The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate
Volume2015(2015), Article ID605830, 7 pages The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate 1Internal Medicine Department, University Hospital of Patras, 26500 Rion, Greece 2University of Patras School of Medicine, 26500 Rion, Greece 3Intensive Care Department, Brugmann University Hospital, 1030 Brussels, Belgium 4Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA Received 22 March 2015; Revised 29 June 2015; Accepted 1 July 2015 Copyright 2015 Dimitrios Velissaris et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option. Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years. Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gas . Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and Continue reading >>
2 Pathophysiology Of Acute Hemorrhagic Shock
Pathophysiology of Acute Hemorrhagic Shock A variety of definitions of hemorrhagic shock have arisen as more understanding of the mechanisms involved have been developed. Several definitions could be considered to be archaic but in general remain accurate (see Box 2-1 ). A modern definition of shock would acknowledge first that shock is inadequate tissue perfusion and inadequate removal of cellular waste products and second that shock is a failure of oxidative metabolism that can involve defects of oxygen (1) delivery, (2) transport, or (3) utilization, or combinations of all three. The diagnoses of clinical signs of shock are primarily related to organ failure, but organ failure is secondary to failure of the cells. Shock is used in reflections drawn from experiences with gunshot wounds. "Shock is the manifestation of the rude unhinging of the machinery of life." Many authors have described the "vicious cycles" in shock (see Figure 2-1 ). They may cascade in a variety of ways such as decreased cardiac output, which leads to a decreased blood pressure, which in turn leads to decreased tissue per- Suggested Citation:"2 Pathophysiology of Acute Hemorrhagic Shock." Institute of Medicine. 1999. Fluid Resuscitation: State of the Science for Treating Combat Casualties and Civilian Injuries. Washington, DC: The National Academies Press. doi: 10.17226/9625. Viciouscirclesinshock.Initiationofshockcanoccuratanypoint, buttheendpointisoftenthesame.Source:Reprinted,withpermission,from Davisetal.,(1995,p.145).Copyright1995byMosby-YearBook,Inc. fusion. Increased cardiac work may lead to failing myocardial function and decreased coronary perfusion. Decreased tissue perfusion at the cellular level leads to microcirculatory damage, cellular aggregation, and microcirculatory obstruction, Continue reading >>
Acidosis
For acidosis referring to acidity of the urine, see renal tubular acidosis. "Acidemia" redirects here. It is not to be confused with Academia. Acidosis is a process causing increased acidity in the blood and other body tissues (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma. The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal pH. Acidosis is said to occur when arterial pH falls below 7.35 (except in the fetus – see below), while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes. The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g., healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.[1] Signs and symptoms[edit] General symptoms of acidosis.[2] These usually accompany symptoms of another primary defect (respiratory or metabolic). Nervous system involvement may be seen with acidosis and occurs more often with respiratory acidosis than with metabolic acidosis. Signs and symptoms that may be seen i Continue reading >>
Acidosis, Shock, Metabolic Acidosis: Causes & Diagnoses | Symptoma.com
ECG may be normal in other causes of cardiogenic shock. [patient.info] Severe acidosis, severe hypoxemia a The etiologies of CS are listed. [mhmedical.com] As the stress on the left ventricle mounts, it is unable to overcome the heightened afterload and cardiac output drops leading to worsening hypoperfusion and acidosis. [emdocs.net] ( T81.1- ) psychogenic syncope ( F48.8 ) shock NOS ( R57.9 ) shock complicating or following abortion or ectopic or molar pregnancy ( O00 - O07 , O08.3 ) shock complicating [icd10data.com] Eventually, they will receive critical VBG results that indicate a mild metabolic acidosis, hyperkalemia, and hyponatremia. [emsimcases.com] acidosis Low bicarbonate (15-20mEq/L) Elevated BUN and creatinine Management Steroid Replacement Initial Dose Hydrocortisone 100mg IV preferred but can be given IM if necessary [coreem.net] If left untreated, Addison's disease can cause severe abdominal pain, weakness, low blood pressure, kidney failure and shock. [childrenshospital.org] Urinary salt and water loss cause severe dehydration, plasma hypertonicity, acidosis, decreased circulatory volume, hypotension, and, eventually, circulatory collapse. [merckmanuals.com] There is often times metabolic acidosis. [earthclinic.com] Effectively apply the newest emergency medicine techniques and approaches, including evidence-based therapies for shock; high-cost imaging; evaluation and resuscitation of [books.google.de] [] from hypoxia and metabolic acidosis secondary to lactic acid generation from poor tissue perfusion, impaired hepatic metabolism, and reduced acid excretion. 3, 10 It may [nursingcenter.com] acidosis Management No prophylactic antibiotics (consider if drowned in obviously infected source such as sewage tank) C-spine immobilization only if high concern Continue reading >>
Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to physiologic processes) Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis, types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidos Continue reading >>
Lactic Acidosis: Background, Etiology, Epidemiology
Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe Continue reading >>
Metabolic Acidosis
Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>
What Is Metabolic Acidosis?
Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>
Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside
Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside Antoine Kimmoun , Emmanuel Novy , Thomas Auchet , Nicolas Ducrocq , and Bruno Levy CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France Antoine Kimmoun, Email: [email protected] . Author information Copyright and License information Disclaimer Copyright Kimmoun et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution Continue reading >>
Defining Metabolic Acidosis In Patients With Septic Shock Using Stewart Approach - Sciencedirect
Volume 30, Issue 3 , March 2012, Pages 391-398 Defining metabolic acidosis in patients with septic shock using Stewart approach Author links open overlay panel JihadMallatMD The aim of this study was to define the nature of metabolic acidosis in patients with septic shock on admission to intensive care unit (ICU) using Stewart method. We also aimed to compare the ability of standard base excess (SBE), anion gap (AG), and corrected AG for albumin and lactate (AGcorr) to accurately predict the presence of unmeasured anions (UA). Thirty consecutive patients with septic shock were prospectively included on ICU admission. Stewart equations modified by Figge were used to calculate the strong ion difference and the strong ion gap (SIG). Most patients had multiple underlying mechanisms explaining the metabolic acidosis. Unmeasured anions and hyperchloremia were present in 70% of the patients. Increased UA were present in 23% of patients with normal values of SBE and [HCO3]. In these patients, plasma [Cl] was significantly lower compared with patients with low SBE and increased UA (103 [102-106.6] vs 108 [106-111] mmol/L; P = .01, respectively). Corrected AG for albumin and lactate had the best correlation with SIG (r = 0.94; P < .0001) with good agreement (bias, 0, and precision, 1.22) and highest area under the receiver operating characteristic curve (0.995; 95% confidence interval, 0.87-1) to discriminate SIG acidosis. Patients with septic shock exhibit a complex metabolic acidosis at ICU admission. High UA may be present with normal values of SBE and [HCO3] as a result of associated relative hypochloremic alkalosis. Corrected AG for albumin and lactate offers the most accurate bedside alternative to Stewart calculation of UA. Choose an option to locate/access this article: Continue reading >>
Combined Respiratory And Metabolic Acidosis Caused By Bronchospasm In Anaphylactic Shock
Zieliński J. · Koziorowski A. From the Department of Internal Medicine (Prof. Dr. B. Jochweds) and Department of Pathophysiology (Dr. A. Koziorowski), Institute of Tuberculosis, Warszawa Authors’ address: Dr. Jan Zielinski and Dr. Antoni Koziorowski, Instytut Gruzlicy, Klinika Chorób Wewnetrznych, Plocka 26, Warszawa (Poland) Continue reading >>
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Cardiogenic Shock - Heartupdate.com
Cardiogenic shock is a syndrome caused by a severe insufficiency of the heart pump manifested by the inability to provide the necessary oxygen and tissue nutrients and to remove metabolic activity product of metabolism. The main condition that leads to cardiogenic shock is the acute myocardial infarction in which necrosis is over 40% of the muscle mass of the left ventricle. In AMI, shock usually appears at 6-8 hours after the onset, but it is possible to install and after 1-2 days by extending the myocardial necrosis or by the AMI complications such as ventricular aneurysm, ventricular septal rupture (rupture of the wall that separates the two ventricles) and ventricular wall rupture. Other causes of cardiogenic shock are: diseases of the heart valves, especially aortic and mitral, intra-atrial thrombosis (formation of the clots with fairly large volume inside the atria), myocarditis, and dilated hypertrophic cardiomyopathy, arrhythmias with large increases in ventricular rate. Myocardial area affected of necrosis becomes akinetic (no more participating in heart contractions, becomes inert) and part of the myocardium that surrounds the necrosis is dyskinetic (contractions are weak). To produce cardiogenic shock, necrosis should contain 40-70% of left ventricular mass. Ventricular systolic function is reduced due to the emergence of these myocardial akinetic and dyskinetic areas and the amount of blood pumped during each systoles in the arterial system is greatly reduced; decreases, thereby, the flow-beat and by extension the cardiac output. In infarcted myocardial region over time, it is reproduced scarring with a more reduced surface area than originally allocated to the coronary artery infarction. The scar shows a diastolic dysfunction, not dilating properly during Continue reading >>
Mortality And The Nature Of Metabolic Acidosis In Children With Shock
, Volume 29, Issue2 , pp 286291 | Cite as Mortality and the nature of metabolic acidosis in children with shock Mortality in children with shock is more closely related to the nature, rather than the magnitude (base deficit/excess), of a metabolic acidosis. To examine the relationship between base excess (BE), hyperlactataemia, hyperchloraemia, 'unmeasured' strong anions, and mortality. Prospective observational study set in a multi-disciplinary Paediatric Intensive Care Unit (PICU). Forty-six children, median age 6months (1.514.4), median weight 5kg (3.28.8), admitted to PICU with shock. Predicted mortality was calculated from the paediatric index of mortality (PIM) score. The pH, base excess, serum lactate, corrected chloride, and 'unmeasured' strong anions (Strong Ion Gap) were measured or calculated at admission and 24h. Observed mortality (n=16) was 35%, with a standardised mortality ratio (SMR) of 1.03 (95% CI 0.711.35). There was no significant difference in admission pH or BE between survivors and nonsurvivors. There was no association between elevation of 'unmeasured' anions and mortality, although there was a trend towards hyperchloraemia in survivors (P=0.08). Admission lactate was higher in nonsurvivors (median 11.6 vs 3.3mmol/l; P=0.0003). Area under the mortality receiver operating characteristic curve for lactate was 0.83 (955 CI 0.700.95), compared to 0.71 (95% CI 0.530.88) for the PIM score. Admission lactate level >5mmol/l had maximum diagnostic efficiency for mortality, with a likelihood ratio of 2.0. There is no association between the magnitude of metabolic acidosis, quantified by the base excess, and mortality in children with shock. Hyperlactataemia, but not elevation of 'unmeasured' anions, is predictive of a poor outcome. MortalityMetabolic aci Continue reading >>
Hs Unit 2 Package 2 Flashcards | Quizlet
Subnormal arterial bp, reduced pressure or tension of any kind. Interstitial space: Definition of stages (I&II) Stage I: water moves from the interstitial spaces and the intestinal lumen to restore the normal blood volume. Stage II: Capillary permeability increases under ischemic conditions, allowing fluid to to leave the blood vessels and enter the interstitial spaces, and finally intense tissue deterioration begins in response to inadequate blood flow. A state of deep prolonged unconsciousness, from which one can be aroused but into which one immediately relapses. The flow of blood or other perfusate per unit volume of tissue, as in ventilation:perfusion ratio. Shift of fluid from the intravascular space to a non-functional space (e.g., abdomen or thorax) Results from an immunologically mediated reaction which vasodilator substances such as histamine are released into the blood. These substances cause vasodilation of arterioles & venules along with a marked increase in capillary permeability. Cardiogenic shock is when the heart has been damaged so much that it is unable to supply enough blood to the organs of the body. Severe blood and fluid loss make the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working. *Most common cause blood loss, dehydration, hemorrhage Caused by mechanical obstruction of the flow of blood through the central circulation. blockage of blood flow through the heart, lungs, and blood vessels. Decreased sympathetic control of blood vessel tone due to a defect in the vasomotor center in the brain stem or the sympathetic outflow to the blood vessels. *Most common cause depressant action of drugs, anaesthesia, lack of glucose, spinal cord injury, septic shock, insulin shock, pain, fear. RARE type of Continue reading >>
Causes Of Metabolic Acidosis In Canine Hemorrhagic Shock: Role Of Unmeasured Ions
Causes of metabolic acidosis in canine hemorrhagic shock: role of unmeasured ions 6Clinic of Anesthesiology, Intensive Care Medicine and Pain Management, Krankenhaus Nordwest, Steinbacher Hohl 2-26, 60488 Frankfurt, Germany 1Clinic of Anesthesiology, Ludwig-Maximilians-University, Marchioninistrasse 15, 81377 Munich, Germany 2Department of Thoracic and Vascular Surgery, University of Ulm, Steinhvelstrasse 9, 89075 Ulm, Germany 3Department of General, Visceral and Thoracic Surgery, Clinic of Nuremberg, Prof.-Ernst-Nathan-Strasse 1, 90419 Nuremberg, Germany 4Sangart Inc., 6175 Lusk Blvd., San Diego, CA 92121, USA 5Alliance Pharmaceutical Corp., 4660 La Jolla Village Drive, San Diego, CA 92122, USA 6Clinic of Anesthesiology, Intensive Care Medicine and Pain Management, Krankenhaus Nordwest, Steinbacher Hohl 2-26, 60488 Frankfurt, Germany 7Department of Physiology, Ludwig-Maximilians-University, Pettenkoferstrasse 12, 80336 Munich, Germany Dirk Bruegger: [email protected] ; Gregor I Kemming: [email protected] ; Matthias Jacob: [email protected] ; Franz G Meisner: [email protected] ; Christoph J Wojtczyk: [email protected] ; Kristian B Packert: [email protected] ; Peter E Keipert: [email protected] ; N Simon Faithfull: [email protected] ; Oliver P Habler: [email protected] ; Bernhard F Becker: [email protected] ; Markus Rehm: [email protected] Received 2007 Aug 14; Revisions requested 2007 Sep 28; Revised 2007 Nov 26; Accepted 2007 Dec 14. Copyright 2007 Bruegger et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distr Continue reading >>
