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(BQ) Part 1 book Critical care medicine - Principles of diagnosis and management in the adult presents the following contents: Cardiac arrest and cardiopulmonary resuscitation, air way management in the critically ill adult; arterial, central venous, and pulmonary artery catheters; intra aortic balloon counterpulsation; mechanical ventilation inacute respiratory distress syndrome,...
CRITICAL CARE MEDICINE PRINCIPLES OF DIAGNOSIS AND MANAGEMENT IN THE ADULT CRITICAL CARE MEDICINE PRINCIPLES OF DIAGNOSIS AND MANAGEMENT IN THE ADULT Joseph E Parrillo, MD Chairman, Heart and Vascular Hospital Hackensack University Medical Center Professor of Medicine Rutgers New Jersey Medical School Hackensack, New Jersey R Phillip Dellinger, MD, MS Professor of Medicine Cooper Medical School of Rowan University Director, Critical Care Cooper University Hospital Camden, New Jersey Fourth Edition 1600 John F Kennedy Blvd Ste 1800 Philadelphia, PA 19103-2899 CRITICAL CARE MEDICINE: PRINCIPLES OF DIAGNOSIS AND MANAGEMENT IN THE ADULT Copyright © 2014 by Saunders, an imprint of Elsevier Inc Copyright © 2008, 2002, 1995 by Mosby, Inc., an imprint of Elsevier Inc ISBN: 978-0-323-08929-6 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein) Notices Knowledge and best practice in this field are constantly changing As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein Library of Congress Cataloging-in-Publication Data Critical care medicine : principles of diagnosis and management in the adult / [edited by] Joseph E Parrillo, R Phillip Dellinger.—4th ed p ; cm Includes bibliographical references and index ISBN 978-0-323-08929-6 (hardcover : alk paper) I. Parrillo, Joseph E. II. Dellinger, R Phillip [DNLM: 1. Critical Care. 2. Intensive Care Units. WX 218] RC86.7 616′.028—dc23 2013014389 Executive Content Strategist: William R Schmitt Senior Content Development Specialist: Janice M Gaillard Publishing Services Manager: Patricia Tannian Senior Project Manager: Sharon Corell Senior Book Designer: Louis Forgione Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 To our families Gale, Nicholas, and Jenny Parrillo and Kate, Walker, Lauren, Reid, and Meg Dellinger Contributors Wissam Abouzgheib, MD, FCPP Section Head, Interventional Pulmonary and Assistant Professor of Medicine, Pulmonary and Critical Care, Cooper University Hospital, Camden, New Jersey David Anthony, MD Thomas P Bleck, MD, FCCM Professor, Neurological Sciences, Neurosurgery, Internal Medicine, and Anesthesiology, Rush Medical College, Associate Chief Medical Officer, Critical Care, Rush University Medical Center, Chicago, Illinois Staff Anesthesiologist and Intensivist, Cardiothoracic Anesthesiology, Anesthesiology Institute, Cleveland, Ohio Frank Bowen, MD Shariff Attaya, MD Susan S Braithwaite, MD Fellow, Cardiovascular Disease, Rush University Medical Center, Chicago, Illinois Robert A Balk, MD Director of Pulmonary and Critical Care Medicine, Internal Medicine, Rush University Medical Center, Professor of Medicine, Rush Medical College, Chicago, Illinois Richard G Barton, MD University of Utah Medical Center, Department of Surgery, Salt Lake City, Utah Thaddeus Bartter, MD Interventional Pulmonologist, University of Arkansas for Medical Sciences, Little Rock, Arkansas C Allen Bashour, MD Associate Professor of Anesthesiology, Staff, Department of Cardiothoracic Anesthesia, Anesthesia Institute, Cleveland Clinic, Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio Carolyn Beckes, MD Professor of Medicine, Cooper Medical School of Rowan University, Chief Medical Officer, Cooper University Hospital, Camden, New Jersey Emily Bellavance, MD Assistant Professor of Surgery, Division of Surgical Oncology, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland Karen Berger, PharmD Neurocritical Care Clinical Pharmacist, New York Presbyterian/Weill Cornell Medical Center, New York, New York Julian Bion Professor of Intensive Care Medicine, University of Birmingham, Birmingham, United Kingdom Department of Cardiothoracic Surgery, Cooper University Hospital, Camden, New Jersey Visiting Clinical Professor, Medicine, University of Illinois-Chicago, Chicago, Illinois, Staff Physician, Saint Francis Hospital, Evanston, Illinois Pietro Carioni, MD Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Università degli Studi di Milano, Dipartimento di Anestesia, Rianimazione ed Emergenza Urgenza, Fondazione IRCCS Ca’ Granda–Ospedale Maggiore Policlinico, Milan, Italy Eleonora Carlesso, MD Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Università degli Studi di Milano, Milan, Italy Rodrigo Cartin-Ceba, MD Consultant, Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota Maurizio Cecconi, MD, MD (UK), FRCA Consultant in Anaesthesia and Intensive Care Medicine, St George’s Healthcare NHS Trust, Honorary Senior Lecturer, St George’s University of London, London, United Kingdom Louis Chaptini, MD Assistant Professor of Medicine, Section of Digestive Diseases, Yale University School of Medicine, New Haven, Connecticut Lakhmir S Chawla, MD Associate Professor, Department of Medicine, George Washington University Medical Center, Washington, District of Columbia Ismail Cinel, MD, PhD Professor of Anesthesiology, Marmara University School of Medicine, Director, Intensive Care Unit, Chief Medical Officer, Marmara University Education and Research Hospital, Istanbul, Turkey vii viii Contributors T R Craig, PhD, MRCP, MB, BCh, BAO E Wesley Ely, MD, MPH Brendan D Curti, MD Henry S Fraimow, MD Quinn A Czosnowski, PharmD John F Fraser, MB ChB, PhD, MRCP, FFARCSI, FRCA, FCICM Specialist Registrar, Critical Care Medicine, Regional Intensive Care Unit, Royal Hospitals, Belfast HSC Trust, Belfast, Northern Ireland, United Kingdom Director, Biotherapy and Genitourinary Oncology Research, Earle A Chiles Research Institute, Portland, Oregon Assistant Professor of Clinical Pharmacy, Department of Pharmacy Practice and Pharmacy Administration, University of the Sciences, Philadelphia, Pennsylvania Marion Danis, MD Chief, Bioethics Consultation Service, Department of Bioethics, National Institutes of Health, Bethesda, Maryland R Phillip Dellinger, MD, MS Professor of Medicine, Cooper Medical School of Rowan University, Director, Critical Care, Cooper University Hospital, Camden, New Jersey Fedele J DePalma, MD Gastroenterology Associates, Newark, Delaware Jose Diaz-Gomez, MD Staff Anesthesiologist/Intensivist, Cardiothoracic Anesthesiology, Cleveland Clinic, Assistant Professor of Anesthesiology, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, Ohio Hisham Dokainish, MD, FRCPC, FASE, FACC Associate Professor of Medicine, McMaster University, Director of Echocardiography, Hamilton Health Sciences, Hamilton, Ontario, Canada Guillermo Domínguez-Cherit, MD, FCCM Professor of Medicine, Department of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee Associate Professor of Medicine, Division of Infectious Diseases, Cooper Medical School of Rowan University, Camden, New Jersey Professor in Intensive Care Medicine, Director of Critical Care Research Group, University of Queensland School of Medicine, The Prince Charles Hospital, Brisbane, Australia Yaakov Friedman, BA, MD Associate Professor of Medicine, Rosalind Franklin University of Medicine, Chicago, Illinois Brian M Fuller, MD Assistant Professor, Anesthesiology and Emergency Medicine, Division of Critical Care, Washington University School of Medicine, St Louis, Missouri Ognjen Gajic, MD, MSc Professor of Medicine, Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota Luciano Gattinoni, MD, FRCP Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Università degli Studi di Milano, Dipartimento di Anestesia, Rianimazione ed Emergenza Urgenza, Fondazione IRCCS Ca’ Granda–Ospedale Maggiore Policlinico, Milan, Italy Nandan Gautam, MRCP, DICM, FRCP, FFICM Consultant, Medicine and Critical Care, University Hospital, Birmingham, United Kingdom Director, División of Pulmonary, Anesthesia, and Critical Care, Instituto Nacional de Ciencias Medicas y Nutrición “Salvador Zubiran,” Mexico City, Distrito Federal, Mexico Martin Geisen, MD David J Dries, MSE, MD Fredric Ginsberg, MD Assistant Medical Director, Department of Surgery, HealthPartners Medical Group/Regions Hospital, St Paul, Minnesota, Professor of Surgery and Anesthesiology, Department of Surgery, University of Minnesota, Minneapolis, Minnesota Lakshmi Durairaj, MD Associate Professor, Division of Pulmonary Critical Care and Occupational Medicine, University of Iowa Hospitals and Clinics, Iowa City, Iowa Adam B Elfant, MD Associate Professor of Medicine, Associate Head Division of Gastroenterology, Cooper University Hospital, Camden, New Jersey Clinical and Research Fellow, Department of Intensive Care Medicine, St George’s Healthcare NHS Trust, London, United Kingdom Associate Professor of Medicine, Division of Cardiovascular Disease, Cooper Medical School of Rowan University, Camden, New Jersey H Warren Goldman, MD, PhD Professor and Chairman of Neurosurgery, Cooper Medical School of Rowan University, Chief of Neurosurgery, Cooper University Hospital, Medical Director, Cooper Neurological Institute, Cooper University Hospital, Camden, New Jersey, Professor of Surgery, Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey Bala K Grandhi, MD, MPH Assistant Director, Internal Medicine Residency Program, Central Michigan University, Saginaw, Michigan A B J Groeneveld, Prof Dr., FCCP, FCCM Professor Doctor, Intensive Care, Erasmus MC, Rotterdam, Netherlands David P Gurka, PhD, MD, FACP, FCCP Associate Professor of Medicine, Department of Medicine, Rush Medical College, Director, Section of Critical Care Medicine, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Director, Surgical Intensive Care Unit, Assistant Chief Medical Officer for Critical Care and Safety Quality, Rush University Medical Center, Chicago, Illinois Marilyn T Haupt, MD Chair and Interim Program Director, Internal Medicine, Central Michigan University College of Medicine, Saginaw, Michigan Dustin M Hipp, MD, MBA Resident Physician, Department of Pediatrics, Baylor College of Medicine, Texas Children’s Hospital, Houston, Texas Michael J Hockstein, MD Contributors George Karam, MD Professor of Medicine, Department of Medicine, Louisiana State University Health Sciences Center, Baton Rouge, Louisiana Steven T Kaufman, MD Assistant Professor of Medicine, Endocrinology, Diabetes, and Metabolism, Cooper University Hospital, Camden, New Jersey Jason A Kline, MD Assistant Professor of Medicine, Nephrology, Cooper Medical School of Rowan University, Camden, New Jersey Zoulficar Kobeissi, MD Assistant Professor of Clinical Medicine, Department of Medicine, Weill Cornell Medical College/The Methodist Hospital, Houston, Texas Anand Kumar, MD Associate Professor, Section of Critical Care Medicine, Section of Infectious Diseases, University of Manitoba, Winnipeg, Canada, Rutgers Robert Wood Johnson Medical School, Camden, New Jersey Neil A Lachant, MD Medical Director, 4G SICU, Department of Surgery, Medstar Washington Hospital Center, Washington, District of Columbia Chief, Section of Hematology, Cooper Cancer Institute, Cooper University Hospital, Professor of Medicine, Cooper Medical School of Rowan University, Camden, New Jersey Steven M Hollenberg, MD Franco Laghi, MD Professor of Medicine, Cooper Medical School of Rowan University, Director, Coronary Care Unit, Cooper University Hospital, Camden, New Jersey Robert C Hyzy, MD Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Loyola University of Chicago, Stritch School of Medicine, Chicago, Illinois, Edward Hines Jr Veterans Administration Hospital, Hines, Illinois Associate Professor, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan Rekha Lakshmanan, MD Hani Jneid, MD, FACC, FAHA, FSCAI Stephen E Lapinsky, MB, BCh, MSc, FRCPC Laura S Johnson, MD Marc Laufgraben, MD, MBA Assistant Professor of Medicine, Director of Interventional Cardiology Research, Baylor College of Medicine, The Michael E DeBakey VA Medical Center, Houston, Texas Trauma Surgery, Washington Hospital Center, Washington, District of Columbia Robert Johnson, MD General Surgery, Thoracic Surgery, Saint Louis University Hospital, St Louis, Missouri Amal Jubran, MD Professor of Medicine, Pulmonary and Critical Care Medicine, Loyola University Medical Center, Loyola University Medical Center, Maywood, Illinois, Section Chief, Pulmonary and Critical Care Medicine, Edward Hines Jr Veterans Affairs Hospital, Hines, Illinois ix Intensivist, Critical Care, Mercy Hospital St Louis, St Louis, Missouri Professor, Department of Medicine, University of Toronto, Site Director, Intensive Care Unit, Mount Sinai Hospital, Toronto, Ontario, Canada Associate Professor of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Cooper Medical School of Rowan University, Camden, New Jersey G G Lavery, MD, FJFICMI, FFARCSI Clinical Director, HSC Safety Forum, Public Health Agency, Consultant, Critical Care, Royal Hospital, Belfast HSC Trust, Belfast, Northern Ireland, United Kingdom Kenneth V Leeper, Jr., MD Professor of Medicine, Division of Medicine/Pulmonary and Critical Care, Emory University School of Medicine, Atlanta, Georgia x Contributors Dan L Longo, MD Deputy Editor, New England Journal of Medicine, Professor of Medicine, Harvard Medical School, Boston, Massachusetts Ramya Lotano, MD, FCCP Christopher B McFadden, MD Assistant Professor, Medicine, Cooper Medical School of Rowan University, Camden, New Jersey Todd A Miano, PharmD Assistant Professor of Medicine, Department of Medicine, Cooper University Hospital, Camden, New Jersey Pharmacy Clinical Specialist, Surgical Critical Care, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania Vincent E Lotano, MD Thomas R Mirsen, MD Hospital of the University of Pennsylvania Division of Thoracic Surgery, Director of Thoracic Surgery, Pennsylvania Hospital, Philadelphia, Pennsylvania Dennis G Maki, MD Ovid O Meyer Professor of Medicine, Divisions of Infectious Diseases and Pulmonary/Critical Care Medicine, Attending Physician, Center for Trauma and Life Support, University of Wisconsin Hospital and Clinics, Madision, Wisconsin Andrew O Maree, MD, MSc Consultant Cardiologist, Waterford Regional Hospital, Waterford, Ireland Paul E Marik, MD, FCCM, FCCP Chief, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, Virginia John Marini, MD Professor of Medicine, Pulmonary and Critical Care Medicine, University of Minnesota, Director of Pysiologic and Translational Research, Regions Hospital, St Paul, Minnesota Associate Professor, Neurology, Cooper Medical School of Rowan University, Camden, New Jersey Manoj K Mittal, MBBS Neurocritical Care Fellow, Neurology, Mayo Clinic, Rochester, Minnesota Rui Moreno, MD, PhD Professor, Unidade de Cuidados Intensivos Neurocríticos, Hospital de São José, Centro Hospitalar de Lisboa Central, E.P.E., Lisboa, Portugal Nick Murphy, MB BS, FRCA, DipICM Honorary Senior Lecturer, Clinical Medicine, University of Birmingham, Consultant Intensivist, Critical Care, Queen Elizabeth Hospital, Birmingham, Edgbaston, Birmingham, United Kingdom Katie M Muzevich, PharmD, BCPS Department of Pharmacy, Virginia Commonwealth University Health System, Richmond, Virginia Girish B Nair, MD Fellow, Pulmonary and Critical Care Medicine, Winthrop University Hospital, Rock Hill, South Carolina John C Marshall, MD, FRCSC Michael S Neiderman, MD Henry Masur, MD Hollis O’Neal, MD, MSc Professor of Surgery, Department of Surgery and the Interdepartmental Division of Critical Care Medicine, University of Toronto, St Michael’s Hospital, Toronto, Ontario, Canada Chief, Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Maryland Dirk M Maybauer, MD, PhD Professor in Anaesthesia and Critical Care Medicine, Philipps University of Marburg, Marburg, Germany, Assistant Professor in Anesthesiology and Critical Care Medicine, The University of Texas Medical Branch, Galveston, Texas Marc O Maybauer, MD, PhD, EDIC, FCCP Professor in Anaesthesia and Critical Care Medicine, Philipps University of Marburg, Marburg, Germany, Assistant Professor in Anesthesiology and Critical Care Medicine, The University of Texas Medical Branch, Galveston, Texas Chairman, Department of Medicine, Winthrop University Hospital, Mineola, New York, Professor of Medicine, Department of Medicine, SUNY at Stony Brook, Stony Brook, New York Assistant Professor of Clinical Medicine, Pulmonary and Critical Care Medicine, Louisiana State University Health Sciences Center, Baton Rouge, Louisiana Matthew Ortman, MD Assistant Professor of Medicine, Rutgers Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Cooper Medical School of Rowan University, Division of Cardiology, Department of Medicine, Cooper University Hospital, Camden, New Jersey Luis Ostrosky-Zeichner, MD, FACP, FIDSA Associate Professor of Medicine and Epidemiology, Division of Infectious Diseases, University of Texas Medical School at Houston, Houston, Texas CHAPTER 36 — Postoperative Management of the Cardiac Surgery Patient MEAN ARTERIAL PRESSURE MAP is one of the most commonly measured and manipulated hemodynamic variables in the perioperative period Although MAPs are routinely maintained in the 70 to 80 mm Hg range, target blood pressure may be altered based upon comorbid disease and the intraoperative course of events Hypertensive patients with neurologic or renal disease may have altered autoregulatory curves, which require higher blood pressures for adequate end-organ function Conversely, in patients with friable cardiac tissue, tenuous surgical repairs, or uncorrected aneurysmal disease lower MAPs may be desirable Ideally, intraoperative manipulation of the blood pressure while observing the echo cardiogram and changes in central venous (CVP) and pulmonary artery pressures (PAPs) will allow the practitioner to define optimal blood pressure HYPERTENSION Cardiac surgical patients presenting in the postoperative period with hypertension should be evaluated for routine causes of acute postoperative hypertension and treated accordingly Pain, residual neuromuscular blockade, hypoxemia, hypercarbia, hypothermia, or bladder distention may provoke hypertension If these precipitants are ruled out, pharmacologic lowering of blood pressure with an infusion of a vasodilator, sodium nitroprusside, or nitroglycerin can be initiated The rapid titratability and short duration of action of these medications is desirable as hemodynamic lability is commonplace Alternatively, short-acting or ultrashort-acting dihydropyridine calcium channel blockers (e.g., nicardipine or clevidipine) have been used as they exert maximal effect in the peripheral arterial system with minimal impact on cardiac function.24 While MAP is lowered, serial measurements of cardiac output and urine output should be recorded to assess the patient’s tolerance of a lower blood pressure HYPOTENSION With a reported incidence of 9% to 44%, hypotension is more common than hypertension following cardiac surgery.25 Studies of off-pump CABG surgery compared to on-pump CABG surgery have demonstrated a significant increase in the incidence of hypotension in those patients exposed to CPB.26 Some clinicians also associate the relatively common hypotensive response to more critically ill patients with prolonged medical management prior to surgery Additionally, widespread use of angiotensinconverting enzyme inhibitors has been implicated as a potential contributor.27 Regardless of the predisposing factors, postoperative hypotension demands prompt investigation and treatment From a physiologic standpoint, MAP = central venous pressure (CVP, mm Hg) + cardiac output (CO, L/minute) × systemic vascular resistance (SVR, dyn⋅s⋅cm−5) A decrease in any of these parameters will reduce MAP It is useful to consider the common causes of postoperative hypotension relative to these hemodynamic variables Low CVP corresponds with hypovolemia Decreased CO can occur as a consequence of cardiac insufficiency/cardiogenic shock or 613 new-onset myocardial ischemia Vasoplegia following CPB leads to a depressed SVR Routine causes of hypotension in the acute postoperative period include hypovolemia, cardiac insufficiency/cardiogenic shock, vasoplegia following CPB, new-onset myocardial ischemia, and tamponade Crucial to postoperative management is understanding the patient’s intraoperative hemodynamics and immediate postbypass cardiac function The most readily correctable cause of hypotension is hypovolemia Commonly boluses of crystalloid (500 mL to 1 L of 0.9% normal saline or lactated Ringer’s solution) are administered and the patient’s hemodynamic responses (MAP, CVP, PAP, and cardiac index [CI]) are evaluated Colloid solutions can be used, but some concern exists when administering hetastarch solutions because of its effects on the coagulation cascade and potential contribution to a bleeding diathesis.28 A low preoperative ejection fraction (70 years old), and prolonged CPB times (>120 minutes) correlate with an increased risk of decreased cardiac output in the postbypass period.29 Postoperatively, a depressed CI often manifests early, during separation from CPB in the operating room The pattern observed on hemodynamic monitoring is a depressed CI (200-300 mL/hr) • Hypothermia • Mechanical ventricular assist • Open sternum Secondary Adverse Criteria • Intra-aortic balloon pump counterpulsation support • Long-standing pulmonary hypertension • Operation for: • Acute myocardial infarction • Acute ventricular septal defect • Acute mitral regurgitation (papillary muscle rupture) • Descending aortic aneurysm *Notably few of these are absolute contraindications to ventilator weaning, but they warrant consideration in the aggregate (see text) FiO2, fraction of inspired oxygen; ICU, intensive care unit; PaO2, partial pressure of oxygen in arterial blood after cardiac surgery, there is little evidence to support this approach Tracheostomy timing can be based on the determination at the end of the first ICU week of a patient’s likelihood of successful weaning over the second week If at that time successful weaning is considered unlikely, tracheostomy should be considered Earlier tracheostomy (before the tenth postoperative day) in patients who require prolonged mechanical ventilation after cardiac surgery is associated with lower morbidity and mortality rates as well as decreased ICU and total hospital lengths of stay, and is not associated with an increased occurrence of mediastinitis.57 Venovenous extracorporeal membrane oxygenation and nitric oxide are two other modalities employed infrequently in selected patients with severe refractory respiratory failure after cardiac surgery Nitric oxide has been used most effectively in patients with severe right ventricular dysfunction due to new-onset pulmonary hypertension to reduce right ventricular afterload It is used under a protocol starting at 40 ppm and only continued if there is an immediate beneficial effect (reduction in pulmonary artery systolic pressure of 25% or greater) Weaning nitric oxide is usually first attempted within 24 hours of initiating it using PA pressure change as the weaning parameter and discontinued as soon as possible 617 RENAL CARE Despite significant research efforts and considerable focus on prevention and treatment, acute kidney injury (AKI) following cardiac surgery is associated with a significantly increased risk of morbidity and mortality Although only 1% of patients will experience the most severe form of kidney injury and require some form of renal replacement therapy, this patient population has a 60% in-hospital mortality rate.58 Risk stratification has identified several preoperative and postoperative risk factors for postoperative AKI—these include female gender, left ventricular ejection fraction (LVEF) less than 35%, exposure to angiographic contrast dye, duration of CPB, and low MAP during CPB.59 Causes of AKI are frequently divided into three distinct etiologic categories—prerenal, intrarenal, and postrenal Although these aid in diagnostic evaluation, overlap may exist with multiple pathologic processes occurring in the same patient Postrenal oliguria implies mechanical obstruction of the urologic system from the collecting ducts through the ureters Diagnosis can be confirmed by Foley irrigation, renal and ureteral ultrasound, or computed tomographic scan of the abdomen and pelvis Prerenal causes occur when intravascular volume and cardiac output are insufficient to adequately perfuse the kidneys In this state of ineffective circulating volume, the natural response of the kidneys is retention of blood volume and excretion of a small quantity of concentrated urine If intravascular depletion or a depressed cardiac output persists, compensatory mechanisms may become overwhelmed Thereafter, renal malperfusion becomes pathologic with the onset of acute tubular necrosis (ATN) and intrinsic renal injury Intrinsic renal failure refers to the state of direct damage to the kidney by ischemia or nephrotoxin exposure The most common cause of intrarenal renal failure is ATN This can result from prolonged periods of ischemia or exposure to nephrotoxic antibiotics, or contrast agents Less commonly, certain medications (e.g., nafcillin or furosemide) can cause an inflammatory condition known as acute interstitial nephritis Initial evaluation of the patient with AKI should focus on the patient’s preoperative risk factors, intraoperative course of events, exposure to nephrotoxic agents, and current hemodynamic and intravascular volume status Laboratory parameters to assist in diagnosis of AKI include urine electrolytes, sodium (Na), Cr, blood urea nitrogen (BUN), and microscopic analysis of urine sediment The fractional excretion of sodium (FeNa) or fractional excretion of BUN (FeBUN) is often used to distinguish prerenal causes of renal failure from intrarenal causes In the fluid-overloaded oliguric patient diuretics can be given to assess the patient’s responsiveness and to remove excess volume Although conversion from oliguric to non oliguric renal failure through diuretics does not improve overall prognosis, it can improve oxygenation and hemodynamics.60 If the patient is diuretic nonresponsive or has worsening electrolyte or acid-base imbalance, fluid overload with impairment of oxygenation or worsening heart failure, or has severe uremia, initiation of dialytic support should be considered Several different dialysis modalities exist In 618 PART — CRITICAL CARE CARDIOVASCULAR DISEASE brief, continuous therapies offer more stable hemodynamics but not clear as much solute or fluid per unit of time as intermittent dialysis.61 APPLICATIONS OF ECHOCARDIOGRAPHY AFTER CARDIAC SURGERY The use of ultrasonography in the perioperative period has increased significantly over the past decade In contrast to TEE usually performed by cardiologists and cardiothoracic anesthesiologists in the operating room, focused TTE is well suited for the postoperative period especially for unexplained hypotension and assessment of response to therapeutic interventions Postoperative use of TTE can provide rapid and accurate diagnostic information in patients developing potentially life-threatening conditions Although the image quality obtained in mechanically ventilated patients is usually better with TEE, TTE usually provides adequate views in postcardiotomy patients; and it is noninvasive, fast, performed at the bedside, reproducible, and focused on major cardiac and pleural space abnormalities.62,63 The use of TTE in periresuscitation (life support) care has two goals: (1) to assess the heart function, and (2) to identify treatable conditions The focused echocardiographic evaluation in life support (FEEL) examination is briefly performed during cardiopulmonary resuscitation (CPR) with the primary objective of identifying potentially reversible causes of cardiopulmonary deterioration The identification and appropriate management by TTE in the perioperative period of severe left ventricular dysfunction, pulmonary embolism, hypovolemia, or cardiac tamponade may be lifesaving.64,65 The recommended echocardiographic window to perform the FEEL examination is the subcostal view (Fig 36.2) The FEEL examination may distinguish “true” pulseless electrical activity (PEA) from pseudo-PEA.66 A recent publication demonstrated that in 35% of patients with an ECG diagnosis of asystole, 58% of those with PEA, coordinated cardiac motion was detected (pseudo-PEA) and associated with increased survival Echocardiographic findings altered management in 78% of cases.64 In addition, FEEL protocol can facilitate the early detection of return of spontaneous circulation One of the most common questions in the critically ill is the fluid responsiveness Barbier and associates described the inferior vena cava (IVC) distensibility index in mechanically ventilated patients.67 This index is based on change in size of IVC with respiration as it decreases with size with inspiration and increases with expiration: Distensibility index = IVC max (end expiration) − IVC (end inspiration) IVC (end expiration) In this equation distensibility index is expressed as a percentage A distensibility index greater than 18% predicts fluid responsiveness B A RV RA LV LA C D Figure 36.2 The FEEL examination—the subcostal view A, Orientation of the probe in the epigastrium B, Direction of the ultrasound beam C and D, Identification of cardiac chambers CHAPTER 36 — Postoperative Management of the Cardiac Surgery Patient ∆IVC = 619 2.6 − 1.7 × 100 = 34.6% 1.7 DIns = 2.6cm DExp = 1.7 cm Parasternal view Long axis Short axis (clockwise rotation) Subcostal view IVC (counterclockwise rotation – 90 degrees) Figure 36.3 Inferior vena cava—diameter and distensibility index Counterclockwise rotation from subcostal view (90 degrees) (Courtesy of Dr Achi Oren-Grinberg: Beth Israel Deaconess Medical Center, Boston, MA.) THE FATE EXAMINATION The focused assessed transthoracic echocardiography (FATE) examination is a qualitative POC ultrasonography, which is ideal within the ICU The FATE examination should include qualitative assessment of left and right ventricular function and intravascular volume status as minimum required information (Fig 36.3) It supplements the critical care evaluation in the perioperative setting.68,69 However, focused echocardiography does not replace a comprehensive echocardiogram performed per cardiology specialist whenever quantitative analysis or specific diagnoses such as endocarditis or valvular dysfunction are needed Moreover, the correct application of this tool in postcardiotomy patients depends on the appropriate utilization of ultrasonography findings in the clinical context.70 The main goal of the FATE examination is to better characterize the state of shock/hypotension, volume status, and pleural disease: Hypovolemia (measurement of IVC diameter and distensibility index) Myocardial dysfunction (qualitative evaluation of the right and left ventricles, measurement of cardiac output and pulmonary pressures) including patients with acute respiratory failure Pericardial effusion/tamponade (evaluation of tamponade physiology) Pulmonary embolism (changes in acute right ventricular dysfunction) Pulmonary edema (lines B, “comet tail” artifacts) Pneumothorax (the sliding sign) The appropriate process of applying FATE examination includes (a) acquisition of images, (b) recognition of normal anatomy of the heart, (c) fundamental knowledge of the more relevant diseases, and more importantly (d) applying findings to the clinical context Apical view Pleural examination Figure 36.4 The focused assessed transthoracic echocardiography (FATE) protocol—transthoracic echocardiography views 1, subcostal view; 2, apical view; 3, parasternal view; 4, pleural examination ACQUISITION OF IMAGES Bedside ultrasonography and acquisition of cardiac images are not exclusive of the comprehensive transthoracic examination Moreover, the FATE examination must be considered an extension of the physical examination Thus, before obtaining images with echocardiography it is important to keep in mind the position of the heart within the chest and the direction of the ultrasound beam (Fig 36.4) In addition, thoracic ultrasonography offers better sensitivity and specificity than plain chest radiography The evaluation of the pleurae mandate the knowledge of anatomic structures above and below both diaphragms The acquisition of images can be very challenging in the postcardiotomy patient Most of the time at least one view can be obtained and the goal of exclusion of important disease is achieved Up to 40% of patients in the ICU have limited acquisition of echocardiography views Although the TEE is an invasive technique, the unparalleled quality of ultrasonography examination is well known (Tables 36.1 and 36.2) ROLE OF ULTRASONOGRAPHY IN POSTCARDIOTOMY TAMPONADE Postcardiotomy surgery tamponade (PCST) is perhaps the most important diagnosis in the patient recovering from cardiac surgery Its early recognition and intervention have a direct impact in patients’ outcome The process of diagnosing PCST begins with the identification of clinical signs and confirmation of the diagnosis with appropriate tools subsequently A high index of suspicion should be maintained throughout the early postoperative cardiovascular ICU (CVICU) hours Usually a progressive decrease of cardiac output after increased chest tube drainage and increased filling pressures occurs with PCST.71 Clinical signs such us Beck’s triad (hypotension, distended neck veins, and diminished heart sounds) and pulsus paradoxus are neither sensitive nor specific of PCST.72 Patients with other disorders such as constrictive 620 PART — CRITICAL CARE CARDIOVASCULAR DISEASE Table 36.1 The FATE Protocol: Technique Probe Orientation Marker Depth Helpful Tips 2-3 cm below xiphoid process or RUQ if chest tubes are in place ~3 o’clock 15-25 cm Subcostal–inferior vena cava From the previous view, rotate transducer 90 degrees counterclockwise ~12 o’clock 16-24 cm Apical Find the point of maximal impulse if feasible; otherwise, from anterior axillar line to nipple Third to fourth intercostal space ~3 o’clock 14-18 cm Hold the transducer from the top; apply angulations between 10 and 40 degrees Supine position Keep right atrium to IVC junction on the screen Need to see the IVC merging into right atrium Ensure good contact with the rib (gentle pressure) ~11 o’clock Rotate 90 degrees clockwise from the parasternal–long-axis view, so ~2 o’clock ~2 o’clock 12-20 cm (up to 24 cm with pleural or pericardial effusion) 12-16 cm View Location of Transducer Subcostal Parasternal–long axis Parasternal–short axis Ideally, left lateral decubitus position Aortic valve level: Tilt transducer face slightly upward toward the patient’s right shoulder Mitral valve level: Transducer is perpendicular to chest wall Papillary muscle level: Transducer faces slightly downward toward the patient’s left flank FATE, focused assessed transthoracic echocardiography; IVC, inferior vena cava; RUQ, right upper quadrant Table 36.2 Assessment of Structures with FATE Protocol Assessment Focus View(s) Classification Left ventricular (LV) function (qualitative)—“eyeballing”: thickness of the myocardium Parasternal–long-/short-axis view Apical view, subcostal view Normal function Mild to moderate LV dysfunction Severe LV dysfunction Hyperdynamic Right ventricular function Parasternal–long-/short-axis view Apical view, subcostal view Parasternal–long-/short-axis view Apical view, subcostal view Parasternal–long-axis view Pericardial space Pleural effusion and pericardial effusion Inferior vena cava (IVC) Subcostal view of the IVC Pericardial effusion Tamponade physiology Diameter measurement: 2-3 cm from right atrium Normal diameter: 2.1 cm Respiratory phase variations, ideally on spontaneously breathing patients FATE, focused assessed transthoracic echocardiography pericarditis, severe COPD, morbid obesity, and right ventricular infarction might present with pulsus paradoxus In contrast, this sign can be absent in patients with atrial septal defect, regional tamponade, pulmonary hypertension, COPD with cor pulmonale, aortic insufficiency, and even positive-pressure mechanical ventilation.72 The various clinical presentations of PCST impose limi tations to the FATE examination, especially posterior compartmented effusion In addition, clotted and loculated blood is echo-dense, somewhat more challenging to diagnose, and could be mistaken for the myocardium itself As a rapid screening tool it can very helpful if collapse of the right ventricle is noticed in the long-axis parasternal view or collapse of the right atrium/right ventricle, or left ventricle in the apical or subcostal views (Figs 36.5 to 36.7) In addition, documentation of abnormally increased CHAPTER 36 — Postoperative Management of the Cardiac Surgery Patient 621 B A RV RA LV LA DA C D Figure 36.5 Apical view A, Orientation of the probe in the apex B, Direction of the ultrasound beam C and D, Identification of cardiac chambers and heart valves B A RV Ao LV LA DA C D Figure 36.6 Parasternal—long axis view A, Orientation of the probe in the apex B, Direction of the ultrasound beam C and D, Identification of cardiac chambers and heart valves 622 PART — CRITICAL CARE CARDIOVASCULAR DISEASE B A RV PA Ao RA LA RV C D RV MV E F RV LV G H Figure 36.7 Parasternal—short axis view A, Orientation of the probe in the left parasternal spaces B, Direction of the ultrasound beam C to H, Identification of cardiac chambers and heart valves CHAPTER 36 — Postoperative Management of the Cardiac Surgery Patient Table 36.3 Echocardiographic Findings in Cardiac Tamponade Typical Atypical Right atrium compression in early diastole* Dilated inferior vena cava without respirophasic variability Echo-free space around the heart (circumferential pericardial effusion) Right ventricular diastolic collapse in the late diastole Respirophasic variation of transmitral and transtricuspid flows “Swinging heart” in the pericardial effusion Selective compression of the atria Selective compression of right atrium Bilateral atrial compression Selective compression of right ventricle Selective compression of left ventricle *Right atrial collapse has higher sensitivity (68% vs 60%) than right ventricular collapse but lower specificity (66% vs 90%) in clinical tamponade With hypovolemia this sign of tamponade might precede hemodynamic alterations diameter of the IVC (>2.5 cm) without variability with respiratory phases may help to distinguish from hemorrhagic shock in the setting of severe hypotension in the postoperative period.73 Transesophageal echocardiography is the definitive test whenever FATE examination has no conclusive findings to support PCST despite high suspicion of atypical presentation The performance of echocardiographic evaluations should not delay an emergency surgical reexploration in the setting of postoperative shock The presence of acute bleeding into the pericardial space makes it appear as echolucent space The presence of blood in the pericardium can be graded as small (0.5 cm), moderate (0.5-2 cm), or large (>2 cm) Right atrial systolic collapse that has duration greater than 30% of the entire systole is the most sensitive and specific sign of PCST The best views to recognize this finding are subcostal or apical view on TTE and midesophageal four-chamber view by TEE Doppler ultrasound can reveal a 35% increase respirophasic variation of the tricuspid/mitral E-wave velocity during spontaneous inspiration and a decrease of 25% in the mitral or left ventricle outflow track flow Another important and helpful finding is the paradoxical movement of the interventricular septum (shift of the septum to the left ventricle in diastole and toward the right ventricle in systole) during spontaneous expiration and normalization in controlled ventilation (Table 36.3) Absence of right atrial collapse in cardiac tamponade is seen in severe pulmonary hyper tension, RV dysfunction, COPD with cor pulmonale, and regional posterior tamponade RESCUE APPLICATIONS OF ECHOCARDIOGRAPHY • The use of focused echocardiography in periresuscitation following cardiac surgery intends to identify the four treatable causes of cardiac arrest (severe ventricular 623 dysfunction, pulmonary embolism, hypovolemia, and cardiac tamponade) • The most useful echocardiography view in the setting of advanced cardiac life support is the subcostal It can be performed after cycles of CPR maneuvers • The identification of true PEA arrest has important prognostic implications as this subgroup of patients has worse prognosis in comparison to patients with pseudo-PEA (detection of coordinated cardiac motion) • Post–cardiac surgery tamponade has various clinical presentations and may impose limitations to focused echocardiography, especially in those cases of posterior compartmented effusion MISCELLANEOUS CONSIDERATIONS INTRA-AORTIC BALLOON PUMP WEANING As noted elsewhere in this chapter, most patients with an IABP on arrival in the post–cardiac surgery unit have had the device percutaneously placed preoperatively in the catheterization laboratory Appropriate management requires knowing the indication for its placement In patients with unstable angina or left critical anatomy (usually a left main vessel obstruction, with or without proximal right coronary artery obstruction), the balloon often can be weaned as soon as the bleeding risks associated with removal are considered back to baseline This may occur before extubation while the patient is still sedated These are patients whose indication for IABP insertion has been corrected by the operation, and who not require significant inotropic support, so the device is withdrawn in the early postoperative hours Less common and more challenging are the patients who had an IABP inserted for hemodynamic instability or cardiogenic shock preoperatively In these patients, weaning from mechanical support may occur only after pharmacologic support (inotropes and vasopressors) has been weaned to a level that would allow them to be reinstituted or increased to support the patient after IABP removal These are patients in whom a trial of ventilator weaning on IABP may be appropriate because the balloon unloads the afterload increases seen by a poor ventricle during awakening and ventilator weaning In such patients, the IABP may be removed after extubation, but often ventilatory failure predominates, and the balloon weaning end points (minimal or no pharmacologic support) are reached well before extubation is an option In these patients, mechanical support is weaned (decreasing the balloon augmentation ratio from 1:1 to 1:2 to 1:3, or by decreasing the balloon inflation volume) A normal response is to see the native (unloaded) systolic pressure increase as the MAP remains steady over 30 to 60 minutes If these criteria are met, the balloon usually can be safely removed Patients who have an IABP placed intraoperatively may have had “prophylactic” mechanical support initiated, and, if on minimal pressor and inotrope support, with an anatomically corrective procedure, the device may be removed before extubation, as noted earlier IABPs placed after CPB as an adjunct to weaning (see earlier) are frequently needed for days before successful weaning 624 PART — CRITICAL CARE CARDIOVASCULAR DISEASE ROUTINE ORDER SETS KEY POINTS (Continued) The post–cardiac surgery setting routinely makes good use of preprinted orders that, ideally, reflect a system-wide patient care pathway for the “typical” patient It is important to review and revise these orders regularly to ensure that they remain appropriate in light of changes in accepted treatment principles and the institution’s patient population The review and revision of these order sets should include a review of patient care pathways or protocols Protocol modifications should be part of a process involving surgeons, anesthesiologists, intensivists, nurses, respiratory therapists, pharmacists, infectious disease specialists, and nephrologists • Thrombolytic therapy is a feasible therapy in selected patients who present postcardiotomy stroke • Perioperative hemodynamic perturbations are common in cardiac surgical patients and depend on the patient’s preoperative state, the nature of the surgical procedure, and the degree of intraoperative stunning • Optimal postoperative blood pressure should be determined in the context of the patient’s comorbid conditions and the nature of the surgical procedure • Postoperative hypotension may be secondary to hypovolemia, cardiac insufficiency, vasoplegia, myocardial ischemia, or tamponade • Myocardial stunning and vasoplegia usually require exogenous pharmacologic support and improve over hours to days • Acute tamponade requires immediate recognition and treatment; unfortunately, classic physical examination signs may not manifest • The most common arrhythmia following cardiac surgery is atrial fibrillation, and clinicians must decide whether rate or rhythm control is preferable for their patients • Bleeding following cardiac surgery is relatively common and often requires transfusion of packed red blood cells, platelets, and FFP • Fluid overload is a common cause of poor gas exchange in the early postoperative period and can be readily assessed by reviewing intraoperative fluid balance and postoperative indicators of volume status • Atelectasis is common in these patients and may not become clinically significant until after extubation when sedation and positive-pressure ventilation have been discontinued, especially in patients who are fluid overloaded • Pleural effusions present after chest tubes have been removed are common but usually not require removal by thoracentesis or chest tube thoracostomy unless they cause respiratory symptoms • Patients with baseline abnormal pulmonary function will usually manifest it to a worse degree postoperatively • Unanticipated, severe pulmonary dysfunction may be due to acute lung injury and is usually associated with inflammation and hemodilution related to CPB, particularly after long operations • Postoperative diaphragm dysfunction may account for pulmonary problems in these patients A paralyzed or palsied diaphragm may be suspected by finding an elevated hemidiaphragm on the first postoperative radiograph or after weaning from positive-pressure ventilation • A protocol-driven and respiratory therapist–managed reduction in initial postoperative intubation time has been achieved in many ICUs INTENSIVE CARE UNIT LENGTH OF STAY Initial intubation time is associated with ICU length of stay Most cardiac surgery patients can be extubated early and transferred out of the ICU within 24 hours Rapid patient turnover is achieved in ICUs that use care pathways based on patient parameters and not the length of stay.49 Patientbased parameters for a diuresis protocol would be based on a patient’s weight relative to the preoperative weight, the BUN/Cr, and the CI/preload, not on time (“postoperative day 1”) When time-based parameters are used, they should be based on hours rather than days Pacing wires might be removed routinely after any 12-hour period with no need for pacing or antidysrhythmic therapy, rather than “on postoperative day 2.” Timing of chest tube removal may be based on volume and character of the drainage, rather than on an experientially derived time or postoperative day KEY POINTS • Despite decreased overall mortality risk in coronary artery grafting, postoperative neurologic complications remain the major cause of morbidity and death Among these complications, stroke portends the worse outcome • The most consistent pathophysiologic mechanism of stroke is embolism (>60%), followed by hypoperfusion and hemorrhage • Clinical presentation of postcardiotomy neurologic complications include altered consciousness and coma, focal neurologic deficit, and seizures • Brain CT scan is indicated at any time postcardiotomy patients present unexplained delayed awakening, new focal neurologic deficit, or seizure • Although brain MRI is not usually feasible in the early postoperative period following cardiac surgery, it provides better characterization of the cerebral ischemic lesions and it has a definite prognostic value • The most important initial interventions of patients suffering from postcardiotomy stroke include tracheal intubation (if the patient has a GCS score