(BQ) Part 1 book Marinos the CIU book presents the following contents: Vascular access, preventive practices in the ICU, hemodynamic monitoring, disorders of circulatory flow, cardiac emergencies, blood components, acute respiratory failure, mechanical ventilation.
Marino’s The ICU Book FOURTH EDITION Paul L Marino, MD, PhD, FCCM Clinical Associate Professor Weill Cornell Medical College New York, New York Illustrations by Patricia Gast Marino’s The ICU Book FOURTH EDITION Health Philadelphia • Baltimore • New York • London Buenos Aires • Hong Kong • Sydney • Tokyo Acquisitions Editor:] Brian Brown Product Development Editor: Nicole Dernoski Production Project Manager: Bridgett Dougherty Manufacturing Manager: Beth Welsh Marketing Manager: Dan Dressler Creative Director: Doug Smock Production Services: Aptara, Inc © 2014 by Wolters Kluwer Health/Lippincott Williams & Wilkins Two Commerce Square 2001 Market St Philadelphia, PA 19103 LWW.com 3rd Edition © 2007 by Lippincott Williams & Wilkins - a Wolters Kluwer Business 2nd Edition © 1998 by LIPPINCOTT WILLIAMS & WILKINS All rights reserved This book is protected by copyright No part of this book may be reproduced in any form or by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews Materials appearing in this book prepared by individuals as part of their official duties as U.S.?government employees are not covered by the abovementioned copyright Printed in the USA Library of Congress Cataloging-in-Publication data available on request from the publisher ISBN-13: 9781451188691 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication Application of this information in a particular situation remains the professional responsibility of the practitioner The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions This is particularly important when the recommended agent is a new or infrequently employed drug Some drugs and medical devices presented in this publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320 International customers should call (301) 223-2300 Visit Lippincott Williams & Wilkins on the Internet: at LWW.com Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to 6pm, EST 10 To Daniel Joseph Marino, my 26-year-old son, who has become the best friend I hoped he would be I would especially commend the physician who, in acute diseases, by which the bulk of mankind are cut off, conducts the treatment better than others HIPPOCRATES Preface to Fourth Edition The fourth edition of The ICU Book marks its 23rd year as a fundamental sourcebook for the care of critically ill patients This edition continues the original intent to provide a “generic textbook” that presents fundamental concepts and patient care practices that can be used in any adult intensive care unit, regardless of the specialty focus of the unit Highly specialized topics, such as obstetrical emergencies, burn care, and traumatic injuries, are left to more qualified specialty textbooks This edition has been reorganized and completely rewritten, with updated references and clinical practice guidelines included at the end of each chapter The text is supplemented by 246 original illustrations and 199 original tables, and five new chapters have been added: Vascular Catheters (Chapter 1), Occupational Exposures (Chapter 4), Alternate Modes of Ventilation (Chapter 27), Pancreatitis and Liver Failure ( Chapter 39), and Nonpharmaceutical Toxidromes ( Chapter 55) Each chapter ends with a brief section entitled “A Final Word,” which highlights an insight or emphasizes the salient information presented in the chapter The ICU Book is unique in that it represents the voice of a single author, which provides a uniformity in style and conceptual framework While some bias is inevitable in such an endeavor, the opinions expressed in this book are rooted in experimental observations rather than anecdotal experiences, and the hope is that any remaining bias is tolerable Acknowledgements Acknowledgements are few but well deserved First to Patricia Gast, who is responsible for all the illustrations and page layouts in this book Her talent, patience, and counsel have been an invaluable aid to this author and this work Also to Brian Brown and Nicole Dernoski, my longtime editors, for their trust and enduring support FIGURE 30.4 Mixed venous O2 saturation (SvO2) during successful and failed trials of spontaneous breathing Data from Reference 17 Management There is surprisingly little information on methods for correcting the cardiac dysfunction that develops during spontaneous breathing trials Patients who develop systolic dysfunction should benefit from continuous positive airway pressure (CPAP), which promotes cardiac output by cancelling the afterload-increasing effect of negative intrathoracic pressure (20,21) Since CPAP is delivered noninvasively, it will not prevent the removal of mechanical ventilation, including extubation Respiratory Muscle Weakness Respiratory muscle weakness is always near the top of the list for potential causes of difficulty in removing ventilatory support However, the role of respiratory muscle weakness in difficult-to-wean patients is not clear The following are some potential sources of respiratory muscle weakness in ventilator-dependent patients Potential Sources MECHANICAL VENTILATION: As mentioned earlier (and shown in Figure 30.1), mechanical ventilation is a recognized cause of diaphragm weakness (5), primarily when patients are not allowed to trigger a ventilator breath (6) However, the perception that ventilator-associated dia-phragm weakness can be a source of failed SBTs is not supported by a clinical study showing that the strength of the diaphragm can actually increase during failed trials of spontaneous breathing (22) Furthermore, the notion that diaphragm weakness can be a source of inadequate ventilation is not supported by observations in patients who lack functioning diaphragms (from paralysis or injury), who show no evidence of inadequate ventilation, and have normal levels O2 and CO2 in their blood (23) These findings indicate that diaphragm weakness is not deserving of its reputation as an important factor in prolonging ventilator dependency CRITICAL ILLNESS NEUROMYOPATHY: The conditions known collectively as critical illness polyneuropathy and myopathy are inflammatory conditions involving peripheral nerves and skeletal muscle that typically appear in patients with severe sepsis and multiorgan failure, and are recognized only when patients fail to wean from mechanical ventilation (24) There is no specific treatment for these conditions, and the weakness can persist for months A more detailed description of these conditions is included in Chapter 45 ELECTROLYTE DEPLETION: Magnesium and phosphorous depletion can promote respiratory muscle weakness (24,25), but the clinical relevance of this effect is unproven Nevertheless, deficiencies in these electrolytes should be corrected in patients who fail repeated attempts to discontinue mechanical ventilation Monitoring Uncertainty about the role of respiratory muscle weakness in failure to remove ventilatory support is partly a reflection of the lack of reliable and readily obtained measures of respiratory muscle strength MAXIMUM INSPIRATORY PRESSURE: The standard clinical measure of respiratory muscle strength is the maximum inspiratory pressure (PImax), which is the negative pressure that is generated by a maximum inspiratory effort against a closed airway (27,28) The normal values of PImax vary widely, but mean values of -120 cm H2O and -84 cm H2O have been reported for adult men and women, respectively (28) Ventilation at rest is threatened when the PImax drops to -15 to -30 cm H2O, which are the threshold values for predicting successful trials of spontaneous breathing (see Table 30.2 ) Unfortunately, patients with acute respiratory failure have difficulty performing the maneuvers involved in the measurement of PImax As a result, the PImax is not measured regularly in patients who require ventilatory support ULTRASOUND: Ultrasound has recently emerged as a potential method of assessing diaphragm strength The ultrasound measures of diaphragm strength include the thickness of the diaphragm, and the length of excursion of the diaphragm during inspiration (29) In a preliminary study that used ultrasound assessments of diaphragm strength in patients who were weaned from mechanical ventilation, there was a significant correlation between failed SBTs and diaphragm weakness identified by ultrasound (29) The reliability of ultrasound measurements for detecting diaphragm weakness is uncertain at the present time because the criteria for diaphragm weakness are arbitrary, and have not been validated (This will require ultrasound measurements in large numbers of normal subjects to determine the range of normal measurements.) Management When respiratory muscle weakness is strongly suspected, trials of spontaneous breathing should continue, but should be terminated before patients show evidence of respiratory distress (to avoid aggravating the weakness) Strategies designed to promote muscle strength, such as patient-triggered ventilation and physical rehabilitation (described earlier), are considered particularly important in patients with documented muscle weakness EXTUBATION Once there is evidence that mechanical ventilation is no longer necessary, the next step is to remove the artificial airway This section focuses on removing endotracheal tubes, although some of the principles also apply to removing tracheostomy tubes (The removal of tracheostomy tubes is a more gradual process, and often occurs after patients leave the ICU.) Extubation should never be performed to reduce the work of breathing, because the work of breathing can actually increase after extubation, as demonstrated in Figure 30.2 (The increased work of breathing can be the result of an increased respiratory rate or breathing through a narrowed glottis, but it occurs in patients who tolerate extubation, so it is not always a cause for concern.) The considerations that must be addressed prior to extubation include: (a) the patient’s ability to clear secretions from the airways, and (b) the risk of symptomatic laryngeal edema following extubation Airway Protective Reflexes The ability to protect the airway from aspirated secretions is determined by the strength of the gag and cough reflexes Cough strength can be assessed by holding a piece of paper 1–2 cm from the end of the endotracheal tube and asking the patient to cough If wetness appears on the paper, the cough strength is considered adequate ( 30) Diminished strength or even absence of cough or gag reflexes will not necessarily prevent extubation, but will identify patients who need special precautions to prevent aspiration Laryngeal Edema Upper airway obstruction from laryngeal edema is the major cause of failed extubations, and is reported in 5–22% of patients who have been intubated for longer than 36 hours (3,31,32) Contributing factors include difficult and prolonged intubation, endotracheal tube diameter, and self-extubation The Cuff-Leak Test The cuff-leak test measures the volume of inhaled gas that escapes through the larynx when the cuff on the endotracheal tube is deflated This test is designed to determine the risk of symptomatic upper airway obstruction from laryngeal edema after the endotracheal tube is removed According to a recent analysis of the cuff leak test (33), the absence of an air leak indicates a high risk of upper airway obstruction following extubation, but the presence of an air leak does not indicate a low risk of upper airway obstruction following extubation, regardless of the volume of the leak The value of the cuff leak test has been debated for years, and the test is not universally accepted Since the results of a cuff leak test not alter patient management, including the decision to extubate, the clinical relevance of the test is unproven Pretreatment with Steroids? Two clinical studies have shown that pretreatment with intravenous corticosteroids ( methyl- prednisolone, 20–40 mg every 4–6 hrs) for 12 to 24 hours prior to extubation results in fewer cases of laryngeal edema and upper airway obstruction following extubation, and fewer reintubations (33,34) The results of one of these studies is shown in Figure 30.5 Steroid pretreatment in this study consisted of three doses of intravenous methylprednisolone (20 mg every hours), with the first dose given 12 hours prior to a planned extubation Note that this pretreatment was associated with about a 7-fold decrease in the incidence of symptomatic laryngeal edema following extubation, and a 50% drop in reintubation rate Although the use of corticosteroids for “anything that swells” is questionable (35), the results of the study shown in Figure 30.5 are compelling enough to consider a brief period (12 to 24 hrs) of corticosteroid therapy prior to planned extubations, particularly in patients who have a high risk of post-extubation laryngeal edema (e.g., from prior selfextubations) A single dose of methylprednisolone (40 mg IV) given one hour prior to extubation did not reduce the incidence of post-extubation laryngeal edema in one study (36), so there is no reason to administer steroids only at the time of extubation Postextubation Stridor The first sign of a significant laryngeal obstruction may be stridorous breathing (noisy breathing), also called stridor The sounds may be high-pitched and wheezy, or lowpitched and harsh, but they are always audible without a stethoscope, and they are always most apparent during inspiration This inspiratory prominence is due to the extrathoracic location of laryngeal obstruction because negative intrathoracic pressures generated during inspiration are transmitted to the upper airways outside the thorax, and this results in a narrowing of the extrathoracic airways during inspiration Therefore, extrathoracic obstructions are always magnified during inspiration FIGURE 30.5 Results of a large, multicenter study showing the effects of pretreatment with a corticosteroid (methylprednisolone, 20 mg IV every hrs for the 12 hours prior to extubation) on the incidence of post-extubation laryngeal edema and the rate of reintubation Data from Reference 30 Post-extubation stridor is apparent within 30 minutes of extubation in a large majority (∼80%) of cases (30), but delays in appearance of up to hours can occur (personal observation) Reintubation is not always re-quired, but close scrutiny is required because there is no proven method for reducing laryngeal edema after extubation Aerosolized Epinephrine Inhalation of an epinephrine aerosol (2.5 mL of 1% epinephrine) is a popular practice for post-extubation stridor However, while effective in children ( 36), this practice is unproven in adults Aerosol therapy with a racemic mixture of epinephrine (which has equal amounts of the levo- and dextro- isomers) is also popular for post-extubation stridor, but clinical studies in children have shown no advantage with racemic epinephrine over standard (l-isomer) epinephrine (37) Noninvasive Ventilation Noninvasive ventilation (which is described on pages 526–531) is effective in reducing the rate of reintubation when used immediately after extubation in patients with a high risk of laryngeal edema (38), but similar success has not been demonstrated in patients who develop post-extubation respiratory failure (39) Thus, the benefit of noninvasive ventilation occurs when it is used as a preventive measure early after extubation A FINAL WORD Be Vigilant The ultimate goal of mechanical ventilation is to no longer need it, and the introductory quote by Sir William Osler is intended to emphasize that vigilance is required to identify when you have reached this goal in a timely manner Vigilance involves early recognition of candidates for trials of unassisted breathing (with daily assessments using the readiness criteria in Table 30.1 ), and early recognition that the candidates can sustain spontaneous ventilation (with trials of spontaneous breathing) This approach will free patients from mechanical ventilation without delay, and end the misfortune of being tethered to a machine REFERENCES Clinical Practice Guidelines MacIntyre NR, Cook DJ, Ely EW Jr, et al Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American College of Chest Physicians, the American Associa-tion for Respiratory Care, and the American College of Critical Care Med-icine Chest 2001; 120(Suppl):375S–395S Reviews MacIntyre NR Evidence-based assessments in the ventilator discontinuation process Respir Care 2012; 57:1611–1618 McConville JF, Kress JP Weaning patients from the ventilator New Engl J Med 2012; 367:2233–2239 Thille AW, Cortes-Puch I, Esteban A Weaning from the ventilator and extubation in ICU Curr Opin Crit Care 2013; 19:57–64 Preliminary Concerns Petrof BJ, Jaber S, Matecki S Ventilator-induced diaphragm dysfunction Curr Opin Crit Care 2010; 16:19–25 Sassoon CSH, Zhu E, Caiozzo VJ Assist-control mechanical ventilation attenuates ventilator-induced diaphragm dysfunction Am J Respir Crit Care Med 2004; 170:626– 632 Mendez-Tellez PA, Needham DM Early physical rehabilitation in the ICU and ventilator liberation Respir Care 2012; 57:1663–1669 Barr J, Fraser GL, Puntillo K, et al Clinical practice guidelines for the management of pain, agitatiom, and delirium in adult patients in the intensive care unit Crit Care Med 2013; 41:263–306 Kreiger BP, Isber J, Breitenbucher A, et al Serial measurements of the rapid-shallow breathing index as a predictor of weaning outcome in elderly medica l patients Chest 1997; 112:1029–1034 Spontaneous Breathing Trials 10 Mehta S, Nelson DL, Klinger JR, et al Prediction of post-extubation work of breathing Crit Care Med 2000; 28:1341–1346 11 Ely W, Baker AM, Dunagen DP, et al Effect of duration of mechanical ventilation of identifying patients capable of breathing spontaneously N Engl J Med 1996; 335:1864–1869 12 Bouley GH, Froman R, Shah H The experience of dyspnea during weaning Heart Lung 1992; 21:471–476 13 Raghavan N, Webb K, Amornputtisathaporn N, O’Donnell DE Recent advances in pharmacotherapy for dyspnea in COPD Curr Opin Pharmacol 2011; 11:204–210 Failure of Spontaneous Breathing 14 Grasso S, Leone A, De Michele M, et al Use of N-terminal pro-brain natriuretic peptide to detect acute cardiac dysfunction during weaning failure in difficult-towean patients with chronic obstructive pulmonary disease Crit Care Med 2007; 35:96–105 15 Srivastava S, Chatila W, Amoateng-Adjepong Y, et al Myocardial ischemia and weaning failure in patients with coronary artery disease: an update Crit Care Med 1999; 27:2109–2112 16 Nishimura Y, Maeda H, Tanaka K, et al Respiratory muscle strength and hemodynamics in heart failure Chest 1994; 105:355–359 17 Papanickolaou J, Makris D, Saranteas T, et al New insights into weaning from mechanical ventilation: left ventricular diastolic dysfunction is a key player Intensive Care Med 2011; 37:1976–1985 18 Jubran A, Mathru M, Dries D, Tobin MJ Continuous recordings of mixed venous oxygen saturation during weaning from mechanical ventilation and the ramifications thereof Am Rev respir Crit Care Med 1998; 158:1763–1769 19 Zapata L, Vera P, Roglan A, et al B-type natriuretic peptides for prediction and diagnosis of weaning failure from cardiac origin Intensive Care Med 2011; 37:477– 485 20 Naughton MT, Raman MK, Hara K, et al Effect of continuous positive airway pressure on intrathoracic and left ventricular transmural pressures in patients with congestive heart failure Circulation 1995; 91:1725–1731 21 Bradley TD, Holloway BM, McLaughlin PR, et al Cardiac output response to continuous positive airway pressure in congestive heart failure Am Rev Respir Crit Care Med 1992; 145:377–382 22 Swartz MA, Marino PL Diaphragm strength during weaning from mechanical ventilation Chest 1985; 88:736–739 23 LaRoche CM, Carroll N, Moxham J, Green M Clinical significance of severe isolated diaphragm weakness Am Rev Respir Dis 1988; 138:862–866 24 Hudson LD, Lee CM Neuromuscular sequelae of critical illness N Engl J Med 2003; 348:745–747 25 Benotti PN, Bistrian B Metabolic and nutritional aspects of weaning from mechanical ventilation Crit Care Med 1989; 17:181–185 26 Malloy DW, Dhingra S, Solren F, et al Hypomagnesemia and respiratory muscle power Am Rev Respir Dis 1984; 129:427–431 27 Mier-Jedrzejowicz A, Brophy C, Moxham J, Geen M Assessment of diaphragm weakness Am Rev Respir Dis 1988; 137:877–883 28 Bruschi C, Cerveri I, Zoia MC et al Reference values for maximum respiratory mouth pressures: A population-based study Am Rev respir Dis 1992; 146:790–793 29 Kim WY, Suh HJ, Hong S-S, et al Diaphragm dysfunction assessed by ultrasonography: Influence on weaning from mechanical ventilation Crit Care Med 2011; 39:2627–2630 Extubation 30 Khamiees M, Raju P, DeGirolamo A, et al Predictors of extubation outcome in patients who have successfully completed a spontaneous breathing trial Chest 2001; 120:12621270 31 Franỗois B, Bellisant E, Gissot V, et al, for the Association des Réanimateurs du Centre-Quest (ARCO) 12-h pretreatment with methylprednisolone versus placebo for prevention of postextubation laryngeal oedema: a randomized double-blind trial Lancet 2007; 369:1083–1089 32 Jaber S, Chanques G, Matecki S, et al Post-extubation stridor in intensive care unit patients Risk factors evaluation and importance of the cuff test Intensive Care Med 2003; 29:63–74 33 Ochoa ME, del Carmen Marín M, Frutos-Vivar F, et al Cuff-leak test for the diagnosis of upper airway obstruction in adults: a systematic review and meta-analysis Intensive Care Med 2009; 35:1171–1179 34 Cheng K-C, Hou C-C, Huang H-C, et al Intravenous injection of methylprednisolone reduces the incidence of post-extubation stridor in intensive care unit patients Crit Care Med 2006; 34:1345–1350 35 Shemie, S Steroids for anything that swells: Dexamethasone and postextubation airway obstruction Crit Care Med: 1996; 24:1613–1614 36 Gaussorgues P, Boyer F, Piperno D, et al Do corticosteroids prevent postintubation laryngeal edema? A prospective study of 276 adults Crit Care Med 1988; 16:649– 652 37 Nutman J, Brooks LJ, Deakins K, et al Racemic versus l-epinephrine aerosol in the treatment of postextubation laryngeal edema: results from a prospective, randomized, doubleblind study Crit Care Med 1994; 22:1591–1594 38 Nava S, Gregoretti C, Fanfulla F, et al Noninvasive ventilation to prevent respiratory failure after extubation in high-risk patients Crit Care Med 2005; 33:2465–2470 39 Hess D The role of noninvasive ventilation in the ventilator discontinuation process Respir Care 2012; 57:1619–1625 ... catheter like the one shown in Figure 1. 6 The features of this catheter are shown in Table 1. 5 Table 1. 5 Selected Features of Hemodialysis Catheters Hemodialysis catheters are the wide-body catheters... typically 16 –20 gauge catheters that are 1 2 inches in length Peripher-al catheters are inserted using a catheter-over-needle device like the one shown in Figure 1. 3 The catheter fits snugly over the. .. rates in the 16 gauge and 18 gauge channels when compared to the 16 and 18 gauge peripheral catheters in Table 1. 2 This, of course, is due to the much longer length of central venous catheters,