Pocket Guide to Critical Care Pharmacotherapy Pocket Guide to Critical Care Pharmacotherapy

Total Page:16

File Type:pdf, Size:1020Kb

Pocket Guide to Critical Care Pharmacotherapy Pocket Guide to Critical Care Pharmacotherapy Pocket Guide to Critical Care Pharmacotherapy Pocket Guide to Critical Care Pharmacotherapy By John Papadopoulos, BS, PharmD, FCCM, BCNSP Associate Professor of Pharmacy Practice Arnold & Marie Schwartz College of Pharmacy and Health Sciences Brooklyn, New York and Critical Care Pharmacist Clinical Instructor of Medicine Department of Medicine New York University Medical Center New York, New York © 2008 Humana Press Inc., a part of Springer Science+Business Media 999 Riverview Drive, Suite 208 Totowa, New Jersey 07512 humanapress.com All rights reserved. No part of this book may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise without written permission from the Publisher. All papers, comments, opinions, conclusions, or recommendations are those of the author(s), and do not necessarily reflect the views of the publisher. Due diligence has been taken by the publishers, editors, and authors of this book to assure the accuracy of the information published and to describe generally accepted practices. The contributors herein have carefully checked to ensure that the drug selections and dosages set forth in this text are accurate and in accord with the standards accepted at the time of publication. Notwithstanding, as new research, changes in government regulations, and knowledge from clinical experience relating to drug therapy and drug reactions constantly occurs, the reader is advised to check the product information provided by the manufacturer of each drug for any change in dosages or for additional warnings and contraindications. This is of utmost importance when the recommended drug herein is a new or infre- quently used drug. It is the responsibility of the treating physician to determine dosages and treatment strategies for individual patients. Further it is the responsibility of the health care provider to ascertain the Food and Drug Administration status of each drug or device used in their clinical practice. The publisher, editors, and authors are not responsible for errors or omissions or for any consequences from the application of the information presented in this book and make no warranty, express or implied, with respect to the contents in this publication. This publication is printed on acid-free paper. ∞ ANSI Z39.48-1984 (American Standards Institute) Permanence of Paper for Printed Library Materials. Cover design by Karen Schulz Production Editor: Amy Thau For additional copies, pricing for bulk purchases, and/or information about other Humana titles, contact Humana at the above address or at any of the following numbers: Tel.: 1-800-SPRINGER; Fax: 973-256- 8314; or visit our Website: http://humanapress.com Photocopy Authorization Policy: Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Humana Press Inc., provided that the base fee of US $30.00 per copy is paid directly to the Copyright Clearance Center at 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license from the CCC, a separate system of payment has been arranged and is acceptable to Humana Press Inc. The fee code for users of the Transactional Reporting Service is: [978-1-934115-45-9/08 $30.00]. Printed in the United States of America. 10 9 8 7 6 5 4 3 2 1 eISBN 13: 978-1-59745-488-9 Library of Congress Control Number: 2007938421 This handbook is dedicated to my wife Maria, my children, Theodore Thomas and Eleni Thalia, and my mother Eleni. I am grateful for your collective understanding of my professional commitment. Preface Critical care medicine is a cutting-edge medical field that is highly evidence-based. Studies are continuously published that alter the approach to patient care. As a criti- cal care clinician, I am aware of the tremendous commit- ment required to provide optimal evidence-based care. Pocket Guide to Critical Care Pharmacotherapy covers the most common ailments observed in adult critically-ill patients. I utilize an algorithmic, easy-to-follow, system- atic approach. Additionally, I provide references and web links for many disease states, for clinicians who want to review the available literature in greater detail. The contents of this handbook should be utilized as a guide and in addition to sound clinical judgment. Consult full prescribing information and take into consideration each drug’s pharmacokinetic profile, contraindications, warnings, precautions, adverse reactions, potential drug interactions, and monitoring parameters before use. Every effort was made to ensure the accuracy of Pocket Guide to Critical Care Pharmacotherapy. The author, edi- tor, and publisher are not responsible for errors or omis- sions or for any consequences associated with the utilization of the contents of this handbook. John Papadopoulos, BS, PharmD, FCCM, BCNSP vii Contents Preface .......................................................................... vii Editor ............................................................................. xi List of Tables .............................................................. xiii 1. Advance Cardiac Life Support ........................ 1 2. Cardiovascular.................................................. 21 3. Cerebrovascular ............................................... 55 4. Critical Care ...................................................... 65 5. Dermatology ...................................................101 6. Endocrinology ................................................103 7. Gastrointestinal ..............................................109 8. Hematology .....................................................119 9. Infectious Disease ..........................................125 10. Neurology ........................................................131 11. Nutrition ..........................................................137 12. Psychiatric Disorders.....................................143 13. Pulmonary .......................................................149 14. Renal .................................................................155 Index ............................................................................183 ix Editor David R. Schwartz, MD • Section Chief, Critical Care Medicine, Assistant Professor of Medicine, Department of Medicine, New York University Medical Center, New York, New York xi List of Tables Chapter 1 1.1. ACLS Pulseless Arrest Algorithm 1.2. Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm 1.3. Pulseless Electrical Activity Algorithm 1.4. Asystole Algorithm 1.5. Bradycardia Algorithm (slow [HR <60 bpm] or Relatively Slow) 1.6. Tachycardia Algorithm Overview 1.7. Management of Stable Atrial Fibrillation/ Atrial Flutter 1.8. Management of Narrow Complex Stable Supraventricular Tachycardia (QRS < 0.12 s) 1.9. Management of Stable Ventricular Tachycardia 1.10. Synchronized Cardioversion Algorithm for the Management of Symptomatic Tachycardia 1.11. Common Drugs Utilized During ACLS 1.12. Pulseless Electrical Activity: Causes (HATCH HMO pH) and Management 1.13. Pharmacological Management of Anaphylaxis/Anaphylactoid Reactions viii xiv List of Tables Chapter 2 2.1. Thrombolysis in Myocardial Infarction (TIMI) Grade Flows 2.2. TIMI Risk Score 2.3. Short-Term Risk of Death of Nonfatal Myocardial Infarction in Patients Presenting with Unstable Angina (Note: Low-Risk Omitted) 2.4. Acute Pharmacological Management of Unstable Angina and Non-ST Elevation Myocardial Infarction 2.5. Acute Pharmacological Management of ST-Elevation Myocardial Infarction (Non-Invasive or Conservative Strategy) 2.6. Considerations in Patients with Right Ventricular Infarctions 2.7. Contraindications to Fibrinolytic Therapy in Patients with ST-Elevation Myocardial Infarction 2.8. Management of Acute Decompensated Heart Failure 2.9. Vaughan Williams Classification of Antiarrhythmics 2.10. Antithrombotic Pharmacotherapy for Patients with Various Diseases 2.11. Causes and Management of Acquired Torsades de Pointes 2.12. Hypertensive Crises 2.13. Management of Catecholamine Extravasation 2.14. Prevention of Venous Thromboembolism in the ICU Patient List of Tables xv 2.15. Management of Deep-Vein Thrombosis and Pulmonary Embolism 2.16. Management of Elevated INRs in Patients Receiving Warfarin Pharmacotherapy Chapter 3 3.1. General Supportive Care for Patients with an Acute Cerebrovascular Accident 3.2. Blood Pressure Management in the Setting of an Acute Cerebrovascular Accident 3.3. Alteplase Inclusion and Exclusion Criteria for CVA Indication 3.4. Modified National Institute of Health Stroke Scale 3.5. Alteplase Administration Protocol for CVA Indication 3.6. Management of an Alteplase-Induced Intrac- ranial Hemorrhage 3.7. Management of Intracranial Hypertension (ICP > 20 mmHg) Chapter 4 4.1. General Drug Utilization Principles in ICU Care 4.2. Management of Severe Sepsis and Septic Shock 4.3. Sedation, Analgesia, and Delirium Guidelines 4.4. Modified Ramsey Sedation Scale 4.5. Riker Sedation-Agitation Scale 4.6. Confusion Assessment Method for the Diagnosis of Delirium in ICU Patients 4.7. Neuromuscular Blocker Use in the Intensive Care Unit xvi List of Tables 4.8. Reversal of Nondepolarizing Neuromuscular Blockers 4.9. Factors that Alter the Effects of Neuromuscu- lar Blockers 4.10. Management of Malignant Hyperthermia 4.11. Use of Packed Red Blood Cell Transfusions and Erythropoietin in Critically-Ill Patients 4.12.
Recommended publications
  • Dopamine: a Role in the Pathogenesis and Treatment of Hypertension
    Journal of Human Hypertension (2000) 14, Suppl 1, S47–S50 2000 Macmillan Publishers Ltd All rights reserved 0950-9240/00 $15.00 www.nature.com/jhh Dopamine: a role in the pathogenesis and treatment of hypertension MB Murphy Department of Pharmacology and Therapeutics, National University of Ireland, Cork, Ireland The catecholamine dopamine (DA), activates two dis- (largely nausea and orthostasis) have precluded wide tinct classes of DA-specific receptors in the cardio- use of D2 agonists. In contrast, the D1 selective agonist vascular system and kidney—each capable of influenc- fenoldopam has been licensed for the parenteral treat- ing systemic blood pressure. D1 receptors on vascular ment of severe hypertension. Apart from inducing sys- smooth muscle cells mediate vasodilation, while on temic vasodilation it induces a diuresis and natriuresis, renal tubular cells they modulate sodium excretion. D2 enhanced renal blood flow, and a small increment in receptors on pre-synaptic nerve terminals influence nor- glomerular filtration rate. Evidence is emerging that adrenaline release and, consequently, heart rate and abnormalities in DA production, or in signal transduc- vascular resistance. Activation of both, by low dose DA tion of the D1 receptor in renal proximal tubules, may lowers blood pressure. While DA also binds to alpha- result in salt retention and high blood pressure in some and beta-adrenoceptors, selective agonists at both DA humans and in several animal models of hypertension. receptor classes have been studied in the treatment of
    [Show full text]
  • Rutamarin: Efficient Liquid–Liquid Chromatographic Isolation from Ruta Graveolens L
    molecules Article Rutamarin: Efficient Liquid–Liquid Chromatographic Isolation from Ruta graveolens L. and Evaluation of Its In Vitro and In Silico MAO-B Inhibitory Activity Ewelina Kozioł 1, Simon Vlad Luca 2,3, Hale Gamze A˘galar 4 , Begüm Nurpelin Sa˘glık 4 , Fatih Demirci 4,5, Laurence Marcourt 6 , Jean-Luc Wolfender 6 , Krzysztof Jó´zwiak 7 and Krystyna Skalicka-Wo´zniak 1,* 1 Independent Laboratory of Natural Products Chemistry, Department of Pharmacognosy, Medical University of Lublin, 20-093 Lublin, Poland; [email protected] 2 Department of Pharmacognosy, Grigore T. Popa University of Medicine and Pharmacy Iasi, 700115 Iasi, Romania; [email protected] 3 Biothermodynamics, TUM School of Life and Food Sciences Weihenstephan, Technical University of Munich, 85354 Freising, Germany 4 Department of Pharmacognosy, Faculty of Pharmacy, Anadolu University, Eskisehir 26470, Turkey; [email protected] (H.G.A.); [email protected] (B.N.S.); [email protected] (F.D.) 5 Faculty of Pharmacy, Eastern Mediterranean University, Famagusta 99628, Cyprus 6 Institute of Pharmaceutical Sciences of Western Switzerland, IPSWS, University of Geneva, CMU, 1211 Geneva 4, Switzerland; [email protected] (L.M.); [email protected] (J.-L.W.) 7 Department of Biopharmacy, Medical University of Lublin, 20-093 Lublin, Poland; [email protected] * Correspondence: [email protected] Academic Editors: Tomasz Tuzimski and James Barker Received: 29 April 2020; Accepted: 5 June 2020; Published: 9 June 2020 Abstract: Naturally occurring coumarins are a group of compounds with many documented central nervous system (CNS) activities. However, dihydrofuranocoumarins have been infrequently investigated for their bioactivities at CNS level.
    [Show full text]
  • Anti-Hypotensive Effects of M6434, an Orally Active a 1-Adrenoceptor Agonist, in Rats
    Anti-Hypotensive Effects of M6434, an Orally Active a 1-Adrenoceptor Agonist, in Rats Tatsuroh Dabasaki, Masato Shimojo, Hiroshi Ishikawa and Akio Uemura Fuji Central Research Laboratory, Mochida Pharmaceutical Co., Ltd., 722 Jimba-aza-Uenohara, Gotemba, Shizuoka 412, Japan Received December 19, 1991 Accepted February 17, 1992 ABSTRACT-The anti-hypotensive effects of M6434 were evaluated and compared with those of other orally active sympathomimetics in rats. Oral administration of M6434 (0.5-2.0 mg/kg) and midodrine (1.0 5.0 mg/kg) also produced a dose-related increase in mean arterial pressure in normotensive rats. The pressor effect of M6434 was about 4 times more potent than that of midodrine. Both M6434 and midodrine caused a dose-dependent decrease in heart rate. The pressor effect of M6434 (1.0 mg/kg) did not diminish after its repeated administration for 7 days. The pretreatment with M6434 (0.5 1.0 mg/kg) and midodrine (2.0 5.0 mg/kg) improved the orthostatic index in the experimental model of postural hypotension in rats. The effect of M6434 on postural hypotension was about 5 times more po tent than that of midodrine. Intravenously injected M6434 (3-300pg/kg) produced a dose-dependent increase in the blood pressure of pithed rats. These results suggest that M6434 possesses a potent anti hypotensive activity which is superior to that of midodrine, and M6434 may be useful in the treatment of essential and postural hypotension. Keywords: M6434, a 1-Agonist, Midodrine, Postural hypotension, Orthostatic index M6434, 2-[(5-chloro-2-methoxyphenyl)azo]-1H-imida in clinical therapy.
    [Show full text]
  • Identification Ofa D1 Dopamine Receptor, Not Linked To
    Br. J. Pharmacol. (1991), 103, 1928-1934 11--" Macmillan Press Ltd, 1991 Identification of a D1 dopamine receptor, not linked to adenylate cyclase, on lactotroph cells 'Danny F. Schoors, *Georges P. Vauquelin, *Hilde De Vos, fGerda Smets, Brigitte Velkeniers, Luc Vanhaelst & Alain G. Dupont Department of Pharmacology, Medical School, Vrije Universiteit Brussel (V.U.B.), Laarbeeklaan 103, B-1090, Brussels, Belgium; *Protein Chemistry Laboratory, Instituut voor Moleculaire Biologie, V.U.B., Paardenstraat 65, St-Genesius-Rode, Belgium and tDepartment of Experimental Pathology, Medical School, V.U.B., Laarbeeklaan 103, B-1090, Brussels, Belgium 1 We studied the lactotroph cells of the rat by both in vivo and in vitro pharmacological techniques for the presence of D1-receptors. Both approaches revealed the presence of a D2-receptor, stimulated by quinpirole (resulting in an inhibition of prolactin secretion) and blocked by domperidone. 2 Administration of fenoldopam, the most selective Dl-receptor agonist currently available, resulted in a dose-dependent decrease of prolactin secretion in vivo (after pretreatment with a-methyl-p-tyrosine) and in vitro (cultured pituitary cells). This increase was dose-dependently blocked by the selective D1-receptor antagonist, SCH 23390, and although the effect of fenoldopam was less than that obtained by D2-receptor stimulation, these data suggest that a D,-receptor also controls prolactin secretion. 3 In order to detect the location of these dopamine receptors, autoradiographic studies were performed by use of [3H]-SCH 23390 and [3H]-spiperone as markers for D1- and D2-receptors, respectively. Specific binding sites for [3H]-SCH 23390 were demonstrated. Fenoldopam dose-dependently reduced [3H]-SCH 23390 binding, but had no effect on [3H]-spiperone binding.
    [Show full text]
  • Effectiveness of Midodrine Treatment in Patients with Recurrent Vasovagal
    Europace (2011) 13, 1639–1647 CLINICAL RESEARCH doi:10.1093/europace/eur200 Syncope and Implantable Loop Recorders Effectiveness of Midodrine treatment in patients with recurrent vasovagal syncope not responding to non-pharmacological treatment (STAND-trial) Downloaded from Jacobus J.C.M. Romme1, Nynke van Dijk2, Ingeborg K. Go-Scho¨ n3,4, Johannes B. Reitsma1, and Wouter Wieling3* 1Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Center, Amsterdam, The Netherlands; 2Department of General Practice/ Family Medicine, 3 4 Academic Medical Center, Amsterdam, The Netherlands; Department of Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands; and Bmeye Cardiovascular http://europace.oxfordjournals.org/ Monitoring B.V., Academic Medical Center, Amsterdam, The Netherlands Received 26 January 2011; accepted after revision 2 June 2011; online publish-ahead-of-print 13 July 2011 Aims Initial treatment of vasovagal syncope (VVS) consists of advising adequate fluid and salt intake, regular exercise, and physical counterpressure manoeuvres. Despite this treatment, up to 30% of patients continue to experience regular episodes of VVS. We investigated whether additional Midodrine treatment is effective in these patients. ..................................................................................................................................................................................... Methods In our study, patients with at least three syncopal and/or severe pre-syncopal recurrences during non-pharmacologi- and results cal treatment were eligible to receive double-blind cross-over treatment starting either with Midodrine or placebo. at Universiteit van Amsterdam on November 15, 2011 Treatment periods lasted for 3 months with a wash-out period of 1 week in-between. At baseline and after each treatment period, we collected data about the recurrence of syncope and pre-syncope, side effects, and quality of life (QoL).
    [Show full text]
  • Electrolyte and Acid-Base
    Special Feature American Society of Nephrology Quiz and Questionnaire 2013: Electrolyte and Acid-Base Biff F. Palmer,* Mark A. Perazella,† and Michael J. Choi‡ Abstract The Nephrology Quiz and Questionnaire (NQ&Q) remains an extremely popular session for attendees of the annual meeting of the American Society of Nephrology. As in past years, the conference hall was overflowing with interested audience members. Topics covered by expert discussants included electrolyte and acid-base disorders, *Department of Internal Medicine, glomerular disease, ESRD/dialysis, and transplantation. Complex cases representing each of these categories University of Texas along with single-best-answer questions were prepared by a panel of experts. Prior to the meeting, program Southwestern Medical directors of United States nephrology training programs answered questions through an Internet-based ques- Center, Dallas, Texas; † tionnaire. A new addition to the NQ&Q was participation in the questionnaire by nephrology fellows. To review Department of Internal Medicine, the process, members of the audience test their knowledge and judgment on a series of case-oriented questions Yale University School prepared and discussed by experts. Their answers are compared in real time using audience response devices with of Medicine, New the answers of nephrology fellows and training program directors. The correct and incorrect answers are then Haven, Connecticut; ‡ briefly discussed after the audience responses, and the results of the questionnaire are displayed. This article and Division of recapitulates the session and reproduces its educational value for the readers of CJASN. Enjoy the clinical cases Nephrology, Department of and expert discussions. Medicine, Johns Clin J Am Soc Nephrol 9: 1132–1137, 2014.
    [Show full text]
  • The Antidepressant-Like Effect of Flavonoids from Trigonella Foenum-Graecum Seeds in Chronic Restraint Stress Mice Via Modulation of Monoamine Regulatory Pathways
    molecules Article The Antidepressant-like Effect of Flavonoids from Trigonella Foenum-Graecum Seeds in Chronic Restraint Stress Mice via Modulation of Monoamine Regulatory Pathways Jiancheng Wang, Cuilin Cheng *, Chao Xin and Zhenyu Wang * Harbin Institute of Technology, 92 West Dazhi Street, Nangang District, Harbin 150001, China; [email protected] (J.W.); [email protected] (C.X.) * Correspondence: [email protected] (C.C.); [email protected] (Z.W.); Tel.: +86-1884-578-1315 (C.C.); +86-1303-996-0001 (Z.W.) Academic Editor: Thomas Efferth Received: 27 February 2019; Accepted: 19 March 2019; Published: 20 March 2019 Abstract: Fenugreek (Trigonella Foenum-Graecum) seeds flavonoids (FSF) have diverse biological activities, while the antidepressant-like effect of FSF has been seldom explored. The aim of this study was to evaluate the antidepressant-like effect of FSF and to identify the potential molecular mechanisms. LC-MS/MS was used for the determination of FSF. Chronic restraint stress (CRS) was used to establish the animal model of depression. Observation of exploratory behavior in the forced swimming test (FST), tail suspension test (TST) and sucrose preference test (SPT) indicated the stress level. The serum corticosterone (CORT) level was measured. The monoamine neurotransmitters (5-HT, NE and DA) and their metabolites, as well as monoamine oxidase A (MAO-A) enzyme activity in the prefrontal cortex, hippocampus and striatum, were evaluated. The protein expression levels of KLF11, SIRT1, MAO-A were also determined by western blot analysis. The results showed that FSF treatment significantly reversed the CRS-induced behavioral abnormalities, including reduced sucrose preference and increased immobility time.
    [Show full text]
  • Drugs-Biologicals FORMULARY for INTERNET PAGE 12 26 18
    AVG ITEM Average Patient Item Charge Code Description BIL AWP /pkg COST Price 25000041 SODIUM and POTASSIUM BICARBONATE TBEF UD $3.61 $0.12 $1.00 25000054 GLIMEPIRIDE TAB 1 MG UD $8.25 $0.11 $1.30 25000086 amLODIPine TAB 5 MG UD $8.65 $0.06 $1.00 25000087 AMMONIA AROMATIC SOLN 15 % (W/V) UD $3.53 $0.17 $1.00 25000090 AMOXICILLIN CAP 500 MG UD $20.12 $0.19 $1.00 25000102 ABACAVIR TAB 300 MG UD $507.10 $8.45 $16.90 25000103 ACAMPROSATE TBEC 333 MG UD $182.38 $0.80 $1.76 25000104 ACARBOSE TAB 25 MG UD $16.70 $0.27 $1.00 25000106 ACETAMINOPHEN SUPP 120 MG UD $5.09 $0.42 $1.00 25000108 ACETAMINOPHEN SUPP 325 MG UD $4.91 $0.44 $1.00 25000109 ACETAMINOPHEN TAB 325 MG UD $12.39 $0.02 $1.00 25000111 ACETAMINOPHEN TAB 500 MG UD $2.34 $0.02 $1.00 25000112 ACETAMINOPHEN SUPP 650 MG UD $3.83 $0.17 $1.00 25000113 ACETAMINOPHEN SOLN 650 MG/20.3 ML UD $75.74 $0.48 $1.22 25000117 ACETAMINOPHEN-CODEINE TAB 300-30 MG UD $12.41 $0.09 $1.00 25000121 ACETYLCYSTEINE SOLN 200 MG/ML (20 %) UD $18.18 $7.66 $15.32 25000140 ALBUTEROL SULFATE NEBU 2.5MG/3ML (0.083 %) UD $8.58 $0.29 $1.00 25000147 ALLOPURINOL TAB 100 MG UD $18.45 $0.12 $1.00 25000150 ALPRAZolam TAB 0.25 MG UD $8.87 $0.09 $1.00 25000151 ALPRAZolam TAB 0.5 MG UD $4.16 $0.04 $1.00 25000182 AMIODARONE TAB 200 MG UD $15.70 $0.20 $1.00 25000184 AMITRIPTYLINE TAB 10 MG UD $8.73 $0.06 $1.00 25000186 AMITRIPTYLINE TAB 25 MG UD $17.46 $0.08 $1.00 25000188 AMITRIPTYLINE TAB 50 MG UD $34.90 $0.16 $1.00 25000205 HYDROCORTISONE ACETATE SUPP 25 MG UD $127.30 $5.75 $11.50 25000206 HEMORRHOIDAL SUPPOSITORY SUPP 0.25
    [Show full text]
  • Midodrine As Adjunctive Support for Treatment of Refractory Hypotension
    Midodrine as adjunctive support for treatment of refractory hypotension in the intensive care unit: a multicenter, randomized, placebo controlled trial (the MIDAS trial) The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Anstey, Matthew H., Bradley Wibrow, Tharusan Thevathasan, Brigit Roberts, Khushi Chhangani, Pauline Yeung Ng, Alexander Levine, Alan DiBiasio, Todd Sarge, and Matthias Eikermann. 2017. “Midodrine as adjunctive support for treatment of refractory hypotension in the intensive care unit: a multicenter, randomized, placebo controlled trial (the MIDAS trial).” BMC Anesthesiology 17 (1): 47. doi:10.1186/s12871-017-0339-x. http://dx.doi.org/10.1186/ s12871-017-0339-x. Published Version doi:10.1186/s12871-017-0339-x Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:32072012 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Anstey et al. BMC Anesthesiology (2017) 17:47 DOI 10.1186/s12871-017-0339-x STUDY PROTOCOL Open Access Midodrine as adjunctive support for treatment of refractory hypotension in the intensive care unit: a multicenter, randomized, placebo controlled trial (the MIDAS trial) Matthew H. Anstey1,2, Bradley Wibrow1,2, Tharusan Thevathasan3, Brigit Roberts1, Khushi Chhangani3, Pauline Yeung Ng3, Alexander Levine4, Alan DiBiasio5, Todd Sarge6 and Matthias Eikermann3,7* Abstract Background: Patients admitted to intensive care units (ICU) are often treated with intravenous (IV) vasopressors.
    [Show full text]
  • Additions and Deletions to the Drug Product List
    Prescription and Over-the-Counter Drug Product List 36TH EDITION Cumulative Supplement Number 10 : October 2016 ADDITIONS/DELETIONS FOR PRESCRIPTION DRUG PRODUCT LIST ABACAVIR SULFATE TABLET;ORAL ABACAVIR SULFATE >A> AB STRIDES ARCOLAB LTD EQ 300MG BASE A 091050 001 Oct 28, 2016 Oct NEWA ACETAMINOPHEN; BUTALBITAL TABLET;ORAL BUTALBITAL AND ACETAMINOPHEN >A> AA MIKART INC 300MG;50MG A 207386 001 Nov 15, 2016 Oct NEWA >D> + NEXGEN PHARMA 300MG;50MG A 090956 001 Aug 23, 2011 Oct CTEC >A> AA + 300MG;50MG A 090956 001 Aug 23, 2011 Oct CTEC ACETAMINOPHEN; BUTALBITAL; CAFFEINE CAPSULE;ORAL BUTALBITAL, ACETAMINOPHEN AND CAFFEINE >D> + NEXGEN PHARMA 300MG;50MG;40MG A 040885 001 Nov 16, 2009 Oct CFTG >A> AB + 300MG;50MG;40MG A 040885 001 Nov 16, 2009 Oct CFTG >A> AB NUVO PHARM INC 300MG;50MG;40MG A 207118 001 Oct 28, 2016 Oct NEWA ACETAZOLAMIDE TABLET;ORAL ACETAZOLAMIDE >A> AB HERITAGE PHARMA 125MG A 205530 001 Oct 27, 2016 Oct NEWA >A> AB 250MG A 205530 002 Oct 27, 2016 Oct NEWA ALBUTEROL SULFATE TABLET;ORAL ALBUTEROL SULFATE >A> @ DAVA PHARMS INC EQ 2MG BASE A 072860 002 Dec 20, 1989 Oct CMS1 ALENDRONATE SODIUM TABLET;ORAL ALENDRONATE SODIUM >D> @ SANDOZ EQ 5MG BASE A 075871 001 Apr 22, 2009 Oct CAHN >D> @ EQ 10MG BASE A 075871 002 Apr 22, 2009 Oct CAHN >D> @ EQ 35MG BASE A 075871 004 Apr 22, 2009 Oct CAHN >D> @ EQ 40MG BASE A 075871 003 Apr 22, 2009 Oct CAHN >D> @ EQ 70MG BASE A 075871 005 Apr 22, 2009 Oct CAHN >A> @ UPSHER-SMITH LABS EQ 5MG BASE A 075871 001 Apr 22, 2009 Oct CAHN >A> @ EQ 10MG BASE A 075871 002 Apr 22, 2009 Oct CAHN >A> @ EQ
    [Show full text]
  • The Serotonin Syndrome
    The new england journal of medicine review article current concepts The Serotonin Syndrome Edward W. Boyer, M.D., Ph.D., and Michael Shannon, M.D., M.P.H. From the Division of Medical Toxicology, he serotonin syndrome is a potentially life-threatening ad- Department of Emergency Medicine, verse drug reaction that results from therapeutic drug use, intentional self-poi- University of Massachusetts, Worcester t (E.W.B.); and the Program in Medical Tox- soning, or inadvertent interactions between drugs. Three features of the sero- icology, Division of Emergency Medicine, tonin syndrome are critical to an understanding of the disorder. First, the serotonin Children’s Hospital, Boston (E.W.B., M.S.). syndrome is not an idiopathic drug reaction; it is a predictable consequence of excess Address reprint requests to Dr. Boyer at IC Smith Bldg., Children’s Hospital, 300 serotonergic agonism of central nervous system (CNS) receptors and peripheral sero- 1,2 Longwood Ave., Boston, MA 02115, or at tonergic receptors. Second, excess serotonin produces a spectrum of clinical find- [email protected]. edu. ings.3 Third, clinical manifestations of the serotonin syndrome range from barely per- This article (10.1056/NEJMra041867) was ceptible to lethal. The death of an 18-year-old patient named Libby Zion in New York updated on October 21, 2009 at NEJM.org. City more than 20 years ago, which resulted from coadminstration of meperidine and phenelzine, remains the most widely recognized and dramatic example of this prevent- N Engl J Med 2005;352:1112-20. 4 Copyright © 2005 Massachusetts Medical Society. able condition.
    [Show full text]
  • Drug and Medication Classification Schedule
    KENTUCKY HORSE RACING COMMISSION UNIFORM DRUG, MEDICATION, AND SUBSTANCE CLASSIFICATION SCHEDULE KHRC 8-020-1 (11/2018) Class A drugs, medications, and substances are those (1) that have the highest potential to influence performance in the equine athlete, regardless of their approval by the United States Food and Drug Administration, or (2) that lack approval by the United States Food and Drug Administration but have pharmacologic effects similar to certain Class B drugs, medications, or substances that are approved by the United States Food and Drug Administration. Acecarbromal Bolasterone Cimaterol Divalproex Fluanisone Acetophenazine Boldione Citalopram Dixyrazine Fludiazepam Adinazolam Brimondine Cllibucaine Donepezil Flunitrazepam Alcuronium Bromazepam Clobazam Dopamine Fluopromazine Alfentanil Bromfenac Clocapramine Doxacurium Fluoresone Almotriptan Bromisovalum Clomethiazole Doxapram Fluoxetine Alphaprodine Bromocriptine Clomipramine Doxazosin Flupenthixol Alpidem Bromperidol Clonazepam Doxefazepam Flupirtine Alprazolam Brotizolam Clorazepate Doxepin Flurazepam Alprenolol Bufexamac Clormecaine Droperidol Fluspirilene Althesin Bupivacaine Clostebol Duloxetine Flutoprazepam Aminorex Buprenorphine Clothiapine Eletriptan Fluvoxamine Amisulpride Buspirone Clotiazepam Enalapril Formebolone Amitriptyline Bupropion Cloxazolam Enciprazine Fosinopril Amobarbital Butabartital Clozapine Endorphins Furzabol Amoxapine Butacaine Cobratoxin Enkephalins Galantamine Amperozide Butalbital Cocaine Ephedrine Gallamine Amphetamine Butanilicaine Codeine
    [Show full text]