DOCSLIB.ORG

METABOLIC Acidosis Or Alkalosis Acidosis Or Alkalosis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
METABOLIC Acidosis Or Alkalosis Acidosis Or Alkalosis Very important Extra information References : • GUYTON AND HALL 12th edition • LINDA 5th edition * Guyton corners, anything that is colored with grey is EXTRA explanation Acid Base Disorders Objectives : • To explain the principles of blood gas and acid-base analysis • To interpret blood gas analysis and diagnose various acid base disorders • Describe causes of acid base disorders • Understand use of acid base nomograms 2 Contact us : [email protected] Disturbances of Acid-Base Balance Acid-base disturbances may be either RESPIRATORY or METABOLIC. pH problems due to pH problems arising a respiratory from acids or bases of disorder a non-CO2 origin RESPIRATORY METABOLIC acidosis or alkalosis acidosis or alkalosis. • Linda corner: o Disturbances of acid-base balance are among the most common conditions in all of clinical medicine. Acid- base disorders are characterized by an abnormal concentration of H+ in blood, reflected as abnormal pH. Acidemia is an increase in H+ concentration in blood (decrease in pH) and is caused by a pathophysiologic process called acidosis. Alkalemia, on the other hand, is a decrease in H+ concentration in blood (increase in pH) and is caused by a pathophysiologic process called alkalosis. o Disturbances of acid-base balance are described as either metabolic or respiratory, depending on whether the primary disturbance is in HCO3− or CO2. There are four simple acid-base disorders, where simple means that only one acid-base disorder is present. When there is more than one acid-base disorder present, the condi- tion is called a mixed acid-base disorder. 3 Disturbances of acid-base balance • Linda corner: Disturbances of acid-base balance are described as either metabolic or respiratory, depending on whether the primary disturbance is in HCO3− or CO2. There are four simple acid-base disorders, where simple means that only one acid-base disorder is present. When there is more than one acid-base disorder present, the condi- tion is called a mixed acid-base disorder. Metabolic acid-base disturbances are primary disor- ders involving HCO3−. Metabolic acidosis is caused by a decrease in HCO3− concentration that, according to the Henderson-Hasselbalch equation, leads to a de- crease in pH. This disorder is caused by gain of fixed H+ in the body (through overproduction of fixed H+, ingestion of fixed H+, or decreased excretion of fixed H+) or loss of HCO3−. Metabolic alkalosis is caused by an increase in HCO3− concentration that, according to the Henderson-Hasselbalch equation, leads to an increase in pH. This disorder is caused by loss of fixed H+ from the body or gain of HCO3−. Respiratory acid-base disturbances are primary disorders of CO2 (i.e., disorders of respiration). Respiratory acidosis is caused by hypoventilation, which results in CO2 retention, increased PCO2, and decreased pH. Respiratory alkalosis is caused by hyperventilation, which results in CO2 loss, decreased PCO2, and increased pH. When there is an acid-base disturbance, several mechanisms are utilized in an attempt to keep the blood pH in the normal range. The first line of defense is buffering in ECF and ICF. In addition to buffering, two types of compensatory responses attempt to nor- malize the pH: respiratory compensation and renal compensation. A helpful rule of thumb to learn is this: If the acid-base disturbance is metabolic (i.e., disturbance of HCO3−), then the compensatory response is respiratory to adjust the PCO2; if the acid-base distur- bance is respiratory (i.e., disturbance of CO2), then the compensatory response is renal (or metabolic) to adjust the HCO3− concentration. Another helpful rule is this: The compensatory response is always in the same direction as the original disturbance. For example, in metabolic acidosis, the primary disturbance is a decrease in the blood HCO3− concentration. The respiratory compensation is hyperventilation, which decreases the PCO2. In respiratory acidosis, the primary disturbance is increased PCO2. The renal compensation increases the HCO3− concentration. As each acid-base4 disorder is presented, the buff- ering and compensatory responses are discussed in detail. Table 7-2 presents a summary of the four simple acid-base disorders and the expected compensatory responses that occur in each. 4 Respiratory Acidosis Associated with Respiratory failure Impaired gas (e.g. COPDs like Inadequate alveolar diffusion emphysema). ventilation ( pulmonary edema) Characterized by ↑ Pco2 (hypercapnia) and ↓ plasma pH. Initial response is : Increased conversion of CO2 to H+ and HCO3 Increase in ECF [H+] and plasma [HCO3-]. Renal SECRETION OF H+ INCREASED [ COMPENSATORY MECHANISM ] ABSORPTION OF HCO3 عملية التنفس وهي أخذ اﻷكسجين وطرح ثاني أكسيد الكربون : Alveolar ventilation • • the kidney act as a compensatory mechanism to correct respiratory acidosis caused 5 by the lung Respiratory Acidosis ACUTELY CHRONICALLY 1 mEq/L [HCO3-] per 10 mm Hg 3.5 mEq/L [HCO3-] per 10 ↑ in Pco2 mm Hg ↑ in Pco2 (tissue buffering) (renal acid excretion) normal HCO3 : 24mEq/L . normal pCo2: 40 mmHg • Linda corner: Disturbances of blood pH can be caused by a primary disturbance of HCO3− concentration or a primary disturbance of PCO2. Such disturbances are best under- stood by considering the Henderson-Hasselbalch equation for the HCO3−/CO2 buffer. Recall that the equation states− that blood pH is determined by the ratio of the HCO3 concentration to the CO2 concentration. Thus, changes in either HCO3− concentration or PCO2 will produce a change in pH. Two types of compensatory responses attempt to normalize the pH: respiratory compensation and renal compensation If the acid-base disturbance is respiratory (i.e., disturbance of CO2), then the compensatory response is renal (or metabolic) to adjust the HCO3− concentration. The compensatory response is always in the same direction as the original disturbance. 6 Respiratory Acidosis Respiratory Acidosis ↓ plasma pH ↑ Pco2 ↑ plasma [HCO3-] - the diagram shows the acid base disorders. The shaded area show the range of values usually seen for each of the disorders. - the reason why the HCO3 is high in respiratory acidosis is because it compensate the disorder. In other words, respiratory acidosis is compensated by metabolic alkalosis. Why?? The Henderson-hasselbalch equation can be used to understand why the increased HCO3 conc. is a compensatory response. It's used to normalize the ratio of HCO3/CO2 . Because when CO2 increase the ration will decrease leading to low ph. But when HCO3 also increase the PH will be normal 7 Respiratory Alkalosis Characterised by: Reduced plasma Pco2 (hypocapnia) and elevated pH - in high altitude, the O2 is less, so ↓ Pco & ↑ plasma pH to compensate this loss 2 hyperventilation is triggered leading to depletion of Co2. Thus respiratory alkalosis may occur. Causes: (results from ↑ ventilation and ↓ Pco2 ) - HCO3 buffering reaction is increased gas exchange mainly due to shifted to left to decrease the HYPERVENTILATION (Anxiety / fear/High altitude) amount of HCO3 and increase extracellular amount of Co2 − Reduction in Pco shifts buffering reaction to the left - In alkalosis, the loss of HCO3 2 helps return the plasma pH + - Decrease in ECF [H ] and plasma [HCO3 ] toward normal. COMPENSATORY MECHANISM : Decreased : + *↓ Renal Secretion of H - - + *↓ Absorption of HCO3 (still an excess of HCO3 relative to H ). 8 Davenport Diagram Acid-base alterations Respiratory Alkalosis ↑ plasma pH ↓ Pco2 ↓ plasma [HCO3-] renal compensation for respiratory alkalosis consist of decrease excretion of H+ and From the diagram : decreased synthesis of new • PH : 7.6 “HIGH” HCO3. Therefore decrease its • HCO3- : 20 “low” reabsorption. And again the ration • Pco2 : 20 “low” of HCO3/Co2 in the equation will be normalized 9 Metabolic Acidosis & Alkalosis Metabolic acidosis and alkalosis ( Non-Co2) includes all situations other than those in which primary problem is respiratory. By definition, metabolic acidosis and alkalosis cannot be due to excess retention or loss of CO2 Does arterial Pco2 remain unchanged in these cases? NO! ↑ [H+] in acidosis will reflexly stimulate ventilation to lower Pco2. Conversely, ventilation will be inhibited in alkalosis to restore [H+]. Remember, plasma Pco2 changes during metabolic acidosis / alkalosis are a result of, not cause of, compensatory reflex responses to non-respiratory abnormalities. الرئة ليست السبب في تغير الهيدروجين لكنها تساعد في تعديل هذا التغيير عن طريق التحكم بالتنفس 10 Metabolic Acidosis Characterized by : - DECREASED [HCO3-] (<25mM) and pH. - Reduction in pH + ↑ in ECF H+ concentration Caused by : * Increased acid production * Impaired acid excretion. • Guyton corner : In metabolic acidosis, an excess of H over HCO3 occurs in the tubular fluid primarily because of decreased filtration of HCO3−. This decreased filtration of HCO3− is caused mainly by a decrease in the extracellular fluid con- centration of HCO3−. In respiratory acidosis, the excess H+ in the tubular fluid is due mainly to the rise in extracellular fluid PCO2, which stimulates H+ secretion. As discussed previously, with chronic acidosis, regard- less of whether it is respiratory or metabolic, there is an increase in the production of NH4+, which further con- tributes to the excretion of H+ and the addition of new HCO3− to the extracellular fluid. With severe chronic acidosis, as much as 500 mEq/day of H+ can be excreted in the urine, mainly in the form of NH4+; this excretion, in turn, contributes up to 500 mEq/day of new HCO3 that is added to the blood. Thus, with chronic acidosis, increased secretion of H+ by the tubules helps eliminate excess H+ from the body and increases the quantity of HCO3− in the extracellular fluid. This process increases the HCO3− part of the bicarbonate buffer system which, in accordance with the Henderson-Hasselbalch equation, helps raise the extracellular pH and corrects the acidosis. If the acidosis is metabolically mediated, additional compensation by the lungs causes a reduction in Pco2, also helping to correct the acidosis. 11 Addition of Severe fixed acids diarrhoea loss (e.g. diabetic of bicarbonate Heavy exercise ketoacidosis ). from intestines.
Load more

Recommended publications
  • BSCI440, Spring 2011, Dr. Higgins
    Chapter Guides: http://virtual.yosemite.cc.ca.us/rdroual/Course%20Materials/Physiology%20101/Chapte r%20Notes/Fall%202011/chapter_5%20Fall%202011.htm “One time, we had a guy perform who was supposed to be a master of kung fu. Turns out he was a male stripper. Surprised the hell out of us all.” “If you ever get stung by an anemone off the Great Barrier Reef, I want your last thought as you die to be 'damn, Higgins told me about this shit.'” “They knew the dose for this furry meatloaf; some of you know it as a cat.” “Experience and treachery will always overcome youth and exuberance.” *holding up a shoe* “So this is urine, right?” “Isn't that great? That's almost pornographic!” - in reference to a flowchart “The next time your roommate goes to vomit, run in and check their pupils and blood pressure. It’s all for science….the next time you get the stomach flu, think of me.” Lecture 1: Multicellularity & Homeostasis Homeostasis (Chapter 1) Why multicellularity? o surface:volume problem (nutrients), greater specialization, compartmentalization, homeostasis o homeostasis – maintenance of a constant, optimal internal environment Identify 4 basic cell types in mammalian systems o neuron, muscle, epithelial (exocrine vs endocrine), connective o organ systems: endocrine, nervous, musculoskeletal, cardiovascular, respiratory, urinary (osmotic pressure, pH, & ion content), gastrointestinal (absorb & excrete), reproductive, immune, integumentary Understand concept & examples of homeostasis o by isolating internal body fluids by regulating the composition of the fluids surrounding the cells & tissues, organ systems eliminate the need for each cell to respond to changes in the external environment o system sets desired reference level, and makes adjustment via feedback Design closed loop, negative feedback system to control a physical parameter 1 o levels go beyond set point → error signal to integrating center → regulatory mechanisms activate effectors → response → change in regulated variable o stimulus → sensory system → comparator with reference → effector for output o e.g.
    [Show full text]
  • Circulating Extracellular Vesicles As Biomarkers and Drug Delivery Vehicles in Cardiovascular Diseases
    biomolecules Review Circulating Extracellular Vesicles As Biomarkers and Drug Delivery Vehicles in Cardiovascular Diseases Renata Caroline Costa de Freitas 1,2 , Rosario Dominguez Crespo Hirata 2 , Mario Hiroyuki Hirata 2 and Elena Aikawa 1,3,4,* 1 Center for Interdisciplinary Cardiovascular Sciences, Division of Cardiovascular Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA; [email protected] 2 Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo 05508-000, Brazil; [email protected] (R.D.C.H.); [email protected] (M.H.H.) 3 Center for Excellence in Vascular Biology, Division of Cardiovascular Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA 4 Department of Human Pathology, Sechenov First Moscow State Medical University, 119992 Moscow, Russia * Correspondence: [email protected]; Tel.: +1-617-730-7755 Abstract: Extracellular vesicles (EVs) are composed of a lipid bilayer containing transmembrane and soluble proteins. Subtypes of EVs include ectosomes (microparticles/microvesicles), exosomes, and apoptotic bodies that can be released by various tissues into biological fluids. EV cargo can modulate physiological and pathological processes in recipient cells through near- and long-distance intercellular communication. Recent studies have shown that origin, amount, and internal cargos (nucleic acids, proteins, and lipids) of EVs are variable under different pathological conditions, including cardiovascular diseases (CVD). The early detection and management of CVD reduce premature morbidity and mortality. Circulating EVs have attracted great interest as a potential biomarker for diagnostics and follow-up of CVD. This review highlights the role of circulating EVs Citation: de Freitas, R.C.C.; Hirata, as biomarkers for diagnosis, prognosis, and therapeutic follow-up of CVD, and also for drug delivery.
    [Show full text]
  • Development of a Software to Determine Disturbances in the Acid-Base Balance in Human Blood
    NOTA TÉCNICA Vol. 34, No. 2, Agosto 2013, pp. 175-191 Development of a Software to Determine Disturbances in the Acid-Base Balance in Human Blood A. Reyes-Lazalde∗ ABSTRACT ∗∗ M. Reyes-Monreal In intensive care units, one of the most frequent emergencies occurring ∗ M.E. Pérez-Bonilla in patients in critical condition is acid-base imbalance. The ability ∗ R. Reyes-Luna to proficiently manage such patients is achieved through many years of hospital practice. The correct quantification of such imbalances ∗ Laboratorio de Biología allows for the detection of complex alterations. Although this area Interactiva, Escuela de is fundamental for the clinical management of many patients, non- Biología, BUAP. Blvd. specialist doctors rarely receive the appropriate training. In addition, Valsequillo y Av. San Claudio, the learning required to master this area is difficult for doctors due Edificio 112-A, Col. Jardines to the level of mathematics involved. There are two online support de San Manuel. CP. 72570, programs available on the internet for determining blood pH based on Puebla, Pue. the Stewart Model, along with a spreadsheet for the patient’s collected ∗∗ Dirección General de data. Generally, the calculation of hydrogen ion concentration [H+] Innovación Educativa, BUAP. uses a table of equivalences between pH y [H+] for discontinuous values Blvd. Valsequillo y Av. San of pH, with the Davenport diagram used manually. However, none Claudio, Edificio 1AUB, Col. of these programs unite the methods of classic calculus, chemistry Jardines de San Manuel. CP. and physicochemistry. This study develops software for the teaching 72570, Puebla, Pue. and calculation of acid-base imbalance that combines all the relevant methods, such as the Henderson-Hasselbalch equation, the Siggard- Anderson modified excess base equation, the anion gap calculation, the computational implementation of the Davenport diagram, the calculus of [H+] for any value of pH, the calculus for the compensatory process, and the Stewart Model.
    [Show full text]
  • Study on Acid-Base Balance Disorders and the Relationship
    ArchiveNephro-Urol of Mon SID. 2020 May; 12(2):e103567. doi: 10.5812/numonthly.103567. Published online 2020 May 23. Research Article Study on Acid-Base Balance Disorders and the Relationship Between Its Parameters and Creatinine Clearance in Patients with Chronic Renal Failure Tran Pham Van 1, *, Thang Le Viet 2, Minh Hoang Thi 1, Lan Dam Thi Phuong 1, Hang Ho Thi 1, Binh Pham Thai 3, Giang Nguyen Thi Quynh 3, Diep Nong Van 4, Sang Vuong Dai 5 and Hop Vu Minh 1 1Biochemistry Department, Military Hospital 103, Hanoi, Vietnam 2Nephrology and Hemodialysis Department, Military Hospital 103, Hanoi, Vietnam 3National Hospital of Endocrinology, Hanoi, Vietnam 4Biochemistry Department, Backan Hospital, Vietnam 5Biochemistry Department, Thanh Nhan Hospital, Hanoi, Vietnam *Corresponding author: Biochemistry Department, Military Hospital 103, Hanoi, Vietnam. Email: [email protected] Received 2020 May 09; Accepted 2020 May 09. Abstract Objectives: We aimed to determine the parameters of acid-base balance in patients with chronic renal failure (CRF) and the rela- tionship between the parameters evaluating acid-base balance and creatinine clearance. Methods: The current cross-sectional study was conducted on 300 patients with CRF (180 males and 120 females). Clinical examina- tion and blood tests by taking an arterial blood sample for blood gas measurement as well as venous blood for biochemical tests to select study participants were performed. Results: Patients with CRF in the metabolic acidosis group accounted for 74%, other types of disorders were less common. The average pH, PCO2, HCO3, tCO2 and BE of the patient group were 7.35 ± 0.09, 34.28 ± 6.92 mmHg, 20.18 ± 6.06 mmol/L, 21.47 ± 6.48 mmHg and -4.72 ± 6.61 mmol/L respectively.
    [Show full text]
  • Davenport Diagram Pathology > Renal Pathologies > Renal Pathologies
    Davenport Diagram Pathology > Renal Pathologies > Renal Pathologies DAVENPORT DIAGRAMS: • Davenport diagrams are graphic displays of acid-base states. • They illustrate the dynamic relationships between arterial blood pH, bicarbonate and non-bicarbonate buffers, and the partial pressure of carbon dioxide. • An isopleth represents all possible combinations of bicarbonate and pH values at a given carbon dioxide partial pressure. 4 simple acid-base disorders prior to compensation Graph Features: - The x-axis tracks pH; the healthy homeostatic arterial blood value = 7.4 - Values less than this reflect acidosis; values higher reflect alkalosis. - The y-axis tracks bicarbonate concentration; the healthy homeostatic value 24 millimolar. - Recall that, as bicarbonate concentration increases, pH becomes more alkaline. - Isopleth for a partial pressure of carbon dioxide of 40 mmHg. - A straight line to represent the combination of all non-bicarbonate buffer titration curves. Disorders that cause the blood to become more acidic. • Metabolic acidosis occurs when the reduction in bicarbonate concentration lowers the pH. - Notice that, because this is a non-respiratory disorder, PaCO2 is unaffected. • Respiratory acidosis occurs when the lungs retain excess carbon dioxide, so the partial pressure of carbon dioxide is elevated above normal, which lowers the pH. - Recall that respiratory acidosis produces an elevated bicarbonate concentration, which is reflected in our graph. Disorders that cause the blood to become alkalotic (aka, basic). • Metabolic alkalosis occurs when bicarbonate concentration is elevated. - As in metabolic acidosis, the PaCO2 remains on the 40 mmHg isopleth. 1 / 4 • Respiratory alkalosis occurs when the lungs release too much carbon dioxide - Lowers the PaCO2 and increases pH. Compensatory Mechanisms • The lungs and kidneys respond to acid-base disorders via compensatory mechanisms that bring pH back to normal.
    [Show full text]
  • Development of a Software to Determine Disturbances in the Acid-Base Balance in Human Blood
    NOTA TÉCNICA Vol. 34, No. 2, Agosto 2013, pp. 175-191 Development of a Software to Determine Disturbances in the Acid-Base Balance in Human Blood A. Reyes-Lazalde∗ ABSTRACT ∗∗ M. Reyes-Monreal In intensive care units, one of the most frequent emergencies occurring ∗ M.E. Pérez-Bonilla in patients in critical condition is acid-base imbalance. The ability ∗ R. Reyes-Luna to proficiently manage such patients is achieved through many years of hospital practice. The correct quantification of such imbalances ∗ Laboratorio de Biología allows for the detection of complex alterations. Although this area Interactiva, Escuela de is fundamental for the clinical management of many patients, non- Biología, BUAP. Blvd. specialist doctors rarely receive the appropriate training. In addition, Valsequillo y Av. San Claudio, the learning required to master this area is difficult for doctors due Edificio 112-A, Col. Jardines to the level of mathematics involved. There are two online support de San Manuel. CP. 72570, programs available on the internet for determining blood pH based on Puebla, Pue. the Stewart Model, along with a spreadsheet for the patient’s collected ∗∗ Dirección General de data. Generally, the calculation of hydrogen ion concentration [H+] Innovación Educativa, BUAP. uses a table of equivalences between pH y [H+] for discontinuous values Blvd. Valsequillo y Av. San of pH, with the Davenport diagram used manually. However, none Claudio, Edificio 1AUB, Col. of these programs unite the methods of classic calculus, chemistry Jardines de San Manuel. CP. and physicochemistry. This study develops software for the teaching 72570, Puebla, Pue. and calculation of acid-base imbalance that combines all the relevant methods, such as the Henderson-Hasselbalch equation, the Siggard- Anderson modified excess base equation, the anion gap calculation, the computational implementation of the Davenport diagram, the calculus of [H+] for any value of pH, the calculus for the compensatory process, and the Stewart Model.
    [Show full text]
  • Coproporphyrins I and III As Functional Markers of OATP1B Activity: in Vitro and in Vivo Evaluation in Preclinical Species S
    Supplemental material to this article can be found at: http://jpet.aspetjournals.org/content/suppl/2016/02/23/jpet.116.232066.DC1 1521-0103/357/2/382–393$25.00 http://dx.doi.org/10.1124/jpet.116.232066 THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS J Pharmacol Exp Ther 357:382–393, May 2016 Copyright ª 2016 by The American Society for Pharmacology and Experimental Therapeutics Coproporphyrins I and III as Functional Markers of OATP1B Activity: In Vitro and In Vivo Evaluation in Preclinical Species s Hong Shen, Jun Dai, Tongtong Liu, Yaofeng Cheng, Weiqi Chen, Chris Freeden, Yingru Zhang, W. Griffith Humphreys, Punit Marathe, and Yurong Lai Pharmaceutical Candidate Optimization, Bristol-Myers Squibb Company, Princeton, New Jersey Received January 12, 2016; accepted February 12, 2016 ABSTRACT Inhibition of organic anion-transporting polypeptide (OATP)1B by 2.6- and 5.2-fold, while rifampicin (15 mg/kg, oral) in- Downloaded from function can lead to serious clinical drug-drug interactions, thus creased the AUCs by 2.7- and 3.6-fold, respectively. As the a thorough evaluation of the potential for this type of interaction systemic exposure increased, the excretion of both isomers must be completed during drug development. Therefore, sensitive in urine rose from 1.6- to 4.3-fold in monkeys. In agreement and specific biomarkers for OATP function that could be used with this finding, the AUC of rosuvastatin (RSV) in cynomolgus in conjunction with clinical studies are currently in demand. In monkeys increased when OATP1B inhibitors were coadminis- the present study, preclinical evaluations were conducted to tered.
    [Show full text]
  • (Renal Physiology 10 &11) Acid-Base Balance 2 & 3
    (Renal Physiology 10 &11) Acid-Base Balance 2 & 3 Buffer System & Acid Base Disorders Ahmad Ahmeda [email protected] 1 Respiratory Regulation of Acid-Base Balance Pulmonary expiration of CO2 normally BALANCES metabolic formation of CO2. Changes in alveolar ventilation can alter plasma Pco2 - ↑ ventilation, ↓Pco2, ↑pH - ↓ ventilation, ↑ Pco2, ↓ pH Changes in [H+] also alters ALVEOLAR VENTILATION. Respiratory Regulation of Acid-Base Balance POWERFUL (1-2 x better than extracellular chemical buffers), but cannot fully rectify disturbances outside respiratory system, i.e. with fixed acids like lactic acid. Acts relatively RAPIDLY to stop [H+] changing too much until renal buffering kicks in but DOES NOT eliminate + - H (or HCO3 ) from body. Abnormalities of respiration can alter bodily [H+] resulting in; - RESPIRATORY ACIDOSIS or - RESPIRATORY ALKALOSIS. Renal Regulation of Acid-Base MOST EFFECTIVE regulator of pH but much SLOWER (i.e. max. activity after 5-6 days) than other processes. Responsible for ELIMINATING the 80 -100 mEq of fixed ACIDS generated each day. Normally, must also PREVENT renal LOSS of freely – - filterable HCO3 in order to preserve this primary buffer system. BOTH PROCESSES are dependent on both H+ filtration / secretion into renal tubules and secretion / reabsorption of - plasma [HCO3 ]. Kidneys also responsible for COMPENSATORY CHANGES in - [HCO3 ] during respiratory acid-base disorders. * IF KIDNEYS FAIL, pH BALANCE WILL FAIL * Renal Regulation of Acid-Base Overall mechanism straightforward: - - large [HCO3 ] continuously filtered into tubules + - large [H ] secreted into tubules + - if more H secreted than HCO3 filtered = a net loss of acid ↑pH - + if more HCO3 filtered than H secreted = a net loss of base ↓pH + - H / HCO3 Control by the Kidney Renal H+ Secretion H+ enters filtrate by FILTRATION through glomeruli and SECRETION into tubules.
    [Show full text]
  • Transformation of the Davenport Diagram to a Computerized Artificial Neural Network
    SCIREA Journal of Medicine http://www.scirea.org/journal/PM April 1, 2018 Volume 2, Issue 1, February 2018 Transformation of the Davenport Diagram to a Computerized Artificial Neural Network TIMOTHY J SMITH, RPH, PHD Department of Physiology and Pharmacology, Thomas J Long School of Pharmacy and Health Sciences, University of the Pacific, Stockton, California 95211 E-Mail:[email protected] (209)946-3168 Abstract The Davenport diagram, which illustrates the interactions of pH, bicarbonate and pCO2 as related to respiratory/metabolic phases of acidosis/alkalosis was transformed into a computerized neural network. This transformation enables computer-assisted prediction of acidosis/alkalosis subtypes on the basis of any two factors from pH, bicarbonate and pCO2. Furthermore, this neural network can eventually be trained to predict changes in acid-base balance on the basis of additional factors; illustrating the utility of neural network analysis as a dynamic predictive tool in healthcare. Keywords: Davenport diagram, neural network, nomogram, acidosis, alkalosis 1 Introduction Many artificial intelligence techniques are useful tools in healthcare. Among these are computerized artificial neural networks, which facilitate prediction of outcomes based upon two or more independent variables. A simple, yet flexible application of neural network analysis is the development of a neural network based upon a nomogram. These nomogram transformations can expand the utility of the nomogram, since additional factors can be used to train the computer to modify predictions beyond the capability of the basic two-dimensional nomogram. Examples of these transformations have been published previously [1,2]. The purpose of this report is to illustrate a neural network transformation based upon the Davenport diagram as a template.
    [Show full text]
  • Blood Ph, Gases, and Electrolytes
    NBS SPECIAL PUBLICATION 450 U.S. DEPARTMENT OF COMMERCE / National Bureau of Standards NATIONAL BUREAU OF STANDARDS The National Bureau of Standards^ was established by an act of Congress March 3, 1901. The Bureau's overall goal is to strengthen and advance the Nation's science and technology and facilitate their effective application for public benefit. To this end, the Bureau conducts research and provides: (1) a basis for the Nation's physical measurement system, (2) scientific and technological services for industry and government, (3) a technical basis for equity in trade, and (4) technical services to pro- mote public safety. The Bureau consists of the Institute for Basic Standards, the Institute for Materials Research, the Institute for Applied Technology, the Institute for Computer Sciences and Technology, the Office for Information Programs, and the Office of Experimental Technology Incentives Program. THE INSTITUTE FOR BASIC STANDARDS provides the central basis within the United States of a complete and consist- ent system of physical measurement; coordinates that system with measurement systems of other nations; and furnishes essen- tial services leading to accurate and uniform physical measurements throughout the Nation's scientific community, industry, and commerce. The Institute consists of the Office of Measurement Services, and the following center and divisions: Applied Mathematics — Electricity — Mechanics — Heat — Optical Physics — Center for Radiation Research — Lab- oratory Astrophysics^ — Cryogenics" — Electromagnetics" — Time and Frequency". THE INSTITUTE FOR MATERIALS RESEARCH conducts materials research leading to improved methods of measure- ment, standards, and data on the properties of well-characterized materials needed by industry, commerce, educational insti- tutions, and Government; provides advisory and research services to other Government agencies; and develops, produces, and distributes standard reference materials.
    [Show full text]
  • Basics of Acid Base Balance
    Basics of Acid Base Balance Red: very important. Green: Doctor’s notes. Pink: formulas. Yellow: numbers. Gray: notes and explanation. Physiology Team 436 – Renal Block Lecture 9 1 For further understanding please check our “Extra Notes” file which contains extra explanation from reference books. Objectives o Lecture: 9 o Lecture 10 & 11 o Define: acid and base. o To define buffer system and discuss the role of blood buffers and to explain their relevant roles in the body. o Explain what is meant by strong o To describe the role of kidneys in the regulation of acid- and weak acids and bases. base balance o To describe the role of lungs in the regulation of acid-base o List and identify the balance names/formulas for the common o To explain the principles of blood gas and acid-base analysis strong acids and strong bases. o To interpret blood gas analysis and diagnose various acid o To explain the role of Henderson- base disorders Hasselbalch equation in acid-base o Describe causes of acid base disorders regulation. o Understand use of acid base nomograms 2 Acid – Base Balance Acid – Base balance ( as known as pH HOMEOSTASIS ) : one of the essential functions of the body, it is concerned with the precise regulation of free (unbound) hydrogen ion concentration in body fluids. When discussing acid - base balance, we are normally concerned with regulation of H+ ion balance ( although HCO3- plays a vital role in this balance ). To avoid disturbances in [H+], and to maintain its homeostasis : (e.g. hydrogen bonding and charge on proteins the amount generated / taken in MUST EQUAL the amount secreted.
    [Show full text]
  • Acid/Base Simulations (Human 7, 11/08/07, 11/4/08 ) Note to Outside Skidmore Readers
    Respiration Physiology (Mammalian Physiology '07/08) Acid/Base Simulations (Human 7, 11/08/07, 11/4/08 ) Note to outside Skidmore readers. The following maneuvers allow the user create a primary respiratory and metabolic acidosis and alkalosis of any desired amount and to observe the model's attempt to compensate for the disturbance. They are also each available in simpler form as acid-base vignettes via links on this page. 1) Learning four interventions that are useful in acid-base simulation After a brief introductory demo, you will 'experiment' on your own with each of the four interventions below by changing the listed variables (and any appropriate others you may find useful in any Help Info on: screen under View summary of all variables ) so as to effect an acid-base disturbance and follow its' compensatory correction. The techniques to be utilized to effect the desired acid-base disturbance include the following: a) Infusion - simulates an IV infusion of controlled time, duration and content. [IFMIN, IFVOL, IFBIC] b) Control of metabolism- controlling metabolism so that it produces more or less acid [BACID] c) Control of ventilation- controlling ventilation via the use of the artificial respirator [ARTRES, ARVOL, ARRT] d) Control of atmospheric CO2- controlling atmospheric % CO2 [FCO2AT] 1 2) Sample simulated acid-base intervention- induction of metabolic alkalosis via infusion of bicarbonate a) Set tables under View Output: for acid-base output (and possible use in plotting on a Davenport diagram) PH, PCO2A, BICARB, AVENT, IFMIN, EXBIC (note: look these up in Help) b) Set up the infusion (note order in which variables are set) 1) IFMIN = 60 2) IFBIC = 240 (Run for 0 min, 0 printouts) 3) IFVOL = 1000 c) run for 1H, 10 (min) between printouts d) Characterize acid-base status at 0.0, 0.5 & 1.0 hour (by a Davenport plot if available), identify the primary acid base problem and secondary compensations (if present).
    [Show full text]