expected for a given decrease in HCO3- concentration. David's HCO3 concentration is decreased to 8 mEq/L (normal, 24 mEq/L). The rules can be used to predict the expected decrease in Pco, for this decrease in HCO3. If David's actual Pc 02 is the same as the predicted Pm,, the respiratory compensation is considered to be appropriate, and no other acid-base abnormality is present. If David's actual Pc02 is different from the predicted value, then another acid-base disorder is present (in addition to the metabolic acidosis). 'The renal rules shown in the Appendix tell us that in simple metabolic acidosis, the expected change in Pc02 (from the normal value of 40 mm Hg) is 1.3 times the change in HCO3 concentration (from the normal value of 24 mEq/L). Thus, in David's case: Decrease in HCO 3- (from normal) = 24 mEq/L - 8 inEq/L = 16 mEq/L RENAL AND ACID–BASE PHYSIOLOGY 201 Predicted decrease in Pc02 (from normal) = 1.3 x 16 mEq/L = 20.8 mm Hg Predicted Pop, = 40 mm Hg - 20.8 mm Hg = 19.2 mm Hg The predicted Pc02 is 19.2 mm Hg. David's actual Pco 2 was 20 mm Hg. Thus, his degree of respiratory compensation was both appropriate and expected for a person with an HCO3- concentration of 8 mEq/L; no additional acid-base disorders were present. 3. David's rapid, deep breathing is the respiratory compensation for his metabolic acidosis. This hyperventilation, typically seen in diabetic ketoacidosis, is called Kussmaul respiration. 4. David has type I diabetes mellitus. The beta cells of his endocrine pancreas do not secrete enough insulin, which is absolutely required for storage of ingested nutrients (see below). Even since David developed type I diabetes mellitus in middle school, he has depended on injec- tions of exogenous insulin to store the nutrients he ingests. When David forgot to take his insulin in the morning and then ate a high-carbohydrate meal (orange juice and doughnuts), he was in trouble! If you have not yet studied endocrine physiology, briefly, the major actions of insulin are coordinated for storage of nutrients. They include uptake of glucose into cells and increased synthesis of glycogen, protein, and fat. Therefore, insulin deficiency has the following effects: (1) decreased glucose uptake into cells, resulting in hyperglycemia; (2) increased protein catab- olism, resulting in increased blood levels of amino acids, which serve as gluconeogenic sub- strates; (3) increased lipolysis, resulting in increased blood levels of free fatty acids; and (4) increased hepatic ketogenesis from the fatty acid substrates. The resulting ketoacids are the fixed acids ft-OH-butyric acid and acetoacetic acid. Overproduction of these fixed acids causes diabetic ketoacidosis (discussed in Question 1). 5. The serum anion gap is "about" electroneutrality, which is an absolute requirement for every body fluid compartment (e.g., serum). That is, in every compartment, the concentration of cations must be exactly balanced by an equal concentration of anions. In the serum compart- ment, we usually measure Na' (a cation) and Cl and HCO 3- (anions). When the concentration of Ne is compared with the sum of the concentrations of Cl and HCO 3-, there is a "gap." This gap, the anion gap, is comprised of unmeasured anions and includes plasma albumin, phosphate, sulfate, citrate, and lactate (Figure 4-11). Anion gap 1Unmeasured anions = protein, phosphate, citrate, sulfate HCO3- Cations Anions Figure 4-11 Serum anion gap. (Reprinted with permission from Costanzo LS: BRS Physiology, 3rd ed. Baltimore, Lippincott Williams & Wilkins, 2003, p 198.) 202 PHYSIOLOGY CASES AND PROBLEMS The anion gap is calculated as follows: Anion gap = [Nal ] - ([C1-] + [HCO31) where Anion gap = unmeasured anions in serum or plasma [Nal = plasma Na+ concentration (mEq/L) [C1-] = plasma Cl- concentration (mEq/L) [FICO3] = plasma HCO3- concentration (mEq/L) The normal range for the serum anion gap is 8-16 mEq/l, (average value, 12 mEq/L). David's serum anion gap is: Anion gap = 132 mEq/L - (96 m Eq/L + 8 mEq/L) = 28 mEq/L A calculated anion gap of 28 mEq/L is much higher than the normal value of 12 mEq/L. Why would the anion gap be increased? Since the anion gap represents unmeasured anions, a logi- cal conclusion is that the concentration of unmeasured anions in David's plasma was increased because of the presence of ketoanions, Thus, David had metabolic acidosis with an increased anion gap. To maintain electroneutrality, the decrease in HCO3- concentration (a measured anion) was offset by the increase in ketoanions (unmeasured anions). Did you notice that the anion gap was increased exactly to the same extent that the HCO3- was decreased? In other words, the anion gap of 28 mEq/I, was 16 rnEq/L above the normal value of 12 mEq/L, and the HCO 3- of 8 mEq/L was 16 mEq/L below the normal value of 24 mEq/L.
Load more

Recommended publications
  • 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]
  • 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]
  • 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.
    [Show full text]
  • Approach to Acute Kidney Injury: Differentiation of Prerenal, Postrenal and Intrinsic Renal Disease, Acute Tubular Necrosis and Renal Vascular Disease
    Acute Kidney Injury, Renal Vascular Disease Renal Genital Urianry System 2019 APPROACH TO ACUTE KIDNEY INJURY: DIFFERENTIATION OF PRERENAL, POSTRENAL AND INTRINSIC RENAL DISEASE, ACUTE TUBULAR NECROSIS AND RENAL VASCULAR DISEASE Biff F. Palmer, MD, Office: H5.112; Phone 87848 Email: [email protected] LEARNING OBJECTIVES • Given laboratory tests results and radiographic imaging, be able to diagnose a patients with an increased serum creatinine concentration as having post-renal renal disease and list the common clinical etiologies of urinary obstruction • Given laboratory tests results and radiographic imaging, be able to diagnose a patients with an increased serum creatinine concentration as having pre-renal kidney injury • Given pertinent aspects of the history, physical examination, serum and urine electrolytes, and urinalysis in any patient, be able to distinguish pre-renal renal failure from intrinsic renal disease • Given urine and plasma concentrations of sodium and creatinine in any patient, be able to calculate the fractional excretion of sodium (FENa) and interpret the results • List the renal syndromes associated with use of NSAID’s • List the characteristics of thromboembolic disease of the kidney, multiple choesterol emboli syndrome, renal vein thrombosis, and renal artery stenosis After determining chronicity and assessing the level of renal function, one should attempt to classify the patient with renal disease into one of several syndromes based on the renal structures most affected: pre-renal, post-renal or intrinsic renal disease. This classification is based on the information obtained in the history, physical examination, laboratory tests and selected imaging studies. It is particularly important to identify prerenal and postrenal disorders because theses disorders are often readily reversible.
    [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]
  • Hyperkalemia: This Time, Not the Usual Suspect
    TUBULAR QUIZ Port J Nephrol Hypert 2018; 32(4): 395-397 • Advance Access publication 4 January 2019 Hyperkalemia: this time, not the usual suspect Anna Lima, Pedro Campos, Ana Gaspar, Afonso Santos, Patricia Carrilho Department of Nephrology, Hospital Prof Dr Fernando Fonseca, Lisbon, Portugal Received for publication: Dec 18, 2018 Accepted in revised form: Jan 4, 2019 A 49-year-old Caucasian male was admitted to the acidosis, one important step to search for the cause is emergency department with a three-day history of to calculate the anion gap.1 In this case the anion gap abdominal pain and nausea. These episodes were fre- was normal (AG= Na – (CL+HCO3) =12mmol/L). The next quent and, in the previous four months, he had noticed step was to calculate the urinary anion gap (UAG= (Na+ fatigue, more severe in the lower limbs, and symptoms + K+) – Cl-= 74mmol/L), which was highly positive. So, compatible with postural hypotension. He had no fever we were in presence of a metabolic acidosis with non- or any other symptoms. Lab tests requested by his increased anion gap, positive UAG, hyperkalemia and general practitioner six weeks earlier had revealed acidic urine (pH 5) in a patient with normal renal function hyperkalemia, without other relevant changes. He had matching a type IV (distal) renal tubular acidosis.2 followed a low-potassium diet since then. Past medical history included active smoking habits, intravenous There are many causes for hyperkalemic distal renal drug use (he suspended seventeen years ago), and tubular acidosis, the most common of which is diabetes changed bowel habits with alternating obstipation and mellitus (by definition a hyporeninemic hypoaldoster- diarrhea.
    [Show full text]
  • Chapter 26: Fluid, Electrolyte, and Acid-Base Balance
    Chapter 26: Fluid, Electrolyte, and Acid-Base Balance Chapter 26 is unusual because it doesn’t introduce much new material, but it reviews and integrates information from earlier chapters to cover 3 types of regulation: regulation of fluid volume, regulation of electrolyte (=ion) concentrations, and regulation of pH. • Outline of slides: • 1. Regulating fluid levels (blood/ECF) • Compartments of the body • Regulation of fluid intake and excretion • 2. Regulating ion concentrations (blood/ECF) • 3. Regulating pH (blood/ECF) • Chemical buffers • Physiological regulation • Respiratory • Renal 1 3 subsections to this chapter – we will cover the middle one only briefly. 1 Ch. 26: Test Question Templates • Q1. Given relevant plasma data, classify a patient’s possible acid-base disorder as a metabolic or respiratory acidosis or alkalosis that is or is not fully compensated. Or, if given such a disorder, give expected plasma pH and CO2 level (high, normal, or low). • Example A: Plasma pH is 7.32, CO2 levels in blood are low. What is this? • Example B: A patient’s plasma has a pH of 7.5. Explain how you could make an additional measurement to determine whether the cause of this unusual pH is metabolic or respiratory. • Example C: A patient’s plasma CO2 levels are very low, yet plasma pH is normal. How can this be? 2 Q1. Example A: (slight) metabolic acidosis. Example B: Measure the CO2 level in the plasma. If the high plasma pH is due to a respiratory problem, the CO2 concentration will be low. If the high pH is NOT due to a respiratory problem, the CO2 will not be low, and may be high if the person is undergoing respiratory compensation for a metabolic alkalosis.
    [Show full text]
  • The Electro-Physiology-Feeedback Measures of Interstitial Fluids
    INTERNATIONAL MEDICAL UNIVERSITY The elecTro-Physiology-Feeedback Measures oF inTersTiTial Fluids BY PROFESSOR OF MEDICINE DESIRÉ DUBOUNET IMUNE PRESS 2008 Electro-Physiology -FeedBack Measures of Interstitial Fluids edited by Professor Emeritus Desire’ Dubounet, IMUNE ISBN 978-615-5169-03-8 1 CHAPTER 1 THE ELECTRO-PHYSIOLOGY-FEEDBACK MEASURES OF INTERSTITIAL FLUIDS The interstitial liquid constitutes the true interior volume that bathe the organs of the human body. It is by its presence that all the exchanges between plasma and the cells are performed. With the vascular, lymphatic and nervous systems, it seems to be the fourth communication way of information's between all the cells. No direct methods for sampling interstitial fluid are currently available. The composition of interstitial fluid, which constitutes the environment of the cells and is regulated by the electrical process of electrochemistry. This has previously been sampled by the suction blister or liquid paraffin techniques or by implantation of a perforated capsule or wick. The results have varied, depending on the sampling technique and animal species investigated. In one study, the ion distribution between vascular and interstitial compartments agreed with the Donnan equilibrium; in others, the concentrations of sodium and potassium were higher in interstitial fluid than in plasma. The concentration of protein in interstitial fluid is lower than in plasma, and the free ion activities theoretically differ from those of plasma because of the Donnan effect. In spite of these differences, and for practical reasons only, plasma is used clinically to monitor fluid and electrolytes. The relation between plasma and interstitial fluid is important in treating patients with abnormal plasma volume or homeostasis.
    [Show full text]
  • New Jersey Chapter American College of Physicians Resident
    New Jersey Chapter American College of Physicians Resident Abstract Competition 2018 Submissions Category Name Additional Authors Program Abstract Title Abstract Clinical Vignette Ankit Bansal Ankit Bansal MD, Robert Atlanticare Rare Case of A 62‐year‐old male IV drug abuser with hepatitis C and diabetes presented to the emergency Lyman MS IV, Saraswati Regional Necrotizing department with progressively worsening right forearm pain and swelling for two days after injecting Racherla MD Medical Myositis leading to heroin. Vitals included temperature 98.8°F and heart rate 107 bmp. Physical examination showed Center Thoracic and erythematous skin with surrounding edema and abscess formation of the right biceps extending into (Dominik Abdominal the axilla, and tenderness to palpation of the right upper extremity (RUE). Labs were white blood cell Zampino) Compartment count 16.1 x103/uL with bands 26%, hemoglobin 12.4 g/dL, platelets 89 x103/uL and blood lactate 2.98 Syndrome mmol/L. Patient was admitted to telemetry for sepsis secondary to right arm cellulitis and abscess. Bedside incision and drainage was performed. Blood and wound cultures were drawn and patient was started on Vancomycin and Levofloxacin. On the third day of admission, patient became febrile, obtunded and had signs of systemic toxicity. Labs showed a worsening leukocytosis and lactic acidosis. CT RUE was consistent with complex fluid collection and with extensive gas tracking encircling the entire length of the right biceps brachii muscle. Surgical debridement was performed twice over the next few days. Blood cultures grew corynbacterium and coagulase negative staphylococcus; wound culture grew coagulase negative staphylococcus. Levofloxacin was switched to Aztreonam.
    [Show full text]
  • Acid-Base Disorders Made So Easy Even a Caveman Can Do It
    ACID-BASE DISORDERS MADE SO EASY EVEN A CAVEMAN CAN DO IT Lorraine R Franzi, MS/HSM, RD, LDN, CNSD Nutrition Support Specialist University of Pittsburgh Medical Center Pittsburgh, PA I. LEARNING OBJECTIVES The clinician after participating in the roundtable will be able to: 1) Indicate whether the pH level indicates acidosis or alkalosis. 2) State whether the cause of the pH imbalance is respiratory or metabolic. 3) Identify if there is any compensation for the acid-base imbalance. II. INTRODUCTION Acid-Base balance is an intricate concept which requires an intimate and detailed knowledge of the body’s metabolic pathways used to eliminate the H+ ion. Clinicians may find it daunting to understand when first introduced to the subject. This roundtable session will demonstrate how to analyze blood gas levels in a very elementary manner so as to diagnose any acid-base disorder in a matter of minutes. The body is in a constant state of flux delicately stabilizing the pH so as to maintain its normalcy. In order to prevent untoward effects of alkalosis or acidosis the body has three major buffering systems that it uses to adjust the pH. They are: 1) Plasma protein (Prot-) 2) Plasma hemoglobin (Hb-) 3) Bicarbonate (HCO3-) The Bicarbonate-Carbonic acid system is the most dominate buffering system and controls the majority of the hydrogen ion (H+) equilibrium. Maintaining homeostasis when these acid-base shifts occur is vital to survival. Metabolic and respiratory processes work in unison to keep the H+ normal and static. II. ACID-BASE ABNORMALITIES The four principal acid-base imbalances are illustrated in Table 1.
    [Show full text]
  • A Case-Based Approach to Acid-Base Disorders
    A Case-Based Approach to Acid-Base Disorders Justin Muir, PharmD Clinical Pharmacy Manager, Medical ICU NewYork-Presbyterian Hospital Columbia University Irving Medical Center [email protected] Disclosures None Objectives At the completion of this activity, pharmacists will be able to: 1. Describe acid-base physiology and disease states that lead to acid-base disorders. 2. Demonstrate a step-wise approach to interpretation of acid-base disorders and compensatory states. 3. Analyze contemporary literature regarding the use of sodium bicarbonate in metabolic acidosis. At the completion of this activity, pharmacy technicians will be able to: 1. Explain the importance of acid-base balance. 2. List the acid-base disorders seen in clinical practice. 3. Identify potential therapies used to treat acid-base disorders. Case A 51 year old man with history of erosive esophagitis, diabetes mellitus, chronic pancreatitis, and bipolar disorder is admitted with several days of severe nausea, vomiting, and abdominal pain. 135 87 31 pH 7.46 / pCO 29 / pO 81 861 2 2 BE -3.8 / HCO - 18 / SaO 96 5.6 20 0.9 3 2 • What additional data should be obtained? • What acid base disturbance(s) is/are present? Introduction • Acid base status is tightly regulated to maintain normal biochemical reactions and organ function • Body uses multiple mechanisms to maintain homeostasis • Abnormalities are extremely common in hospitalized patients with a higher incidence in critically ill with more complex pictures • A standard approach to analysis can help guide diagnosis and treatment Important acid-base determinants Blood gas generally includes at least: Normal range Measurement Description (arterial blood) pH -log [H+] 7.35-7.45 pCO2 partial pressure of dissolved CO2 35-45 mmHg pO2 partial pressure of dissolved O2 80-100 mmHg Base excess calculated measure of metabolic acid/base deviation from normal -3 to +3 SO2 calculated measure of Hgb O2 saturation based on pO2 95-100% - HCO3 calculated measure based on relationship of pH and pCO2 22-26 mEq/L Haber RJ.
    [Show full text]
  • Acid-Base Balance
    Intensive Care Nursery House Staff Manual Acid-Base Balance INTRODUCTION: The newborn infant is subject to numerous conditions that may disturb acid-base homeostasis. Management of ventilation, which controls the respiratory component of acid-base balance, is discussed in the section on Respiratory Support (P. 10). This section is a brief discussion of the metabolic aspects of acid-base balance. METABOLIC ACIDOSIS, defined as a base deficit >5 mEq/L on the first day and >4 mEq/L thereafter, occurs from: •Loss of buffer (mainly bicarbonate) or •Excess production of acid or decreased excretion of acid The anion gap is a useful calculation in assessing metabolic acidosis. + - - Anion gap = [Na ] – ([Cl ] + [HCO3 ]) Loss of buffer has no effect on anion gap. Accumulation of organic acid (e.g., lactic acid) causes an increase in anion gap. Normal anion gap: <15 mEq/L Increased anion gap: >15 mEq/L in LBW infants (<2,500 g) >18 mEq/L in ELBW infants (<1,000 g) Newborn infants normally have a base deficit of 1 to 3 mEq/L. Common causes of metabolic acidosis: •Bicarbonate loss, especially via immature kidney or from GI tract •Lactic acidosis from inadequate tissue perfusion and oxygenation (e.g., from asphyxia, shock, severe anemia, hypoxemia, PDA, NEC, excessive ventilator pressures with ↓ cardiac output) •Hypothermia •Organic acidemia due to an inborn error of metabolism (see P. 155) •Excessive Cl in IV fluids •Renal failure •Excessive acid load from high protein formula in preterm (late metabolic acidosis of prematurity ) - •Excretion of HCO3 as metabolic compensation for respiratory alkalosis Dilution acidosis is caused by excessive volume expansion (with saline, Ringer’s lactate or dextrose solutions).
    [Show full text]