Acid-Base Disorders

Total Page:16

File Type:pdf, Size:1020Kb

Acid-Base Disorders Acid-Base Disorders Benson S. Hsu, MD, MBA,* Saquib A. Lakhani, MD,† Michael Wilhelm, MD‡ *Pediatric Critical Care, University of South Dakota, Sanford School of Medicine, Sioux Falls, SD. †Pediatric Critical Care, Yale School of Medicine, New Haven, CT. ‡Pediatric Critical Care, University of Wisconsin School of Medicine and Public Health, Madison, WI. Education Gap To treat critically ill children, a physician must have a clear understanding of acid-base balance. Objectives After completing this article, readers should be able to: 1. Describe the mechanisms regulating acid-base physiology and identify blood gas abnormalities associated with an acid-base imbalance. 2. Recognize the differential diagnosis and clinical and laboratory features associated with metabolic acidosis and metabolic alkalosis as well as how to manage each appropriately. 3. Calculate an anion gap and formulate a differential diagnosis associated with various anion gap values. 4. Identify factors contributing to compensatory changes associated with primary metabolic and respiratory acidoses and alkaloses. INTRODUCTION The body’s ability to maintain acid-base homeostasis is based on a complex set of interactions between the respiratory and metabolic systems. This article reviews normal acid-base physiology and examines disorders of acid-base imbalances, first within a primary metabolic cause and then within a primary respiratory cause. Covering the complex nuances of acid-base control within a limited-scope review article is impossible. Thus, this article focuses on the traditional model based on the Henderson-Hasselbalch equation rather than the strong ion (or Stewart) model, which explores the difference between all the dissociated cations and anions. Using the traditional model, the authors explore the various meta- bolic and respiratory disturbances while addressing the implications of the anion gap on metabolic acidoses. AUTHOR DISCLOSURE Drs Hsu and Lakhani have disclosed no financial relationships relevant to this article. Dr Wilhelm has REGULATION OF ACID-BASE disclosed that he holds stock in Inovio Pharmaceuticals. This commentary does not The Henderson-Hasselbalch Equation contain discussion of an unapproved/ investigative use of a commercial product or Homeostatic control of acid-base balance is critical for all metabolic and phys- device. iologic functions of the human body. The Henderson-Hasselbalch equation Vol. 37 No. 9 SEPTEMBER 2016 361 Downloaded from http://pedsinreview.aappublications.org/ by guest on November 14, 2018 describes the relationship between pH and the bicarbonate ranges and not independently examine any of the variables. fl buffering system (the predominant buffering system in For example, a blood gas with a high PCO2 may re ect a normal plasma) to establish this homeostasis: pH and should be interpreted as nonacidotic (Table 1). þ 4 4 þ þ À The Anion Gap CO2 H2O H2CO3 H HCO3 Use of only the Henderson-Hasselbalch equation is insuf- ¼ þ À= ficient to describe a patient’s metabolic acid-base state com- pH pK log HCO3 H2CO3 pletely. The anion gap further describes the interactions of fi the measured positive charges (cations) and negative charges When accounting for H2CO3, the modi ed equation (anions) to the unmeasured charged particles. The anion gap becomes: equation is based on the understanding that the cations in the ¼ þ À=½ : ∗ pH pK log HCO3 0 03 Pco2 plasma balance the anions in the plasma at equilibrium. The “measureable” positive and negative charges in the Examination of the modified equation reveals the impor- serum refer to those measured with a standard electrolyte À panel. To calculate the anion gap, positive charges include tance of bicarbonate ion (HCO3 ) and dissolved carbon þ þ dioxide (PCO2) in the determination of pH. The pK is the sodium (Na ) and potassium (K ) while negative charges À À include bicarbonate (HCO ) and chloride (ClÀ). In normal pH at which the bicarbonate ion (HCO3 )andcarbon 3 dioxide (CO2) are equal. This value is approximately conditions, the measured cations exceed the measured 6.35. The 0.03 constant is used to describe the PCO2 anions (the normal anion gap), which is predominantly solubility. When changes occur in the pH due to PCO2 accounted for by the serum proteins. This normal value changes, the predominant system involved is the respira- for the anion gap ranges from 12 to 20 mEq/L (12–20 þ tory system. When changes in pH occur due to changes in mmol/L) when the K concentration is included and 8 to À 16 mEq/L (8-16 mmol/L) when it is not included. HCO3 , the predominant system involved is the metabolic À system. However, the system favors the HCO at physiologic þ þ À À 3 Anion Gap ¼ Na þ K À HCO þ Cl pH, therefore, the buffering ability of the metabolic system 3 ’ is dependent on the body s ability to eliminate CO2 through In the setting of low serum protein, such as hypoalbumi- the respiratory system. Thus, it is evident that two comple- nemia, the normal unmeasured anions are decreased and mentary systems, respiratory and metabolic, are used to the anion gap narrows. Thus, with critical illness when describe changes to the body’s pH. protein concentrations are oftenlow,anelevatedconcen- Clinically, the acid-base state is normally determined by tration of unmeasured anions can frequently be masked a blood gas sample. Although the gold standard remains by an apparently normal (falsely low) anion gap. Conse- arterial blood gas measurement, use of the venous or quently, the combination of the modified Henderson- capillary blood gas sample is prevalent within the pediatric Hasselbalch equation and the anion gap calculation begins population due to the relative ease in obtaining these sam- to illustrate an individual patient’sacid-basebalance. ples. Although minor differences exist within pH and PCO2 among the different blood gas sample types, these differ- ences can be accounted for during interpretation by assum- ing expected slight increases in PCO2 and decreases in pH TABLE 1. General Reference Ranges for Arterial for venous samples. As expected due to the location of the and Venous Blood Gases blood draw, venous blood gas samples are unreliable for PO2 measurements. Because capillary blood gradually transitions ARTERIAL VENOUS between arterial and venous states, the PCO2 and pH norma- pH 7.38 – 7.42 7.36 – 7.38 tive values often are between the arterial and venous norma- – – tive values. Of note, a blood gas machine measures the pH PO2 (mm Hg) 80 100 30 50 À – – and the partial pressure of the gases, but the HCO3 ion PCO2 (mm Hg) 38 42 43 48 concentration is a calculated value. À – – HCO3 (mmol/L) 22 24 25 26 In examining blood gases, acidosis occurs when the pH À¼ ¼ ¼ value is lower than normal. In contrast, alkalosis occurs HCO3 bicarbonate, PCO2 partial pressure of carbon dioxide, PO2 partial pressure of oxygen. Reference normal values are laboratory-dependent when the pH value is higher than normal. It is important to and may vary due to differing techniques. À characterize pH in context of PCO2 and HCO3 reference 362 Pediatrics in Review Downloaded from http://pedsinreview.aappublications.org/ by guest on November 14, 2018 The human body has a natural inclination toward a desired Extending from this initial assessment, additional clues from equilibrium, which accounts for the common finding of results of blood gas analysis and a basic metabolic panel reflect- compensatory changes in the opposite direction. Within set- ing the anion gap can help discern a primary metabolic versus tings of respiratory derangement leading to changes in the respiratory cause. Determining the acute or chronic nature of the pH, the compensatory mechanism occurs within the meta- compensation adds additional diagnostic information. bolic system. For respiratory acidosis (commonly arising due to an increase of PCO2), the body compensates by creating À METABOLIC ACIDOSIS metabolic alkalosis (from a retention of HCO3 ). In contrast, for respiratory alkalosis (commonly arising from a decrease A combination of the anion gap calculation and knowledge of of PCO2), the body compensates by creating metabolic acidosis the pH state within the body is required to describe metabolic À (from a loss of HCO3 ) (Table 2). Metabolic compensation to acidosis. The regulation of the acid-base state, as noted by the respiratory derangements often takes hours to days to estab- Henderson-Hasselbalch equation, is based on the buffering À lish. In comparison, compensatory mechanisms within the effect of HCO3 . However, from an electroneutrality view- respiratory system for primary metabolic derangements gen- point, use of the anion gap calculation can further differentiate erally occur more rapidly, often over minutes to hours. causes for the metabolic acidosis. Because reference values in the calculation of unmeasured anions or anion gap vary among laboratories, clinicians must be aware of normal values ASSESSMENT AND DETERMINATION OF for the laboratories they use. As noted previously, due to the ACID-BASE STATE importance of homeostasis, normal gap versus increased gap The first step in the assessment of an acid-base imbalance acidosis indicate vastly different clinical pictures. for a patient is to determine a primary respiratory versus primary metabolic etiology. A detailed history and compre- Hyperchloremic (Non-anion Gap) Metabolic Acidosis À À hensive physical examination can offer clues to the present- Chloride (Cl ) has an important relationship to HCO3 ing cause. Such evaluation may reveal a neurologic
Recommended publications
  • Mechanical Ventilation Bronchodilators
    A Neurosurgeon’s Guide to Pulmonary Critical Care for COVID-19 Alan Hoffer, M.D. Chair, Critical Care Committee AANS/CNS Joint Section on Neurotrauma and Critical Care Co-Director, Neurocritical Care Center Associate Professor of Neurosurgery and Neurology Rana Hejal, M.D. Medical Director, Medical Intensive Care Unit Associate Professor of Medicine University Hospitals of Cleveland Case Western Reserve University To learn more, visit our website at: www.neurotraumasection.org Introduction As the number of people infected with the novel coronavirus rapidly increases, some neurosurgeons are being asked to participate in the care of critically ill patients, even those without neurological involvement. This presentation is meant to be a basic guide to help neurosurgeons achieve this mission. Disclaimer • The protocols discussed in this presentation are from the Mission: Possible program at University Hospitals of Cleveland, based on guidelines and recommendations from several medical societies and the Centers for Disease Control (CDC). • Please check with your own hospital or institution to see if there is any variation from these protocols before implementing them in your own practice. Disclaimer The content provided on the AANS, CNS website, including any affiliated AANS/CNS section website (collectively, the “AANS/CNS Sites”), regarding or in any way related to COVID-19 is offered as an educational service. Any educational content published on the AANS/CNS Sites regarding COVID-19 does not constitute or imply its approval, endorsement, sponsorship or recommendation by the AANS/CNS. The content should not be considered inclusive of all proper treatments, methods of care, or as statements of the standard of care and is not continually updated and may not reflect the most current evidence.
    [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]
  • Metabolic Alkalosis in Adults with Stable Cystic Fibrosis Fahad Al-Ghimlas*,1, Marie E
    The Open Respiratory Medicine Journal, 2012, 6, 59-62 59 Open Access Metabolic Alkalosis in Adults with Stable Cystic Fibrosis Fahad Al-Ghimlas*,1, Marie E. Faughnan1,2 and Elizabeth Tullis1,2 1Department of Medicine, University of Toronto, Canada 2St. Michael’s Hospital, Li Ka Shing Knowledge Institute, Canada Abstract: Background: The frequency of metabolic alkalosis among adults with stable severe CF-lung disease is unknown. Methods: Retrospective chart review. Results: Fourteen CF and 6 COPD (controls) patients were included. FEV1 was similar between the two groups. PaO2 was significantly higher in the COPD (mean ± 2 SD is 72.0 ± 6.8 mmHg,) than in the CF group (56.1 ± 4.1 mmHg). The frequency of metabolic alkalosis in CF patients (12/14, 86%) was significantly greater (p=0.04) than in the COPD group (2/6, 33%). Mixed respiratory acidosis and metabolic alkalosis was evident in 4 CF and 1 COPD patients. Primary metabolic alkalosis was observed in 8 CF and none of the COPD patients. One COPD patient had respiratory and metabolic alkalosis. Conclusions: Metabolic alkalosis is more frequent in stable patients with CF lung disease than in COPD patients. This might be due to defective CFTR function with abnormal electrolyte transport within the kidney and/ or gastrointestinal tract. Keywords: Cystic fibrosis, metabolic alkalosis. BACKGROUND METHODS Cystic fibrosis (CF) is a multi-system disease that is After obtaining ethics approval, a retrospective chart and caused by mutations in a 230 kb gene on chromosome 7 database review was performed on clinically stable CF encoding 1480 aminoacid polypeptide, named cystic fibrosis patients (Toronto CF Database) and COPD patients (Chest transmembrane regulator (CFTR) [1].
    [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]
  • The Basic Principles of Acid-Base Regulation*
    The Basic Principles of Acid-Base Regulation* ORHAN MUREN, M.D. Associate Professor of Medicine and Anesthesiology, Medical College of Virginia, Health Sciences Division of Virginia Commonwealth University, Richmond, Virginia Acid-base homeostasis refers to those chemical In normal people, the concentration of H• is and physiological processes which maintain the hy­ approximately 40 nanomoles ( n moles) per liter of drogen ion (H•) activity in body fluids at the levels plasma. One nanomole equals 10-9 moles. However, compatible with life and normal functioning. This is it would be more correct to indicate the thermo­ an enormous task due to the fact that reactions which dynamic activities rather than the concentrations, produce H• and reactions which consume H• are the two being related as follows: continously occurring in human beings. On one hand there is acid production (fixed activity ----.- = activity coefficient and volatile acid) and on the other hand acid elimi­ concentration nation (fixed and volatile acid). Normally in a given time, such as in a day, acid elimination is equal At infinite dilution the activity coefficient is to acid production. Whenever there is imbalance equal to one. However, in concentrations in body between input and output, acid-base disturbances fluids, it is much less than one. The pH meter will occur. electrode responds to hydrogen ion activity and not Many biochemical processes require optimum concentration. However, it is customary to work in H• ion concentration. Changes in H• concentration concentrations, and values for the different equilib­ markedly affect the catalytic activity of enzymes. rium constants are adjusted accordingly, as indicated Myocardial and muscular contraction, vascular tone, by a prime after a symbol such as K'.
    [Show full text]
  • Ketoalkalosis: Masked Presentation of Diabetic Ketoacidosis with Literature Review
    Case Report J Endocrinol Metab. 2017;7(6):194-196 Ketoalkalosis: Masked Presentation of Diabetic Ketoacidosis With Literature Review Vinod Kumara, Sushant M. Nanavatia, c, Fnu Komala, Luis Carlos Ortiza, Namrata Paula, Manhedar Kumarb, Patrick Michaela, Monisha Singhal Abstract sis would be masqueraded by alkalosis. We present a unique case of 25 years old female with DKA and alkalemia. Most dreaded complication in type 1 diabetes mellitus remains dia- betic ketoacidosis (DKA): plasma blood glucose > 250 mg/dL, serum Case Report bicarbonate < 18 mEq/L, anion gap metabolic acidosis and ketosis. Insulin deficiency with high levels of glucagon and stress hormones causing ketogenesis in liver, elevated lipolysis in peripheral tissues, and A 25-year-old female with type 1 diabetes mellitus presented increased free fatty acids contribute the formation of ketones leading with complaints of intractable vomiting, generalized weakness to metabolic acidosis. And hence DKA is also termed as ketoacidosis. and abdominal pain. Six hours prior to arrival to emergency Unusually, patients with diuretic use, alkali ingestion, intractable vom- department (ED), she started to experience diffuse abdominal iting, or hypercortisolism may present with alkalemia in DKA. Con- pain around periumbilical area and subsequently started in- traction (Metabolic) Alkalosis masquerades metabolic acidosis with tractable non-bilious vomiting. At home, she was prescribed anion gap and low to normal bicarbonate that uncovers on provision of to insulin detemir 25 units once a day along with insulin aspart intravenous fluids. We present a case of a 25-year-old female with DKA 6 units along with three meals. She stated of adherent to insu- presenting with intractable vomiting, alkalotic pH and high anion gap.
    [Show full text]
  • Metabolic Alkalosis a Brief Pathophysiologic Review
    CJASN ePress. Published on June 25, 2020 as doi: 10.2215/CJN.16041219 Metabolic Alkalosis A Brief Pathophysiologic Review Michael Emmett Abstract Metabolic alkalosis is a very commonly encountered acid-base disorder that may be generated by a variety of exogenous and/or endogenous, pathophysiologic mechanisms. Multiple mechanisms are also responsible for Divisions of Internal the persistence, or maintenance, of metabolic alkalosis. Understanding these generation and maintenance Medicine and mechanisms helps direct appropriate intervention and correction of this disorder. The framework utilized in Nephrology, Department of this review is based on the ECF volume-centered approach popularized by Donald Seldin and Floyd Rector in Medicine, Baylor the 1970s. Although many subsequent scientific discoveries have advanced our understanding of the University Medical pathophysiology of metabolic alkalosis, that framework continues to be a valuable and relatively Center at Dallas, straightforward diagnostic and therapeutic model. Dallas, Texas CJASN 15: ccc–ccc, 2020. doi: https://doi.org/10.2215/CJN.16041219 Correspondence: Dr. Michael Emmett, Department of Medicine, Baylor Introduction profile, or Gamblegram (Figure 2), shows why the 2 University Medical Metabolic alkalosis is a primary acid-base disorder increased [HCO3 ] must be accompanied by a re- Center at Dallas, 3500 that increases the serum bicarbonate concentration duction of [Cl2](independentof[Na1]), a reduction Gaston Avenue, Room 2 [HCO3 ] (this is usually approximated by its surro- of the [AG2], or both (7,8). In fact, metabolic alkaloses H-102, Dallas, TX 2 75246-2096. Email: gate the venous total [CO2]) above 30 meq/L (1), reproducibly increase the [AG ] to a small degree, 1 Michael.Emmett@ causing the arterial blood [H ]tofall,i.e., the arterial mostly owing to increased negative charge density of BSWHealth.org blood pH increases into the alkaline range (.7.45).
    [Show full text]
  • Management of Critically Ill Patients David Tofovic 34 Y.O
    Management of Critically Ill Patients David Tofovic 34 y.o. M • Presents with to the ED via EMS. • Per Brother/Chart Review: • Unable to provide history. • PMHx: SLE, Type 1 Diabetes (well controlled) • PSHx: Tonsillectomy, Insulin Pump (recently • Last seen earlier that morning by neighbor. removed) • Sister states she found him down at home. • Allergies: NKDA • Home Meds • Started CPR, neighbor called 911. • Prednisone (unknown dose or duration) • Sister is a nurse, believed that she couldn’t • Cellcept (mycophenolate) feel a pulse • Glargine • Lispro • Complained of “cold and and a bad cough” • SHx: No tobacco, no EtOH, no illicits several days prior. • FHx: SLE, HTN, DLD, stroke • Initial rhythm: asystole • Epi x 1 • ROSC 34 y.o. M • Vitals: • Physical Exam: • T: 38.3°C • General: nonresponsive • HR: 130s • BP: 76/44 • CVS: RRR, no m/r/g/c • RR: 24 • Lung: tachypnea, coarse breathe • Pox: 88% on bag and mask sounds bilaterally • Per EMR: Wgt 88 kgs • Neuro: PERRL, GCS 7 • Per EMR: Hgt 184 cm • Extremities: Radial, DP and PT 2+, no lower extremity pitting edema • Skin: No rashes, no ulcers 34 y.o. M • CBC: 13>17&50.1<294 • RFP: 122/7.3/81/5/74/5.53/1369 • Ca/Mg/Phos: 7.8/2.24/3.3 • INR/PTT: 2.2/64 • LFT • AST ~2100 • ALT ~1800 • ALKPHOS >3000 • Tbili: 6.5 • Dbili:4.1 • Alb: 3.3 • Tp: 6.4 • ABG: 6.9/55/18/3.1 • Lactate: 4.8 • Beta-hydroxybutyrate: 6.3 What’s wrong? systems systems Systems Based • CVS • Infectious • Pulmonary • Heme • Neuro/Psych • Supportive (FASTHUGS BID) • GU • Lines • GI • CODE • Endo/Rheum • Dispo • Infectious • PT/OT • Heme Procotalized Medicine You don’t look so good.
    [Show full text]
  • It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis
    SCIENCE IN RENAL MEDICINE www.jasn.org It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis Robert G. Luke and John H. Galla Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio ABSTRACT Maintenance of metabolic alkalosis generated by chloride depletion is often attributed aspiration, chloruretic diuretics, NaNO3 to volume contraction. In balance and clearance studies in rats and humans, we infusion (an effect of un-reabsorbable showed that chloride repletion in the face of persisting alkali loading, volume anions), and prior hypercapnia (post- contraction, and potassium and sodium depletion completely corrects alkalosis hypercapnic CDA) were all used to gen- by a renal mechanism. Nephron segment studies strongly suggest the corrective erate CDA. These studies establish that 2 response is orchestrated in the collecting duct, which has several transporters Cl repletion by NaCl or KCl—but not integral to acid-base regulation, the most important of which is pendrin, a luminal replacement of Na+ and K+ losses without 2 2 Cl/HCO3 exchanger. Chloride depletion alkalosis should replace the notion of Cl —fully corrects CDA in the mainte- contraction alkalosis. nance phase. The issue of the specific role of ECF volume depletion was not re- J Am Soc Nephrol 23: 204–207, 2012. doi: 10.1681/ASN.2011070720 solved at this time. To separate chloride from volume re- pletion, we first studied rats with selective Chloridedepletionisthecommonestofthe identical to that in the plasma of the dogs CDA produced by peritoneal dialysis 3 three major causes of metabolic alkalosis; with stable alkalemia. These isometric in- against NaHCO3 and a normal serum po- theothersrelatetopotassiumdepletion/ fusions completely corrected alkalosis by tassium concentration.
    [Show full text]
  • Severe Alkalemia (Ph 7.85): Compatible with Life? a Triple Acid
    ISSN 2474-3666 Case Report Mathews Journal of Case Reports Severe Alkalemia (pH 7.85): Compatible with Life? A Triple Acid-Base Conundrum Kishan B Patel1, James Espinosa2, Joan Wiley3, Nicholas Roy4, Alan Lucerna5 1Department of Emergency medicine/ Internal Medicine resident at Rowan-SOM in Stratford, NJ, USA. 2Assistant professor, Department of Emergency at Rowan-SOM and an attending physician at Kennedy USA. 3Associate program director of emergency medicine residency at Rowan School of Osteopathic Medicine and an attending physician at Kennedy USA. 4Pulmonary Critical Care, Kennedy University Hospital, Washington Twp, NJ, USA. 5Pulmonary Critical Care, Rowan-SOM, Stratford, NJ, USA. Corresponding Author: Kishan B Patel, Department of Emergency medicine/ Internal Medicine resident at Rowan-SOM in Stratford, NJ, USA, Tel: 765-448-8000; Email: [email protected] Received Date: 12 Feb 2016 Copyright © 2016 Patel KB Accepted Date: 10 Jun 2016 Citation: Patel KB, Espinosa J, Wiley J, Roy N, et al. (2016). Published Date: 13 Jun 2016 Severe Alkalemia (pH 7.85): Compatible with Life? A Triple Acid-Base Conundrum. M J Case. 1(2): 010. ABSTRACT Acid- Base disorders are a common occurrence seen in emergency medicine. An infrequent occurrence is one with a triple acid base disorder in which one of the derangement predominates to generate an alkalemia with a pH of > 7.60. Severe alkalemia with a pH > 7.65 is associated with a high mortality rate. Early recognition and aggressive management of the underlying acid base disorders is imperative for survival. Here we describe a case in which a patient presented with a gapped metabolic acidosis, presumed secondary to diabetic ketoacidosis, as well as a concurrent severe metabolic alka- losis with a pH of 7.85 and a respiratory alkalosis, which was secondary to a paradoxical unexpected respiratory response.
    [Show full text]
  • Metabolic Alkalosis James Strom, MD Objectives Readings I. Recognition
    Metabolic Alkalosis James Strom, MD Objectives 1. Recognize the electrolyte and blood gas findings that characterize simple and mixed metabolic alkaloses. 2. Understand the contributory roles of bicarbonate load, H+ loss, and increased tubular bicarbonate reabsorption. 3. Understand the generation and maintenance phases of metabolic alkalosis. 4. Understand the categorization and pathophysiology of chloride responsive and chloride resistant alkalosis. 5. Understand the roles of aldosterone and hypokalemia. 6. Review the therapy of metabolic alkalosis. Readings Rose and Rennke, pages 140-151. Rennke and Denker, pages 145-156. I. Recognition A. Simple Disorder 1. Elevated pH (reduced H+ concentration) - 2. Elevated HCO3 3. Adaptive (compensatory) rise in PaCO2 - 0.6 - 0.7 mm Hg per 1 mEq/L rise in HCO3 Example: pH 7.48 PaCO2 46 mm Hg - HCO3 34 mEq/L Tufts University School of Medicine Page 1 Metabolic Alkalosis James Strom, MD B. Mixed Disorder Bicarbonate increased beyond levels anticipated in response to another disorder Example: pH 7.38 PaCO2 65 mm Hg - HCO3 37 mEq/L Pathophysiologic Diagnosis: Mixed respiratory acidosis and metabolic alkalosis a. Low pH indicates acidemia (though mild) b. High PaCO2 of 65 identifies a respiratory acidosis - c. In simple respiratory acidosis, HCO3 rises ~ 0.3mEq/L for each 1 mm Hg rise in PaCO2 (to about 32 mEq/L for PaCO2 65) - d. Further increase in HCO3 to 37 indicates metabolic alkalosis Clinical Diagnosis: COPD and diuretic therapy C. Clinical Importance 1. Clue to an underlying disorder like volume depletion or primary aldosteronism 2. Interferes with ventilation in COPD 3. Combined metabolic and respiratory alkaloses can be severe II.
    [Show full text]
  • Acid Base Disorders – November 2017
    CrackCast Show Notes – Acid Base Disorders – November 2017 www.canadiem.org/crackcast Chapter 124 – Acid Base Disorders Episode Overview: 1. Describe an approach to acid-base problems 2. List a DDx for Resp Acidosis, Resp Alkalosis, Met Acidosis, Met Alkalosis 3. List causes of an elevated AGMA 4. List causes of NAGMA 5. List 5 complications of bicarbonate therapy Wisecracks 1. What are causes of a LOW anion gap? 2. Why do patients with hyperventilation have lip and extremity paresthesias, carpopedal spasm, muscle cramps, lightheadedness, and syncope? Key Points: Patients with an acute severe metabolic acidosis rely on a robust respiratory compensation; in these cases, the adequacy of the ventilatory response should be assessed and augmented, with non-invasive or invasive ventilation, if needed. • The strong ion difference = ([Na+ + K+ ] − [Cl− ]). When significantly less than 40, an acidosis is present. • The delta gap (ΔG) = (AG − 12) − (24 − [HCO3 − ]). Its calculation determines if the anion gap is accounted for by the change in serum bicarbonate concentration. An elevated anion gap and ΔG more than 6 indicates that a metabolic alkalosis in addition to a metabolic acidosis is likely to be present. • Patients who have a chronic respiratory acidosis (eg, in chronic obstructive pulmonary disease) are at risk for dangerous alkalemia if they are ventilated with routine parameters. Blood gas analysis in these cases should be performed frequently and settings titrated to the serum pH. • Alcoholic ketoacidosis may be manifested similarly to diabetic ketoacidosis but is much less common; insulin is contraindicated in alcoholic ketoacidosis. • When an elevated anion gap is recognized, the initial assessment focuses on identifying one of four causes: ketoacidosis, toxic ingestions, lactic acidosis, and renal failure.
    [Show full text]