Surgical Critical Care and Emergency Surgery E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
This is a unique question-and-answer book for surgical residents and trainees, concentrating on the growing subspecialty of surgery in critical care and emergency surgery. This book covers all surgical aspects of critical care and acute or emergency surgery, making it an ideal learning and review text for surgical trainees and those professionals specializing in these fields. The second edition includes full revised and updated questions throughout, with additional topics addressed in a new companion website.
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Veröffentlichungsjahr: 2018
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Table of Contents
Cover
Title Page
Contributors
About the Companion Website
Part One: Surgical Critical Care
1 Respiratory and Cardiovascular Physiology
2 Cardiopulmonary Resuscitation, Oxygen Delivery, and Shock
3 ECMO
4 Arrhythmias, Acute Coronary Syndromes, and Hypertensive Emergencies
5 Sepsis and the Inflammatory Response to Injury
6 Hemodynamic and Respiratory Monitoring
7 Airway and Perioperative Management
8 Acute Respiratory Failure and Mechanical Ventilation
9 Infectious Disease
10 Pharmacology and Antibiotics
11 Transfusion, Hemostasis, and Coagulation
12 Analgesia and Anesthesia
13 Delirium, Alcohol Withdrawal, and Psychiatric Disorders
14 Acid‐Base, Fluid, and Electrolytes
15 Metabolic Illness and Endocrinopathies
16 Hypothermia and Hyperthermia
17 Acute Kidney Injury
18 Liver Failure
19 Nutrition Support in Critically Ill Patients
20 Neurocritical Care
21 Thromboembolism
22 Transplantation, Immunology, and Cell Biology
23 Obstetric Critical Care
24 Pediatric Critical Care
25 Envenomations, Poisonings, and Toxicology
26 Common Procedures in the ICU
27 Diagnostic Imaging, Ultrasound, and Interventional Radiology
Part Two: Emergency Surgery
28 Neurotrauma
29 Blunt and Penetrating Neck Trauma
30 Cardiothoracic and Thoracic Vascular Injury
31 Abdominal and Abdominal Vascular Injury
32 Orthopedic and Hand Trauma
33 Peripheral Vascular Trauma
34 Urologic Trauma and Disorders
35 Care of the Pregnant Trauma Patient
36 Esophagus, Stomach, and Duodenum
37 Small Intestine, Appendix, and Colorectal
38 Gallbladder and Pancreas
39 Liver and Spleen
40 Incarcerated Hernias
41 Necrotizing Soft Tissue Infections and Other Soft Tissue Infections
42 Obesity and Bariatric Surgery
43 Thermal Burns, Electrical Burns, Chemical Burns, Inhalational Injury, and Lightning Injuries
44 Gynecologic Surgery
45 Cardiovascular and Thoracic Surgery
46 Pediatric Surgery
47 Geriatrics
48 Telemedicine and Telepresence for Surgery and Trauma
49 Statistics
50 Ethics, End‐of‐Life, and Organ Retrieval
Index
End User License Agreement
List of Tables
Chapter 03
Table 3.1 The RESP score at ECMO initiation.
Chapter 04
Table 4.1 CHA
2
DS
2
‐VASc calculation.
Chapter 07
Table 7.1 The Original and Modified Mallampati Classification classes.
Chapter 10
Table 10.1 Method of elimination of neuromuscular blocking agents.
Table 10.2 Alvimopan prescription limitations.
Table 10.3 Risk factors for MDR pathogens.
Chapter 11
Table 11.1
Chapter 12
Table 12.1 Richmond Agitation and Sedation Scale (RASS).
Chapter 13
Table 13.1 Confusion assessment method to assess delirium (CAM).
Table 13.2 Richmond Agitation Sedation Score (RASS).
Chapter 17
Table 17.1 The KDIGO criteria stages of AKI.
Chapter 18
Table 18.1 Three‐month mortality rates by MELD score.
Chapter 21
Table 21.1 The AAOS recommendations.
Chapter 22
Table 22.1 CYP3A4 inhibitors: increase tacrolimus levels.
Table 22.2 CYP3A4 inducers: decrease tacrolimus levels.
Chapter 28
Table 28.1 Glasgow Coma Scale.
Table 28.2 Brain injury guidelines.
Chapter 29
Table 29.1 Denver screening criteria.
Table 29.2 Injury scale for blunt cerebrovascular injury.
Chapter 34
Table 34.1 Treatment options, adapted from the European Association of Urology
Guidelines on Urological Trauma.
Chapter 39
Table 39.1 Classification of hepatic tumors.
Table 39.2 MELD estimated three‐month mortality.
Chapter 41
Table 41.1 The Laboratory Risk Indicator for Necrotizing Fascitis (LRINEC) score.
Chapter 42
Table 42.1 BMI classification.
Chapter 46
Table 46.1 Pediatric vital sign normal ranges.
Table 46.2 The OI and OSI cutoffs for determining the severity of ARDS in pediatric patients.
Table 46.3 The American Association for the Surgery of Trauma Organ Injury Scale (AAST‐OIS) for pancreatic injuries. Reproduced with permission from Moore
et al.
(1990)
Journal of Trauma
,
30
, 1427–1429.
Chapter 49
Table 49.1 Design of a cohort study.
List of Illustrations
Chapter 01
Figure 1.1 The influence of catheter dimensions on the gravity‐driven infusion of water.
Figure 1.2
Figure 1.3 The cardiac cycle illustrated.
Figure 1.4
Figure 1.5
Figure 1.6
Chapter 04
Figure 4.1
Figure 4.2 (A) Normal electrocardiogram pattern in the precordial leads V1–3. (B) changes in Brugada syndrome (type B).
Figure 4.3
Figure 4.4
Figure 4.5 12‐lead ECG with arrows showing pericarditis.
Figure 4.6 How to measure ST elevation.
Figure 4.7
Figure 4.8
Figure 4.9
Figure 4.10 12 lead ECG with solid arrows showing prolonged QT interval.
Figure 4.11
Figure 4.12
Figure 4.13
Figure 4.14
Figure 4.15 Right‐sided chest ECG.
Figure 4.16 12 lead ECG with arrows inferior MI.
Figure 4.17 RT sided chest lead ECG.
Figure 4.18
Chapter 07
Figure 7.1
Chapter 08
Figure 8.1
Figure 8.2
Figure 8.3
Chapter 10
Figure 10.1
Chapter 11
Figure 11.1
Chapter 14
Figure 14.1
Chapter 24
Figure 24.1
Figure 24.2
Figure 24.3
Figure 24.4
Chapter 25
Figure 25.1a Ulceration to lower extremities.
Figure 25.1b Ulceration to lower extremities.
Chapter 27
Figure 27.1 The FAST exam.
Chapter 28
Figure 28.1
Figure 28.2
Figure 28.3 Algorithm for the diagnosis and management of blunt cerebrovascular injuries in adults.
Chapter 29
Figure 29.1 The vascular anatomy and zones of the neck.
Figure 29.2 A seat belt sign over the neck in Zone I. A full color version of this figure appears in the plate section of this book.
Figure 29.3 Axial CT scan of a Jefferson fracture with bilateral anterior and posterior ring disruption.
Figure 29.4 Axial CT scan of C2 vertebrae with right pedicle and lamina fractures
Chapter 31
Figure 31.1 Retroperitoneal zones.
Chapter 32
Figure 32.1
Figure 32.2
Figure 32.3 Gustilo and Anderson type IIIA open tibia fracture. A full‐color version of this figure appears in the plate section of this book.
Figure 32.4 A full‐color version of this figure appears in the plate section of this book.
Figure 32.5 A lateral wrist x‐ray with a volarly dislocated lunate (white arrow) indicating a perilunate dislocation.
Chapter 33
Figure 33.1 Pulsatile hemorrhage from the right thigh, a vascular “hard sign.” A full color version of this figure appears in the plate section of this book.
Figure 33.2 Temporary intravascular shunting of the superficial femoral artery. A full color version of this figure appears in the plate section of this book.
Figure 33.3
Chapter 34
Figure 34.1
Figure 34.2
Figure 34.3
Figure 34.4
Figure 34.5
Figure 34.6 Shariat
et al.
nomogram to predict need for exploration in cases of renal trauma.
Chapter 37
Figure 37.1 A full color version of this figure appears in the plate section of this book.
Figure 37.2
Figure 37.3 A full color version of this figure appears in the plate section of this book.
Figure 37.4 A full color version of this figure appears in the plate section of this book.
Figure 37.5
Chapter 39
Figure 39.1
Figure 39.2 Couinaud’s eight segments of the liver.
Figure 39.3
Figure 39.4
Figure 39.5
Chapter 40
Figure 40.1
Figure 40.2
Chapter 41
Figure 41.1 Trunk and extremity necrotizing soft‐tissue infection. Head at top of photo, left arm to right of photo.
Figure 41.2 Scalp necrotizing soft‐tissue infection; right ear is to the right, face anteriorly.
Chapter 43
Figure 43.1 An escharotomy.
Chapter 45
Figure 45.1 Large right pulmonary embolus on CT scan.
Figure 45.2 Free esophageal perforation into the right pleural cavity.
Chapter 46
Figure 46.1
Chapter 49
Figure 49.1 Normal and asymmetric distributions.
Figure 49.2
Guide
Cover
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Surgical Critical Care and Emergency Surgery
Clinical Questions and Answers
Second Edition
Edited by
Forrest “Dell” Moore, MD, FACS
Vice Chief of SurgeryAssociate Trauma Medical DirectorJohn Peter Smith Health Network/Acclaim Physician GroupFort Worth, TX, USA
Peter Rhee, MD, MPH, FACS, FCCM, DMCC
Professor of Surgery at USUHS, Emory, and MorehouseChief of Surgery and Senior Vice President of GradyAtlanta, GA, USA
Gerard J. Fulda, MD, FACS, FCCM
Associate Professor, Department of SurgeryJefferson Medical College, Philadelphia, PAChairman Department of SurgeryPhysician Leader Surgical Service LineChristiana Care Health Systems, Newark, DE, USA
This second edition first published 2018© 2018 by John Wiley & Sons Ltd
Edition HistoryJohn Wiley & Sons Ltd (1e, 2012)
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.
The right of Forrest “Dell” Moore, Peter Rhee, and Gerard J. Fulda, to be identified as the authors of the editorial in this work has been asserted in accordance with law.
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Limit of Liability/Disclaimer of WarrantyThe contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
Library of Congress Cataloging‐in‐Publication Data
Names: Moore, Forrest “Dell”, editor. | Rhee, Peter, 1961– editor. | Fulda, Gerard J., editor.Title: Surgical critical care and emergency surgery : clinical questions and answers / edited by Forrest “Dell” Moore, Peter Rhee, Gerard J. Fulda.Description: 2e. | Hoboken, NJ : Wiley, 2017. | Includes bibliographical references and index. |Identifiers: LCCN 2017054466 (print) | LCCN 2017054742 (ebook) | ISBN 9781119317982 (pdf) | ISBN 9781119317951 (epub) | ISBN 9781119317920 (pbk.)Subjects: | MESH: Critical Care–methods | Surgical Procedures, Operative–methods | Wounds and Injuries–surgery | Emergencies | Critical Illness–therapy | Emergency Treatment–methods | Examination QuestionsClassification: LCC RD93 (ebook) | LCC RD93 (print) | NLM WO 18.2 | DDC 617/.026–dc23LC record available at https://lccn.loc.gov/2017054466
Cover Design: WileyCover Images: (Background) © Paulo Gomez/Hemera/Gettyimages; (Inset image) © jacoblund/Gettyimages
Contributors
Joanelle A. Bailey, MDResident In SurgeryRutgers New Jersey Medical SchoolNewark, NJ, USA
Adam D. Fox, DOAssistant Professor of SurgerySection Chief, TraumaDivision of Trauma Surgery and Critical CareRutgers NJMSAssociate Trauma Medical Director NJ Trauma CenterUniversity HospitalNewark, NJ, USA
Erin M. Garvey, MDPediatric Surgery FellowPhoenix Children’s HospitalPhoenix, AZ, USA
Alan Cook, MDClinical Assistant ProfessorDepartment of SurgeryUniversity of Arizona Phoenix CampusChandler Regional Medical CenterChandler, AZ, USA
Lewis J. Kaplan, MDAssociate Professor of SurgeryPerelman School of Medicine, University of PennsylvaniaDepartment of SurgeryDivision of Trauma, Surgical Critical Care and Emergency SurgerySection Chief, Surgical Critical CarePhiladelphia VA Medical CenterPhiladelphia, PA, USA
J. Craig Egan, MDChief, Division of Pediatric SurgeryDirector, Pediatric Surgical Critical CarePhoenix Children’s HospitalPhoenix, AZ, USA
Allyson Cook, MDSurgical Critical Care FellowStanford UniversityStanford, CA, USA
Stephen L. Barnes, MDProfessor of Surgery & AnesthesiaDivision Chief of Acute Care SurgeryUniversity of Missouri School of MedicineMU HealthColumbia, MO, USA
Jeffrey P. Coughenour, MDAssociate Professor of Surgery & Emergency MedicineDivision of Acute Care SurgeryUniversity of Missouri School of MedicineMU HealthColumbia, MO, USA
Christopher S. Nelson, MDAssistant Professor of SurgeryDivision of Acute Care SurgeryUniversity of Missouri School of MedicineMU HealthColumbia, MO, USA
Andrew J. Young, MDStaff SurgeonNaval HospitalBremerton, WA, USA
Adrian A. Maung, MDAssociate Professor of SurgerySection of General SurgeryTrauma and Surgical Critical CareDepartment of SurgeryYale School of MedicineAdult Trauma Medical Director Yale New Haven HospitalNew Haven, CT, USA
CPT Clay M. Merritt, DOGeneral Surgery ResidentWilliam Beaumont Army Medical CenterEl Paso, TX, USA
Andrew Tang, MDAssociate professor of surgeryBanner University Medical Center‐TucsonTucson, AZ, USA
Matthew B. Singer, MDAcute Care SurgeryThe Institute of Trauma and Acute Care, Inc.Pomona, CA, USA
Omar K. Danner, MDChief of Surgery for MSMGrady Memorial HospitalAssociate Professor of SurgeryDirector of TraumaDepartment of SurgeryMorehouse School of MedicineAtlanta, GA, USA
Matthew Martin, MDClinical Professor of SurgeryUniversity of Washington School of MedicineSeattle, WAProfessor of SurgeryUniformed Services University for the Health SciencesBethesda, MD, USA
Aaron Cunningham, MDGeneral Surgery ResidentOregon Health Sciences UniversityPortland, OR, USA
Mubeen Jafri, MDAssistant Professor of SurgeryOregon Health Sciences UniversityPortland, OR, USA
Brett D. Crist, MDAssociate ProfessorDepartment of Orthopaedic SurgeryVice Chairman of Business DevelopmentDirector Orthopaedic Trauma ServiceDirector Orthopaedic Trauma FellowshipUniversity of MissouriColumbia, MO, USA
Gregory J. Della Rocca, MDAssociate ProfessorDepartment of Orthopaedic SurgeryUniversity of MissouriColumbia, MO, USA
Joshua Dilday, DOCPT MC, US ArmyGeneral Surgery ResidentWilliam Beaumont Army Medical CenterEl Paso, TX, USA
Courtney McKinney, PharmDClinical Pharmacist, Chandler Regional Medical CenterClinical Instructor, Department of Pharmacy Practice and ScienceUniversity of Arizona College of Pharmacy Tucson, AZ, USA
Rondi Gelbard, MDAssistant Professor of SurgeryAssociate Medical Director, Surgical ICUAssociate Program Director, Surgical Critical Care FellowshipEmory University School of MedicineAtlanta, GA, USA
Barret Halgas, MDCPT MC, US ArmyGeneral Surgery ResidentWilliam Beaumont Army Medical CenterEl Paso, TX, USA
LTC Eric Ahnfeldt, DOChairman, Military Committee for American Society of Metabolic and Bariatric SurgeryDirector, Metabolic and Bariatric SurgeryProgram DirectorGeneral Surgery ResidencyWilliam Beaumont Army Medical CenterEl Paso, TX, USA
Daniel Roubik, MDCPT MC, US ArmyGeneral Surgery ResidentWilliam Beaumont Army Medical CenterEl Paso, TX, USA
Andy Michaels, MDClinical Associate Professor of SurgeryOregon Health and Science UniversitySurgeonTacoma Trauma TrustMedecins Sans Frontiers/Doctors Without BordersInternational Committee of the Red Cross, Portland, OR, USA
Cathy Ho, MDAcute Care Surgery FellowBanner University Medical CenterTucson, AZ, USA
Narong Kulvatunyou, MDAssociate ProfessorProgram Director Surgical Critical Fellowship/Acute Care Surgery FellowshipUniversity of Arizona Health Science CenterDepartment of Surgery, Section of Trauma, Critical Care & Emergency SurgeryTucson, AZ, USA
Herb A. Phelan, MDProfessor of SurgeryUniversity of Texas Southwestern Medical CenterDepartment of SurgeryDivision of Burns/Trauma/Critical CareDallas, TX, USA
Juan C. Duchesne, MDProfessor of SurgerySection Chief TraumaDepartment of Tulane SurgeryTICU Medical DirectorNorman McSwain Level I Trauma CenterNew Orleans, LA, USA
Gregory Peirce, MDMAJ MC, US ArmyChief of General SurgeryWeed Army Community HospitalFort Irwin, CA, USA
Therese M. Duane, MDProfessor of Surgery, University of North TexasChief of Surgery and Surgical SpecialtiesJohn Peter Smith Health NetworkFort Worth, TX, USA
Asser Youssef, MDClinical Associate Professor of SurgeryUniversity of Arizona College of Medicine ‐ PhoenixPhoenix, AZ, USA
Jeremy Juern, MDAssociate Professor of SurgeryMedical College of WisconsinMilwaukee, WI, USA
Kenji Inaba, MDAssociate Professor of Surgery Emergency Medicine and AnesthesiaDivision of Trauma and Critical CareLAC + USC Medical Center University of Southern CaliforniaLos Angeles, CA, USA
Marquinn D. Duke, MDTrauma Medical DirectorNorth Oaks Medical CenterClinical Instructor of Surgery, Tulane UniversityClinical Assistant Professor of SurgeryLouisiana State UniversityNew Orleans, LA, USA
Jacob Swann, MDMAJ MC, US ArmyGeneral Surgery ResidentWilliam Beaumont Army Medical CenterEl Paso, TX, USA
Stephen M. Welch, DODepartment of SurgeryDivision of Acute Care SurgeryUniversity of Missouri Health CareColumbia, MO, USA
Muhammad Numan Khan, MDResearch FellowDivision of Trauma, Critical Care, Emergency General Surgery, and BurnsDepartment of SurgeryUniversity of Arizona,Tucson, AZ, USA
Bellal Joseph, MDProfessor of SurgeryVice Chair of ResearchDivision of Trauma, Critical Care, Emergency General Surgery, and BurnsDepartment of SurgeryUniversity of Arizona,Tucson, AZ, USA
Bryan C. Morse, MS, MDAssistant Professor of SurgeryEmory University SOM‐Department of SurgeryGrady Memorial HospitalAtlanta, GA, USA
Jay J. Doucet, MDProfessor of SurgeryHead, Division of Trauma, Surgical Critical Care, Burns & Acute Care SurgeryUniversity of California San Diego Health, San Diego, CA, USA
Vishal Bansal, MDTrauma Medical DirectorScripps Mercy HospitalSan Diego, CA, USA
Yousef Abuhakmeh, DOCPT MC, US ArmyGeneral Surgery ResidentWilliam Beaumont Army Medical CenterEl Paso, TX, USA
Leslie Kobayashi, MDAssociate Professor of Clinical SurgeryDivision of Trauma, Surgical Critical Care, Burns and Acute Care SurgeryUCSD Medical CenterSan Diego, CA, USA
Remigio J. Flor, MDCPT MC, USARMYGeneral Surgery ResidencyWilliam Beaumont Army Medical CenterEl Paso, TX, USA
Keneeshia N. Williams, MDAssistant Professor of SurgeryEmory University SOM‐Department of SurgeryGrady Memorial HospitalAtlanta, GA, USA
Faisal Shah Jehan, MDResearch FellowDivision of Trauma, Critical Care, Emergency General Surgery, and BurnsDepartment of SurgeryUniversity of ArizonaTucson, AZ, USA
John Watt, MDAssociate Program DirectorGeneral Surgery ResidencyWilliam Beaumont Army Medical CenterAcute Care SurgeonChandler Regional Medical CenterChandler, AZ, USA
Nicholas Thiessen, MDAcute Care SurgeonChandler Regional Medical CenterChandler, AZ, USA
K. Aviva Bashan‐Gilzenrat, MDAssistant Professor of SurgeryDivision of Acute Care SurgeryMorehouse School of MedicineGrady HealthAtlanta, GA, USA
Jonathan Nguyen, DOAssistant Professor of SurgeryDivision of Acute Care SurgeryMorehouse School of MedicineGrady HealthAtlanta, GA, USA
Kalterina Latifi, MSDirector, eHealth CenterWestchester Medical Center Health NetworkValhalla, NY, USA
Rifat Latifi, MDProfessor of Surgery, New York Medical CollegeDirector, Department of SurgeryChief, Divisions of Trauma and General SurgeryWestchester Medical CenterProfessor of Surgery, NYMCValhalla, NY, USA
Raquel M. Forsythe, MDAssistant Professor of Surgery and Critical Care MedicineUniversity of Pittsburgh Medical CenterPresbyterian HospitalPittsburgh, PA, USA
Anthony Sciscione, MDDirector of Obstetrics and Gynecology Residency Program and Maternal Fetal MedicineChristiana Care Healthcare SystemNewark, DelawareProfessor of Obstetrics and GynecologyJefferson Medical CollegePhiladelphia, PA, USA
Filip Moshkovsky, DOAssistant Professor of Clinical SurgeryUniversity of Perelman School of MedicineTraumatology, Surgical Critical Care and Emergency SurgeryReading Health SystemReading, PA, USA
Marcin Jankowski, DODepartment of SurgeryDivision of Trauma and Surgical Critical CareHahnemann University HospitalDrexel University College of MedicinePhiladelphia, PA, USA
Frederick Giberson, MDClinical Assistant Professor of SurgeryJefferson Health SystemPhiladelphia, PA, USAProgram Director, General Surgery ResidencyVice Chair of Surgical EducationChristiana Care Health SystemNewark, DE, USA
Mark Cipolle, MDDirector of Outcomes Research, Surgical Service LineChristiana Care Health SystemNewark, DE, USA
Luis Cardenas, DOMedical Director, Surgical Critical CareProgram Director, Surgical Critical Care FellowshipChristiana Care Health SystemNewark, DE, USA
Michelle Strong, MDMedical Director of Shock Trauma ICUSt. David’s South Austin Medical CenterAustin, TX, USA
Peter Bendix, MDDepartment of SurgerySection of Trauma and Acute Care SurgeryUniversity of Chicago MedicineChicago, IL, USA
Ali Salim, MDProfessor of SurgeryHarvard Medical SchoolDivision Chief of Trauma, Burns and Surgical Critical CareBrigham and Women’s HospitalBoston, MA, USA
LTC Joseph J. DuBose, MDAssociate Professor of Surgery, Uniformed ServicesUniversity of the Health SciencesAssociate Professor of Surgery, University of MarylandR Adams Cowley Shock Trauma CenterUniversity of Maryland Medical System,Baltimore, MD, USA
Erin Palm, MDDivision of Trauma and Critical CareLAC + USC Medical Center, University of Southern CaliforniaLos Angeles, CA, USA
Jorge Con, MDDirector Trauma, eHealth and International Research FellowshipWestchester Medical CenterValhalla, NY, USA
Emily Cantrell, MDTrauma and Acute Care Surgery FellowDivision of Trauma, Surgical Critical Care, Burns and Acute Care SurgeryUCSD Medical CenterSan Diego, CA, USA
Amelia Simpson, MDTrauma and Acute Care Surgery FellowDivision of Trauma, Surgical Critical Care, Burns and Acute Care SurgeryUCSD Medical CenterSan Diego, CA, USA
Michelle G. Hamel, MDTrauma and Acute Care Surgery FellowDivision of Trauma, Surgical Critical Care, Burns and Acute Care SurgeryUCSD Medical CenterSan Diego, CA, USA
Amy V. Gore, MDResident In SurgeryRutgers New Jersey Medical SchoolNewark, NJ, USA
Ashley McCusker, MDAcute Care Surgery FellowBanner University Medical CenterTucson, AZ, USA
Terence O’Keeffe, MB, ChB, MSPHProfessor, Surgery Division Chief, Trauma, Critical Care,Burn and Emergency Surgery Chief of Staff,Banner University Medical CenterTucson, AZ, USA
Gerard J. Fulda, MDAssociate Professor, Department of SurgeryJefferson Medical College, Philadelphia, PA, USChairman Department of SurgeryPhysician Leader Surgical Service LineChristiana Care Health Systems, Newark, DE, USA
About the Companion Website
This book is accompanied by a companion website:
www.wiley.com/go/moore/surgical_criticalcare_and_emergency_surgery
The website features:
MCQs
Part OneSurgical Critical Care
1Respiratory and Cardiovascular Physiology
Marcin Jankowski, DO and Frederick Giberson, MD
All of the following are mechanisms by which vasodilators improve cardiac function in acute decompensated left heart failure except:
Increase stroke volume
Decrease ventricular filling pressure
Increase ventricular preload
Decrease end‐diastolic volume
Decrease ventricular afterload
Most patients with acute heart failure present with increased left‐ventricular filling pressure, high systemic vascular resistance, high or normal blood pressure, and low cardiac output. These physiologic changes increase myocardial oxygen demand and decrease the pressure gradient for myocardial perfusion resulting in ischemia. Therapy with vasodilators in the acute setting can often improve hemodynamics and symptoms.
Nitroglycerine is a powerful venodilator with mild vasodilatory effects. It relieves pulmonary congestion through direct venodilation, reducing left and right ventricular filling pressures, systemic vascular resistance, wall stress, and myocardial oxygen consumption. Cardiac output usually increases due to decreased LV wall stress, decreased afterload, and improvement in myocardial ischemia. The development of “tachyphylaxis” or tolerance within 16–24 hours of starting the infusion is a potential drawback of nitroglycerine.
Nitroprusside is an equal arteriolar and venous tone reducer, lowering both systemic and vascular resistance and left and right filling pressures. Its effects on reducing afterload increase stroke volume in heart failure. Potential complications of nitroprusside include cyanide toxicity and the risk of “coronary steal syndrome.”
In patients with acute heart failure, therapeutic reduction of left‐ventricular filling pressure with any of the above agents correlates with improved outcome.
Increased ventricular preload would increase the filling pressure, causing further increases in wall stress and myocardial oxygen consumption, leading to ischemia.
Answer: C
Marino, P. (2014)
The
ICU
Book
, 4th edn, Lippincott Williams & Wilkins, Philadelphia, PA,
chapter 13
.
Mehra, M.R. (2015) Heart failure: management, in
Harrison’s Principles of Internal Medicine
, 19th edn (eds D. Kasper, A. Fauci, S. Hauser,
et al.
), McGraw‐Hill, New York.
Which factor is most influential in optimizing the rate of volume resuscitation through venous access catheters?
Laminar flow
Length
Viscosity
Radius
Pressure gradient
The forces that determine flow are derived from observations on ideal hydraulic circuits that are rigid and the flow is steady and laminar. The Hagen‐Poiseuille equation states that flow is determined by the fourth power of the inner radius of the tube (Q = Δp πr4/ 8µL ), where P is pressure, μ is viscosity, L is length, and r is radius. This means that a two‐fold increase in the radius of a catheter will result in a sixteen‐fold increase in flow. As the equation states, the remaining components of resistance, such as pressure difference along the length of the tube and fluid viscosity, are inversely related and exert a much smaller influence on flow. Therefore, cannulation of large central veins with long catheters are much less effective than cannulation of peripheral veins with a short catheter. This illustrates that it is the size of the catheter and not the vein that determines the rate of volume infusion (see Figure 1.1).
Figure 1.1 The influence of catheter dimensions on the gravity‐driven infusion of water.
Answer: D
Marino, P. (2014)
The
ICU
Book
, 4th edn, Lippincott Williams & Wilkins, Philadelphia, PA,
chapter 12
.
Choose the correct physiologic process represented by each of the cardiac pressure‐volume loops in
Figure 1.2
.
Figure 1.2
Increased preload, increased stroke volume,
Increased afterload, decreased stroke volume
Decreased preload, increased stroke volume,
Decreased afterload, increased stroke volume
Increased preload, decreased stroke volume,
Decreased afterload, increased stroke volume
Decreased preload, decreased stroke volume,
Increased afterload, decreased stroke volume
Decreased preload, increased stroke volume,
Increased afterload, decreased stroke volume
One of the most important factors in determining stroke volume is the extent of cardiac filling during diastole or the end‐diastolic volume. This concept is known as the Frank–Starling law of the heart. This law states that, with all other factors equal, the stroke volume will increase as the end‐diastolic volume increases. In Figure 1.2A, the ventricular preload or end‐diastolic volume (LV volume) is increased, which ultimately increases stroke volume defined by the area under the curve. Notice the LV pressure is not affected. Increased afterload, at constant preload, will have a negative impact on stroke volume. In Figure 1.2B, the ventricular afterload (LV pressure) is increased, which results in a decreased stroke volume, again defined by the area under the curve.
Answer: A
Mohrman, D. and Heller, L. (2014)
Cardiovascular Physiology
, 8th edn, McGraw‐Hill, New York, chapter 3.
A 68‐year‐old patient is admitted to the SICU following a prolonged exploratory laparotomy and extensive lysis of adhesions for a small bowel obstruction. The patient is currently tachycardic and hypotensive. Identify the most effective way of promoting end‐organ perfusion in this patient.
Increase arterial pressure (total peripheral resistance) with vasoactive agents
Decrease sympathetic drive with heavy sedation
Increase end‐diastolic volume with controlled volume resuscitation
Increase contractility with a positive inotropic agent
Increase end‐systolic volume
This patient is presumed to be in hypovolemic shock as a result of a prolonged operative procedure with inadequate perioperative fluid resuscitation. The insensible losses of an open abdomen for several hours in addition to significant fluid shifts due to the small bowel obstruction can significantly lower intravascular volume. The low urine output is another clue that this patient would benefit from controlled volume resuscitation.
Starting a vasopressor such as norepinephrine would increase the blood pressure but the effects of increased afterload on the heart and the peripheral vasoconstriction leading to ischemia would be detrimental in this patient. Lowering the sympathetic drive with increased sedation will lead to severe hypotension and worsening shock. Increasing contractility with an inotrope in a hypovolemic patient would add great stress to the heart and still provide inadequate perfusion as a result of low preload. An increase in end‐systolic volume would indicate a decreased stroke volume and lower cardiac output and would not promote end‐organ perfusion.
According to the principle of continuity, the stroke output of the heart is the main determinant of circulatory blood flow. The forces that directly affect the flow are preload, afterload and contractility. According to the Frank–Starling principle, in the normal heart diastolic volume is the principal force that governs the strength of ventricular contraction. This promotes adequate cardiac output and good end‐organ perfusion.
Answer: C
Levick, J.R. (2013)
An Introduction to Cardiovascular Physiology
, Butterworth and Co. London.
Which physiologic process is least likely to increase myocardial oxygen consumption?
Increasing inotropic support
A 100% increase in heart rate
Increasing afterload
100% increase in end‐diastolic volume
Increasing blood pressure
Myocardial oxygen consumption (MVO2) is primarily determined by myocyte contraction. Therefore, factors that increase tension generated by the myocytes, the rate of tension development and the number of cycles per unit time will ultimately increase myocardial oxygen consumption. According to the Law of LaPlace, cardiac wall tension is proportional to the product of intraventricular pressure and the ventricular radius.
Since the MVO2 is closely related to wall tension, any changes that generate greater intraventricular pressure from increased afterload or inotropic stimulation will result in increased oxygen consumption. Increasing inotropy will result in increased MVO2 due to the increased rate of tension and the increased magnitude of the tension. Doubling the heart rate will approximately double the MVO2 due to twice the number of tension cycles per minute. Increased afterload will increase MVO2 due to increased wall tension. Increased preload or end‐diastolic volume does not affect MVO2 to the same extent. This is because preload is often expressed as ventricular end‐diastolic volume and is not directly based on the radius. If we assume the ventricle is a sphere, then:
Therefore
Substituting this relationship into the Law of LaPlace
This relationship illustrates that a 100% increase in ventricular volume will result in only a 26% increase in wall tension. In contrast, a 100% increase in ventricular pressure will result in a 100% increase in wall tension. For this reason, wall tension, and therefore MVO2, is far less sensitive to changes in ventricular volume than pressure.
Answer: D
Klabunde, R.E. (2011)
Cardiovascular Physiology Concepts
, 2nd edn. Lippincott, Williams & Wilkins, Philadelphia, PA.
Rhoades, R. and Bell, D.R. (2012)
Medical Physiology: Principles for Clinical Medicine
, 4th edn, Lippincott, Williams & Wilkins, Philadelphia, PA.
A 73‐year‐old obese man with a past medical history significant for diabetes, hypertension, and peripheral vascular disease undergoes an elective right hemicolectomy. While in the PACU, the patient becomes acutely hypotensive and lethargic requiring immediate intubation. What effects do you expect positive pressure ventilation to have on your patient’s cardiac function?
Increased pleural pressure, increased transmural pressure, increased ventricular afterload
Decreased pleural pressure, increased transmural pressure, increased ventricular afterload
Decreased pleural pressure, decreased transmural pressure, decreased ventricular afterload
Increased pleural pressure, decreased transmural pressure, decreased ventricular afterload
Increased pleural pressure, increased transmural pressure, decreased ventricular afterload
This patient has a significant medical history that puts him at high risk of an acute coronary event. Hypotension and decreased mental status clearly indicate the need for immediate intubation. The effects of positive pressure ventilation will have direct effects on this patient’s cardiovascular function. Ventricular afterload is a transmural force so it is directly affected by the pleural pressure on the outer surface of the heart. Positive pleural pressures will enhance ventricular emptying by promoting the inward movement of the ventricular wall during systole. In addition, the increased pleural pressure will decrease transmural pressure and decrease ventricular afterload. In this case, the positive pressure ventilation provides cardiac support by “unloading” the left ventricle resulting in increased stroke volume, cardiac output and ultimately better end‐organ perfusion.
Answer: D
Cairo, J.M. (2016) Extrapulmonary effects of mechanical ventilation, in
Pilbeam’s Mechanical Ventilation. Physiological and Clinical Applications
, 6th edn, Elsevier, St. Louis, MO, pp. 304–314
Following surgical debridement for lower extremity necrotizing fasciitis, a 47‐year‐old man is admitted to the ICU. A Swan‐Ganz catheter was inserted for refractory hypotension. The initial values are CVP
=
5 mm Hg, MAP
=
50 mm Hg, PCWP
=
8 mm Hg, PaO
2
=
60 mm Hg, CO
=
4.5 L/min, SVR
=
450 dynes
·
sec/cm
5
, and O
2
saturation of 93%. The hemoglobin is 8 g/dL. The most effective intervention to maximize perfusion pressure and oxygen delivery would be which of the following?
Titrate the FiO
2
to a SaO
2
> 98%
Transfuse with two units of packed red blood cells
Fluid bolus with 1 L normal saline
Titrate the FiO
2
to a PaO
2
> 80
Start a vasopressor
To maximize the oxygen delivery (DO2) and perfusion pressure to the vital organs, it is important to determine the factors that directly affect it. According to the formula below, oxygen delivery (DO2) is dependent on cardiac output (Q), the hemoglobin level (Hb), and the O2 saturation (SaO2):
This patient is likely septic from his infectious process. In addition, the long operation likely included a significant blood loss and fluid shifts so hypovolemic/hemorrhagic shock is likely contributing to this patient’s hypotension. The low CVP, low wedge pressure indicates a need for volume replacement. The fact that this patient is anemic as a result of significant blood loss means that transfusing this patient would likely benefit his oxygen‐carrying capacity as well as provide volume replacement. Fluid bolus is not inappropriate; however, two units of packed red blood cells would be more appropriate. Titrating the PaO2 would not add any benefit because, according to the above equation, it contributes very little to the overall oxygen delivery. Starting a vasopressor in a hypovolemic patient is inappropriate at this time and should be reserved for continued hypotension after adequate fluid resuscitation. Titrating the FiO2 to a saturation of greater than 98% would not be clinically relevant. Although the patient requires better oxygen‐carrying capacity, this would be better solved with red blood cell replacement.
Answer: B
Marino, P. (2014)
The
ICU
Book
, 4th edn, Lippincott Williams & Wilkins, Philadelphia, PA,
chapter 2
.
To promote adequate alveolar ventilation, decrease shunting, and ultimately improve oxygenation, the addition of positive end‐expiratory pressure (PEEP) in a severely hypoxic patient with ARDS will:
Limit the increase in residual volume (RV)
Limit the decrease in expiratory reserve volume (ERV)
Limit the increase in inspiratory reserve volume (IRV)
Limit the decrease in tidal volume (TV)
Increase pCO
2
Patients with ARDS have a significantly decreased lung compliance, which leads to significant alveolar collapse. This results in decreased surface area for adequate gas exchange and an increased alveolar shunt fraction resulting in hypoventilation and refractory hypoxemia. The minimum volume and pressure of gas necessary to prevent small airway collapse is the critical closing volume (CCV). When CCV exceeds functional residual capacity (FRC), alveolar collapse occurs. The two components of FRC are residual volume (RV) and expiratory reserve volume (ERV).
The role of extrinsic positive end‐expiratory pressure (PEEP) in ARDS is to prevent alveolar collapse, promote further alveolar recruitment, and improve oxygenation by limiting the decrease in FRC and maintaining it above the critical closing volume. Therefore, limiting the decrease in ERV will limit the decrease in FRC and keep it above the CCV thus preventing alveolar collapse.
Limiting an increase in the residual volume would keep the FRC below the CCV and promote alveolar collapse. Positive‐end expiratory pressure has no effect on inspiratory reserve volume (IRV) or tidal volume (TV) and does not increase pCO2.
Answer: B
Rimensberger, P.C. and Bryan, A.C. (1999) Measurement of functional residual capacity in the critically ill. Relevance for the assessment of respiratory mechanics during mechanical ventilation.
Intensive Care Medicine
,
25
(5), 540–542.
Sidebotham, D., McKee, A., Gillham, M., and Levy, J. (2007)
Cardiothoracic Critical Care
, Butterworth‐Heinemann, Philadelphia, PA.
Which of the five mechanical events of the cardiac cycle is described by an initial contraction, increasing ventricular pressure and closing of the AV valves?
Ventricular diastole
Atrial systole
Isovolumic ventricular contraction
Ventricular ejection (systole)
Isovolumic relaxation
The repetitive cellular electrical events resulting in mechanical motions of the heart occur with each beat and make up the cardiac cycle. The mechanical events of the cardiac cycle correlate with ECG waves and occur in five phases described in Figure 1.3.
Ventricular diastole (mid‐diastole): Throughout most of ventricular diastole, the atria and ventricles are relaxed. The AV valves are open, and the ventricles fill passively.
Atrial systole: During atrial systole a small amount of additional blood is pumped into the ventricles.
Isovolumic ventricular contraction: Initial contraction increases ventricular pressure, closing the AV valves. Blood is pressurized during isovolumic ventricular contraction.
Ventricular ejection (systole): The semilunar valves open when ventricular pressures exceed pressures in the aorta and pulmonary artery. Ventricular ejection (systole) of blood follows.
Isovolumic relaxation: The semilunar valves close when the ventricles relax and pressure in the ventricles decreases. The AV valves open when pressure in the ventricles decreases below atrial pressure. Atria fill with blood throughout ventricular systole, allowing rapid ventricular filling at the start of the next diastolic period.
Figure 1.3 The cardiac cycle illustrated.
Answer: C
Kibble, J.D. and Halsey, C.R. (2015) Cardiovascular physiology, in
Medical Physiology: The Big Picture
, McGraw‐Hill, New York, pp. 131–174.
Barrett, K.E., Barman, S.M., Boitano, S., and Brooks, H.L. (2016) The heart as a pump, in
Ganong’s Review of Medical Physiology
(K. E. Barrett, S.M. Barman, S, Boitano, and H.L. Brooks, eds), 25th edn, McGraw‐Hill, New York, pp. 537–553.
A recent post‐op 78‐year‐old man is admitted to the STICU with an acute myocardial infarction and resulting severe hypotension. A STAT ECHO shows decompensating right‐sided heart failure. CVP = 23 cm H
2
0. What is the most appropriate therapeutic intervention at this time?
Volume
Vasodilator therapy
Furosemide
Inodilator therapy
Mechanical cardiac support
The mainstay therapy of right‐sided heart failure associated with severe hypotension as a result of an acute myocardial infarction is volume infusion. However, it is important to carefully monitor the CVP or PAWP in order to avoid worsening right heart failure resulting in left‐sided heart failure as a result of interventricular interdependence. A mechanism where right‐sided volume overload leads to septal deviation and compromised left ventricular filling. An elevated CVP or PAWP of > 15 should be utilized as an endpoint of volume infusion in right heart failure. At this point, inodilator therapy with dobutamine or levosimendan should be initiated. Additional volume infusion would only lead to further hemodynamic instability and potential collapse. Vasodilator therapy should only be used in normotensive heart failure due to its risk for hypotension. Diuretics should only be used in normo‐ or hypertensive heart failure patients. Mechanical cardiac support should only be initiated in patients who are in cardiogenic shock due to left‐sided heart failure.
Acute decompensated heart failure (ADHF) can present in many different ways and require different therapeutic strategies. This patient represents the “low output” phenotype that is often associated with hypoperfusion and end‐organ dysfunction. See Figure 1.4.
Figure 1.4
Answer: D
Mehra, M.R. (2015) Heart failure: management, in
Harrison’s Principles of Internal Medicine
, 19th edn (D. Kasper, A. Fauci, S. Hauser,
et al.
, eds), McGraw‐Hill, New York, chapter 280.
The right atrial tracing in
Figure 1.5
is consistent with:
Figure 1.5
Tricuspid stenosis
Normal right atrial waveform tracing
Tricuspid regurgitation
Constrictive pericarditis
Mitral stenosis
The normal jugular venous pulse contains three positive waves (Figure 1.6). These positive deflections, labeled “a,” “c,” and “v” occur, respectively, before the carotid upstroke and just after the P wave of the ECG (a wave); simultaneous with the upstroke of the carotid pulse (c wave); and during ventricular systole until the tricuspid valve opens (v wave). The “a” wave is generated by atrial contraction, which actively fills the right ventricle in end‐diastole. The “c” wave is caused either by transmission of the carotid arterial impulse through the external and internal jugular veins or by the bulging of the tricuspid valve into the right atrium in early systole. The “v” wave reflects the passive increase in pressure and volume of the right atrium as it fills in late systole and early diastole.
Figure 1.6
Normally the crests of the “a” and “v” waves are approximately equal in amplitude. The descents or troughs of the jugular venous pulse occur between the “a” and “c” wave (“x” descent), between the “c” and “v” wave (“x ” descent), and between the “v” and “a” wave (“y ” descent). The x and x′ descents reflect movement of the lower portion of the right atrium toward the right ventricle during the final phases of ventricular systole. The y descent represents the abrupt termination of the downstroke of the v wave during early diastole after the tricuspid valve opens and the right ventricle begins to fill passively. Normally the y descent is neither as brisk nor as deep as the x descent.
Answer: C
Hall, J.B., Schmidt, G.A., and Wood, L.D.H. (eds) (2005)
Principles of Critical Care
, 3rd edn, McGraw‐Hill, New York.
McGee, S. (2007)
Evidence‐based Physical Diagnosis
, 2nd edn, W. B. Saunders & Co., Philadelphia, PA.
Pinsky, L.E. and Wipf, J.E. (n.d.) University of Washington Department of Medicine
. Advanced Physical Diagnosis. Learning and Teaching at the Bedside.
Edition 1,
http://depts.washington.edu/physdx/neck/index.html
(accessed November 6, 2011).
The addition of PEEP in optimizing ventilatory support in patients with ARDS does all of the following except:
Increases functional residual capacity (FRC) above the alveolar closing pressure
Maximizes inspiratory alveolar recruitment
Limits ventilation below the lower inflection point to minimize shear‐force injury
Improves V/Q mismatch
Increases the mean airway pressure
The addition of positive‐end expiratory pressure (PEEP) in patients who have ARDS has been shown to be beneficial. By maintaining a small positive pressure at the end of expiration, considerable improvement in the arterial PaO2 can be obtained. The addition of PEEP maintains the functional residual capacity (FRC) above the critical closing volume (CCV) of the alveoli, thus preventing alveolar collapse. It also limits ventilation below the lower inflection point minimizing shear force injury to the alveoli. The prevention of alveolar collapse results in improved V/Q mismatch, decreased shunting, and improved gas exchange. The addition of PEEP in ARDS also allows for lower FiO2 to be used in maintaining adequate oxygenation.
PEEP maximizes the expiratory alveolar recruitment; it has no effect on the inspiratory portion of ventilatory support.
Answer: B
Gattinoni, L,, Cairon, M., Cressoni, M.,
et al.
(2006) Lung recruitement in patients with acute respiratory distress syndrome.
New England Journal of Medicine
354
, 1775–1786.
West, B. (2008)
Pulmonary Pathophysiology – The Essentials
, 8th edn, Lippincott, Williams & Wilkins, Philadelphia, PA.
A 70‐year‐old man with a history of diabetes, hypertension, coronary artery disease, asthma and long‐standing cigarette smoking undergoes an emergency laparotomy and Graham patch for a perforated duodenal ulcer. Following the procedure, he develops acute respiratory distress and oxygen saturation of 88%. Blood gas analysis reveals the following:
pH
=
7.43
paO
2
=
55 mm Hg
HCO
3
=
23 mmol/L
pCO
2
=
35 mm Hg
Based on the above results, you would calculate his A‐a gradient to be (assuming atmospheric pressure at sea level, water vapor pressure = 47 mm Hg):
8 mm Hg
15 mm Hg
30 mm Hg
51 mm Hg
61 mm Hg
The A‐a gradient is equal to PAO2 – PaO2 (55 from ABG). The PAO2 can be calculated using the following equation:
Therefore, A‐a gradient (PaO2 – PAO2) = 51 mm Hg.
Answer: D
Marino, P. (2007)
The
ICU
Book
, 3rd edn, Lippincott Williams & Wilkins, Philadelphia, PA, chapter 19.
What is the most likely etiology of the patient in question 13’s respiratory failure and the appropriate intervention?
Pulmonary edema, cardiac workup
Neuromuscular weakness, intubation, and reversal of anesthetic
Pulmonary embolism, systemic anticoagulation
Acute asthma exacerbation, bronchodilators
Hypoventilation, pain control
Disorders that cause hypoxemia can be categorized into four groups: hypoventilation, low inspired oxygen, shunting, and V/Q mismatch. Although all of these can potentially present with hypoxemia, calculating the alveolar‐arterial (A‐a) gradient and determining whether administering 100% oxygen is of benefit, can often determine the specific type of hypoxemia and lead to quick and effective treatment.
Acute hypoventilation often presents with an elevated PaCO2 and a normal A‐a gradient. This is usually seen in patients with altered mental status due to excessive sedation, narcotic use, or residual anesthesia. Since this patient’s PaCO2 is low (35 mm Hg), it is not the cause of this patient’s hypoxemia.
Low inspired oxygen presents with a low PO2 and a normal A‐a gradient. Since this patient’s A‐a gradient is elevated, this is unlikely the cause of the hypoxemia.
A V/Q mismatch (pulmonary embolism or acute asthma exacerbation) presents with a normal PaCO2 and an elevated A‐a gradient that does correct with administration of 100% oxygen. Since this patient’s hypoxemia does not improve after being placed on the nonrebreather mask, it is unlikely that this is the cause.
Shunting (pulmonary edema) presents with a normal PaCO2 and an elevated A‐a gradient that does not correct with the administration of 100% oxygen. This patient has a normal PaCO2, an elevated A‐a gradient and hypoxemia that does not correct with the administration of 100% oxygen. This patient has a pulmonary shunt.
Although an A‐a gradient can vary with age and the concentration of inspired oxygen, an A‐a gradient of 51 is clearly elevated. This patient has a normal PaCO2 and an elevated A‐a gradient that did not improve with 100% oxygen administration therefore a shunt is clearly present. Common causes of shunting include pulmonary edema and pneumonia.
Reviewing this patient’s many risk factors for a postoperative myocardial infarction and a decreased left ventricular function makes pulmonary edema the most likely explanation.
Answer: A
Weinberger, S.E., Cockrill, B.A., and Mande, J. (2008)
Principles of Pulmonary Medicine
, 5th edn. W.B. Saunders, Philadelphia, PA.
You are taking care of a morbidly obese patient on a ventilator who is hypotensive and hypoxic. His peak airway pressures and plateau pressures have been slowly rising over the last few days. You decide to place an esophageal balloon catheter. The values are obtained:
What is the likely cause of the increased peak airway pressures and what is your next intervention?
Decreased lung compliance, increase PEEP to 25 cm H
2
O
Decreased lung compliance, high frequency oscillator ventilation
Decreased chest wall compliance, increase PEEP to 25 cm H
2
O
Decreased chest wall compliance, high‐frequency oscillator ventilation
Decreased lung compliance, bronchodilators
The high plateau pressures in this patient are concerning for worsening lung function or poor chest‐wall mechanics due to obesity that don’t allow for proper gas exchange. One way to differentiate the major cause of these elevated plateau pressures is to place an esophageal balloon. After placement, measuring the proper pressures on inspiration and expiration reveals that the largest contributing factor to these high pressures is the weight of the chest wall causing poor chest‐wall compliance. The small change in esophageal pressures, as compared with the larger change in transpulmonary pressures, indicates poor chest‐wall compliance and good lung compliance. It is why the major factor in this patient’s high inspiratory pressures is poor chest‐wall compliance. The patient is hypotensive, so increasing the PEEP would likely result in further drop in blood pressure. This is why high‐frequency oscillator ventilation would likely improve this patient’s hypoxemia without affecting the blood pressure.
Answer: D
Talmor, D., Sarge, T., O’Donnell, C., and Ritz, R. (2006) Esophageal and transpulmonary pressures in acute respiratory failure
.
Critical Care Medicine
,
34
(5), 1389–1394.
Valenza, F., Chevallard, G., Porro, G.A., and Gattinoni, L. (2007) Static and dynamic components of esophageal and central venous pressure during intra‐abdominal hypertension.
Critical Care Medicine
,
35
(6), 1575–1581.
All of the following cardiovascular changes occur in pregnancy except:
Increased cardiac output
Decreased plasma volume
Increased heart rate
Decreased systemic vascular resistance
Increased red blood cell mass – “relative anemia
”
The following cardiovascular changes occur during pregnancy:
Decreased systemic vascular resistance
Increased plasma volume
Increased red blood cell volume
Increased heart rate
Increased ventricular distention
Increased blood pressure
Increased cardiac output
Decreased peripheral vascular resistance
Answer: B
DeCherney, A.H. and Nathan, L. (2007)
Current Diagnosis and Treatment: Obstetrics and Gynecology
, 10th edn, McGraw‐Hill, New York, chapter 7.
Yeomans, E.R. and Gilstrap, L.C., III. (2005) Physiologic changes in pregnancy and their impact on critical care.
Critical Care Medicine
,
33
, 256–258.
Choose the incorrect statement regarding the physiology of the intra‐aortic balloon pump:
Shortened intraventricular contraction phase leads to increased oxygen demand
The tip of catheter should be between the second and third rib on a chest x‐ray
Early inflation leads to increased afterload and decreased cardiac output
Early or late deflation leads to a smaller afterload reduction
Aortic valve insufficiency is a definite contra‐indication
Patients who suffer hemodynamic compromise despite medical therapies may benefit from mechanical cardiac support of an intra‐aortic balloon pump (IABP). One of the benefits of this device is the decreased oxygen demand of the myocardium as a result of the shortened intraventricular contraction phase. It is of great importance to confirm the proper placement of the balloon catheter with a chest x‐ray that shows the tip of the balloon catheter to be 1 to 2 cm below the aortic knob or between the second and third rib. If the balloon is placed too proximal in the aorta, occlusion of the brachiocephalic, left carotid, or left subclavian arteries may occur. If the balloon is too distal, obstruction of the celiac, superior mesenteric, and inferior mesenteric arteries may lead to mesenteric ischemia. The renal arteries may also be occluded, resulting in renal failure.
Additional complications of intra‐aortic balloon‐pump placement include limb ischemia, aortic dissection, neurologic complications, thrombocytopenia, bleeding, and infection.
The inflation of the balloon catheter should occur at the onset of diastole. This results in increased diastolic pressures that promote perfusion of the myocardium as well as distal organs. If inflation occurs too early it will lead to increased afterload and decreased cardiac output. Deflation should occur at the onset of systole. Early or late deflation will diminish the effects of afterload reduction. One of the definite contraindications to placement of an IABP is the presence of a hemodynamically significant aortic valve insufficiency. This would exacerbate the magnitude of the aortic regurgitation.
Answer: A
Ferguson, J.J., Cohen, M., Freedman, R.J.,
et al.
(2001) The current practice of intra‐aortic balloon counterpulsation: results from the Benchmark Registry.
Journal of American Cardiology
,
38
, 1456–1462.
Hurwitz, L.M. and Goodman, P.C. (2005) Intraaortic balloon pump location and aortic dissection.
American Journal of Roentgenology
,
184
, 1245–1246.
Sidebotham, D., McKee, A., Gillham, M., and Levy, J. (2007)
Cardiothoracic Critical Care
, Butterworth‐Heinemann, Philadelphia, PA.
Choose the
incorrect
statement regarding the West lung zones:
Zone 1 does not exist under normal physiologic conditions
In hypovolemic states, zone 1 is converted to zone 2 and zone 3
V/Q ratio is higher in zone 1 than in zone 3
Artificial ventilation with excessive PEEP can increase dead space ventilation
Perfusion and ventilation are better in the bases than the apices of the lungs
The three West zones of the lung divide the lung into three regions based on the relationship between alveolar pressure (PA), pulmonary arterial pressure (Pa) and pulmonary venous pressure (Pv).
Zone 1 represents alveolar dead space and is due to arterial collapse secondary to increased alveolar pressures (PA > Pa > Pv).
Zone 2 is approximately 3 cm above the heart and represents and represents a zone of pulsatile perfusion (Pa > PA > Pv).
Zone 3 represents the majority of healthy lungs where no external resistance to blood flow exists promoting continuous perfusion of ventilated lungs (Pa > Pv > PA).
Zone 1 does not exist under normal physiologic conditions because pulmonary arterial pressure is higher than alveolar pressure in all parts of the lung. However, when a patient is placed on mechanical ventilation (positive pressure ventilation with PEEP) the alveolar pressure (PA) becomes greater than the pulmonary arterial pressure (Pa) and pulmonary venous pressure (Pv). This represents a conversion of zone 3 to zone 1 and 2 and marks an increase in alveolar dead space. In a hypovolemic state, the pulmonary arterial and venous pressures fall below the alveolar pressures representing a similar conversion of zone 3 to zone 1 and 2. Both perfusion and ventilation are better at the bases than the apices. However, perfusion is better at the bases and ventilation is better at the apices due to gravitational forces.
Answer: B
Lumb, A. (2000)
Nunn’s Applied Respiratory Physiology
, 5 edn, Butterworth‐Heinemann, Oxford.
West, J., Dollery, C., and Naimark, A. (1964) Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures.
Journal of Applied Physiology
,
19
, 713–724.
Choose the correct statement regarding clinical implications of cardiopulmonary interactions during mechanical ventilation:
The decreased trans‐pulmonary pressure and decreased systemic filling pressure is responsible for decreased venous return
Right ventricular end‐diastolic volume is increased due to increased airway pressure and decreased venous return
The difference between trans‐pulmonary and systemic filling pressures is the gradient for venous return
Patients with severe left ventricular dysfunction may have decreased transmural aortic pressure resulting in decreased cardiac output
Patients with decreased PCWP usually improve with additional PEEP
The increased trans‐pulmonary pressure and decreased systemic filling pressure is responsible for decreased venous return to the heart resulting in hypotension. This phenomenon is more pronounced in hypovolemic patients and may worsen hypotension in patients with low PCWP.
Right ventricular end‐diastolic volume is decreased due to the increased transpulmonary pressure and decreased venous return.
Patients with severe left ventricular dysfunction may have decreased transmural aortic pressure resulting in increased
