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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Foreword
- •Foreword
- •Contents of Volume I
- •Contents of Volume II
- •Contributors
- •1.1 Introduction
- •1.4.3 Acute Stroke
- •1.4.4 CNS Infection
- •1.4.1 Sepsis
- •1.4.2 Acute Encephalopathy
- •1.4.5 Severe Community-Acquired Pneumonia
- •1.4.6 Nosocomial Pneumonia
- •1.4.7 Pulmonary Edema
- •1.4.8 Fever
- •References
- •2.1 Introduction
- •2.4 ECG Nomenclature
- •2.4.1 P Wave
- •2.4.2 PR Interval
- •2.4.3 QRS Complex
- •2.4.4 J Point
- •2.4.5 ST Segment
- •2.4.6 T Wave
- •2.4.7 QT Interval
- •2.4.8 U Wave
- •2.4.9 RR Interval
- •2.5.1 P Wave
- •2.5.1.1 Atrial Arrhythmias
- •Atrial Fibrillation
- •Atrial Flutter
- •Atrial Tachycardia
- •Multifocal Atrial Tachycardia
- •2.5.1.2 Interatrial Blocks
- •Intermittent Interatrial Block (I-IAB)
- •Advanced Interatrial Block (A-IAB)
- •2.5.2 P-QRS Ratio
- •2.5.2.1 Shortened P-QRS Ratio
- •Wolff-Parkinson-White Syndrome (WPW)
- •Junctional Rhythm
- •Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
- •2.5.2.3 Prolonged P-QRS Ratio
- •2.5.3 PR Interval
- •2.5.3.1 Shortened PR Interval
- •2.5.3.2 Prolonged PR Interval
- •2.5.3.3 Second-Degree AV Block
- •Advanced AV Block
- •Third-Degree AV Block (Complete Heart Block)
- •2.5.4 PR Segment
- •2.5.4.1 PR-Segment Elevation
- •2.5.4.2 PR-Segment Depression
- •Acute Pericarditis
- •Acute Myocardial Ischemia
- •2.5.5 Q Waves
- •2.5.6 QRS Complex
- •2.5.6.1 Heart Rate
- •2.5.7 QT Interval
- •2.5.8 ST Segment
- •2.5.8.1 ST-Segment Depression
- •2.5.8.2 ST-Segment Elevation
- •2.5.9 T Waves
- •2.5.9.1 Inverted T Wave
- •2.5.9.2 Flattened T Wave
- •2.5.9.3 Peaked T Wave
- •References
- •Further Reading
- •3.1 Introduction
- •3.2.2 Nasogastric Tube
- •3.2.3 Central Venous Catheters
- •3.2.4 Cardiac Devices
- •3.2.5 Arterial Catheters
- •3.3 Cardiopulmonary Abnormalities
- •3.3.1 Pulmonary Edema
- •3.3.2 Acute Respiratory Distress Syndrome
- •3.3.3 Atelectasis
- •3.3.4 Aspiration
- •3.3.5 Pneumonia
- •References
- •4.1 Introduction
- •4.5 Modes of Mechanical Ventilation
- •4.5.1 Volume Control Ventilation
- •4.5.2 Pressure Control Ventilation
- •4.5.3 Pressure Support Ventilation
- •4.6 Patient-Ventilator Interactions
- •4.6.1 Trigger Dyssynchrony
- •4.6.2 Flow Dyssynchrony
- •4.6.3 Cycle Dyssynchrony
- •4.9.1 Acute Respiratory Distress Syndrome
- •4.9.2 Severe Asthma Exacerbation
- •4.11 Summary
- •5.10 Neuromuscular Blockade
- •References
- •5.1 Introduction
- •5.3 Pathobiology
- •5.4 ARDS Phenotypes
- •5.5 Lung-Protective Ventilation
- •5.6 Positive End-Expiratory Pressure
- •5.7 Conservative Fluid Management
- •5.8 Moderate-to-Severe ARDS
- •5.9 Prone Positioning
- •5.11 Corticosteroids
- •5.12 Inhaled Pulmonary Vasodilators
- •5.13 Veno-Venous Extracorporeal Membrane Oxygenation
- •5.14 Survivorship
- •References
- •6.1 Introduction/Epidemiology
- •6.2 Physiology
- •6.2.2 Physiology During COPD Exacerbation
- •6.4 Pharmacologic Treatment
- •6.4.1 Bronchodilators
- •6.4.1.1 Mechanism
- •6.4.2 Glucocorticoid Therapy
- •6.4.2.1 Mechanism
- •6.4.2.4 Duration
- •6.4.3 Antimicrobials
- •6.4.3.1 Antibiotic Patient Selection
- •6.4.4.1 Nonpharmacologic Interventions
- •6.4.4.2 Opioids
- •6.4.4.3 Benzodiazepines
- •6.4.4.4 Dexmedetomidine
- •6.4.4.5 Ketamine
- •6.4.5 Adjunctive Therapies
- •6.4.5.1 Magnesium
- •6.4.5.3 Vitamin D
- •6.4.5.4 Venous Thromboembolism Prophylaxis
- •6.4.5.5 Smoking Cessation
- •6.4.5.6 Bowel Regimen
- •6.4.5.7 Mucolytics
- •6.4.5.8 Nutrition
- •6.4.5.9 Post-Discharge Adjuncts
- •6.5 ICU-Level Interventions
- •6.5.1 Noninvasive Positive-Pressure Ventilation
- •6.5.2 High-Flow Nasal Canula
- •6.5.3 Invasive Mechanical Ventilation
- •6.6 Conclusion
- •References
- •7.1 Introduction
- •7.1.1 What Is Asthma?
- •7.2 Diagnosis
- •7.2.1 Physical Examination
- •7.2.2 Laboratory Data
- •7.2.3 Radiographic Findings
- •7.3.1 Standard-of-Care Therapy
- •7.3.3 Potential Adjunctive Therapies
- •7.3.3.1 Inhaled Corticosteroids (ICSs)
- •7.3.3.4 Intravenous (IV) Aminophylline
- •7.3.3.5 Intravenous (IV) Beta2-Agonists
- •7.3.3.6 Leukotriene Antagonists (LTRAs)
- •7.3.3.7 Intramuscular (IM) or IV Epinephrine
- •7.3.3.8 Inhaled Anesthetics
- •7.3.3.9 Inhaled Helium-Oxygen (Heliox)
- •7.3.3.10 Intravenous Ketamine
- •7.3.4.1 Subcutaneous (SC) Biologics
- •7.4.1 Noninvasive Ventilation (NIV)
- •7.4.2 Invasive Mechanical Ventilation (IMV)
- •7.6.1 Outpatient Follow-Up
- •7.7 Summary
- •References
- •8.1 Introduction
- •8.1.3.2 Anatomic Location
- •8.1.3.3 Chronicity
- •8.1.4 Clinical Presentation
- •8.1.4.1 Symptoms
- •8.1.4.2 Physician Examination
- •8.1.4.3 Cardiopulmonary Compromise
- •8.2.1.1 Clinical Pretest/Scores
- •8.2.1.2 D-Dimer-Level Interpretations
- •8.2.2 Computed Tomography Pulmonary Angiography (CTPA)
- •8.2.3 Mortality Risk Assessment
- •8.2.3.1 PE Severity Index Score
- •8.2.3.2 Prognostic Indicators
- •8.3.2 High-Risk PE
- •8.4 Systemic Thrombolytic Therapy
- •8.4.1.1 High-Risk PE
- •8.4.1.2 Intermediate-Risk PE
- •8.4.1.3 Cardiac Arrest
- •8.5.2 Percutaneous Mechanical Interventions
- •8.5.2.2 Catheter-Directed Thrombolysis
- •8.5.3 Surgical Embolectomy
- •8.5.4 Mechanical Circulatory Support
- •8.6.1 PE Response Team (PERT)
- •8.6.3.1 Renal Dysfunction
- •8.6.3.4 Cancer
- •8.6.3.5 Treatment Failure
- •8.7 Conclusion
- •References
- •9.1.2 ECMO Outcomes
- •9.2 ECMO During Cardiopulmonary Resuscitation (eCPR)
- •9.2.1 Extracorporeal Carbon Dioxide Removal
- •9.3 ECMO Management
- •9.3.3 Fluid Management
- •9.4.1 Coagulation Changes
- •9.4.2 Transfusion Thresholds
- •9.4.3.1 Heparin
- •9.4.3.2 Direct Thrombin Inhibitors
- •9.4.4 Monitoring Anticoagulation
- •9.6.2.1 Opioids
- •9.6.2.2 Ketamine
- •9.6.2.3 Propofol
- •9.6.2.4 Benzodiazepines
- •9.6.2.5 Dexmedetomidine
- •9.7.1 Aminoglycosides
- •9.7.2 Beta-Lactams
- •9.7.4 Antifungals
- •9.9 Other Complications
- •9.9.1 Bleeding
- •9.9.2 Thrombosis
- •9.9.3 Neurologic
- •9.10 Conclusion
- •References
- •10.1 Type 1–5 Myocardial Infarctions
- •10.2 Acute Coronary Syndrome (Type 1 MI)
- •10.3 Clinical Presentation/Evaluation
- •10.4 Non-pharmacologic Therapy
- •10.5 Pharmacologic Therapy
- •10.5.1 Fibrinolytics
- •10.5.2 Anticoagulants
- •10.5.2.1 Heparins
- •10.5.2.2 Direct Thrombin Inhibitors
- •10.5.3 Antiplatelets
- •10.5.3.1 Aspirin
- •10.5.3.2 P2Y12 Inhibitors
- •Clopidogrel
- •Prasugrel
- •Ticagrelor
- •10.5.3.3 Glycoprotein IIb/IIIa Receptor Inhibitors
- •10.5.3.4 Cangrelor
- •10.7 Long-Term Management
- •10.7.1 High Bleed Risk (HBR)
- •10.7.2 Statins
- •10.7.3 Beta-Blockers
- •10.7.5 Mineralocorticoid Receptor Antagonists
- •References
- •11.1 Introduction
- •11.2.2 What is Ejection Fraction?
- •11.4 Understanding Blood Pressure
- •11.5 Preload vs. Afterload
- •11.6 Acute Decompensated Heart Failure
- •11.6.2 Etiology
- •11.8 Treating Volume Overload
- •11.8.1 Loop Diuretics
- •11.9 Intravenous Vasodilators
- •11.10 Cardiogenic Shock
- •11.10.1 Inotrope Clinical Pearl
- •11.12 Digoxin
- •11.12.3 Loading Dose
- •11.12.4 Maintenance Dosing
- •11.12.5 Monitoring
- •11.12.7 Distribution
- •11.12.8 Drug-Drug Interactions
- •11.12.9 Digoxin Toxicity
- •11.13 ADHF Clinical Pearls
- •11.13.3 Avoid Phenylephrine
- •11.13.4 Use Mean Arterial Pressure (MAP)
- •11.14 Guideline-Directed Medical Therapy
- •11.15 Venous Thromboembolism (VTE) Prophylaxis
- •11.16 Conclusion
- •References
- •12.1 Introduction
- •12.3 Diagnostic Findings
- •12.4.1 Oxygen Therapy
- •12.4.2 Pharmacological Management
- •12.4.3 Mechanical Circulatory Support (MCS)
- •12.5 Pulmonary Hypertension
- •12.6 The Pharmacist’s Role
- •12.7 Conclusion
- •References
- •13.1 Introduction
- •13.2 Atrial Arrhythmias
- •13.2.2 Atrioventricular Blocks
- •13.2.3 Atrial Fibrillation
- •13.2.3.2 Anticoagulation
- •13.2.3.3 Rate vs. Rhythm Control
- •13.2.4 Atrial Flutter
- •13.2.5 Supraventricular Tachycardia (SVT)
- •13.3 Ventricular Arrhythmias
- •13.3.1 Premature Ventricular Complexes
- •13.3.2 Ventricular Tachycardia
- •13.3.2.1 Torsades de Pointes
- •13.3.3 Ventricular Fibrillation
- •13.3.4 Ventricular Arrhythmia Treatment Strategies
- •13.3.4.1 ICD Implantation
- •13.3.4.2 Pharmacologic Treatments
- •13.3.4.3 Catheter Ablation
- •13.4 Conclusion
- •References
- •14.1 Introduction
- •14.3.2 Laboratory Assessment
- •14.3.3 Imaging
- •14.3.4 Invasive Hemodynamic Monitoring
- •14.4.1 Distributive
- •14.4.2 Cardiogenic
- •14.4.3 Hypovolemic
- •14.4.4 Obstructive
- •14.5 Management
- •14.6 Conclusion
- •References
- •15.1 Background
- •15.2 Diagnosis
- •15.3 Management
- •References
- •16.1 Introduction
- •16.3 Hemodynamics
- •16.5 Pharmacological Management
- •16.5.1 Hyperosmolar Therapy
- •16.5.3 Barbiturate Coma
- •16.6 Nonpharmacological Treatments
- •16.6.2 Temperature Management
- •16.6.3 Prophylactic Hypothermia
- •16.7 Adjunct Therapies
- •16.7.2 Venous Thromboembolism (VTE) Prophylaxis
- •16.7.3 Antibiotic Prophylaxis
- •16.7.4 Stress Ulcer Prophylaxis (SUP)
- •16.7.5 Tranexamic Acid
- •16.7.6 Glucose Targets
- •16.7.7 Steroids
- •16.8 Complications
- •16.8.1 Paroxysmal Sympathetic Hyperactivity
- •16.8.3 Central Fever
- •16.8.4.1 Diabetes Insipidus
- •16.8.4.3 Cerebral Salt Wasting Syndrome
- •16.9 Conclusion
- •References
- •17.1 Introductory Case
- •17.2 Introduction
- •17.4 Pathophysiology
- •17.5 Acute Therapies
- •17.5.1 Thrombolytic Therapy
- •17.5.2 Thrombectomy
- •17.5.3 Blood Pressure Management
- •17.5.4 Acute Anticoagulation
- •17.5.5 Antiplatelet Therapy
- •17.6 Early Complications
- •17.6.1 Hemorrhagic Conversion
- •17.6.2 Angioedema
- •17.6.3 Malignant Cerebral Edema
- •17.7 Secondary Prevention
- •References
- •18.1 Introduction
- •18.4 Therapeutic Drug Monitoring
- •18.5 Adverse Drug Effects
- •18.7 Anti-seizure Medications
- •18.7.1 Available Parenteral Preparations
- •18.7.1.1 Benzodiazepines: GABAA Receptor Activation
- •18.7.1.2 Other GABAergic Therapies
- •Barbiturates: GABAergic
- •Phenobarbital
- •Pentobarbital Infusion
- •Propofol Infusion: GABAergic
- •18.7.1.3 Second-Line Non-anesthetic ASMs
- •Levetiracetam: Synaptic Vesicle Protein 2A Binding

Contributors
xxiii
Emaad J. Iqbal New York-Presbyterian Hospital, Columbia University Irving
Medical Center, New York, NY, USA
ChristineS.Ji Department of Pharmacy, Beth Israel Deaconess Medical Center,
Boston, MA, USA
HeatherJohnson University of Pittsburgh Medical Center, Pittsburgh, PA, USA
University of Pittsburgh, Pittsburgh, PA, USA
Lesly V. Jurado Hernández
Department of Pharmacy, Novant Health New
Hanover Regional Medical Center, Wilmington, NC, USA
AdaSelinaJutba, PharmD, BCCCP Department of Pharmacy, Memorial Hermann Memorial City Medical Center, Houston, TX, USA
NidhiKataria Department of Laboratory Medicine and Pathology, Mayo Clinic,
Rochester, MN, USA
MichaelT.Kenes Michigan Medicine, Ann Arbor, MI, USA
College of Pharmacy, University of Michigan, Ann Arbor, MI, USA
SoyoungKristi Kim Clinical Pharmacy Specialist, Critical Care, Department of
Pharmacy, Cooper University Health Care, Camden, NJ, USA
BryanD.Kraft Division of Pulmonary, Allergy, and Critical Care Medicine, Duke
University School of Medicine, Durham, NC, USA
Division of Pulmonary and Critical Care Medicine, Washington University School
of Medicine, Saint Louis, MO, USA
JustinKreuter Department of Laboratory Medicine and Pathology, Mayo Clinic,
Rochester, MN, USA
CaitlinE.Kulig Ernest Mario School of Pharmacy, Rutgers the State University of
New Jersey, Piscataway New Jersey and St. Joseph’s University Medical Center,
Paterson, NJ, USA
GiovannaLandi Department of Cardio-Thoracic Surgery, Maastricht University
Medical Centre (MUMNC+), Maastricht, The Netherlands
GraceLee Los Angeles Medical Center, Kaiser Permanente, Los Angeles, CA, USA
Steven M. Lemieux Veterans Administration Connecticut Healthcare System,
West Haven, CT, USA
FannyLi Departments of Clinical Pharmacy and Pharmaceutical Services, Uni-
versity of California, San Francisco Health, San Francisco, CA, USA
DustyLisi Heart Failure, Emory Saint Joseph’s Hospital, Atlanta, GA, USA

xxiv
Contributors
Natasha D. Lopez Department of Pharmacy, Massachusetts General Hospital,
Boston, MA, USA
Uvette Lou Department of Pharmacy, Massachusetts General Hospital, Bos-
ton, MA, USA
SamanthaLuk Department of Pharmacy, Massachusetts General Hospital, Bos-
ton, MA, USA
FabioMacori
Ospedale Santo Spirito Rome, Rome, RM, Italy
KristinMadenci Brigham and Women’s Hospital, Harvard Medical School, Bos-
ton, MA, USA
AhmedA.Mahmoud Houston Methodist Hospital, Houston, TX, USA
Manu L. N. G. Malbrain First Department of Anaesthesiology and Intensive
Therapy, Medical University Lublin, Lublin, Poland
Medical Data Management, Medaman, Geel, Belgium
International Fluid Academy, Lovenjoel, Belgium
MaricarMalinis Section of Infectious Diseases, Yale University School of Medi-
cine, New Haven, CT, USA
Patrick Mazi Washington University in St. Louis, Barnes Jewish Hospital, St.
Louis, MO, USA
Sharon L. McCartney Department of Anesthesiology, Pain, and Perioperative
Medicine, University of Kansas, Kansas City, USA
LauraC. McNamara Department of Medicine, Beth Israel Deaconess Medical
Center, Boston, MA, USA
SachinMehta Department of Anesthesiology, Pain, and Perioperative Medicine,
University of Kansas, Kansas City, USA
AndresF.Miranda-Arboleda Brigham and Women’s Hospital, Harvard Medical
School, Boston, MA, USA
AliciaH.Muratore Division of Gastroenterology and Hepatology, Department of
Medicine, UNC Chapel Hill School of Medicine, Chapel Hill, NC, USA
Andrea M. Nei Department of Pharmacy, Mayo Clinic Hospital—Rochester,
Rochester, MN, USA
HavenNisly Department of Medicine, Duke University School of Medicine, Dur-
ham, NC, USA
CavanO’Kane Ernest Mario School of Pharmacy, Rutgers, the State University of
New Jersey, Piscataway, NJ, USA
Penn Medicine Princeton Medical Center, Plainsboro Township, NJ, USA

Contributors
xxv
RobertOlver Department of Intensive Care Medicine, Victorian Heart Hospital,
Monash Health, Clayton, VIC, Australia
Department of Intensive Care Medicine, Monash Medical Centre, Monash Health,
Clayton, VIC, Australia
AlejandroNarváezOrozco University of Antioquia, Medellín, Colombia
Alex Panuccio Los Angeles Medical Center, Kaiser Permanente, Los Ange-
les, CA, USA
MonaK.Patel
Pulmonary, Critical Care & Sleep Medicine, NYU Langone Health,
NYU Grossman School of Medicine, New York, USA
TylerPeck Beth Israel Deaconess Medical Center, Harvard Medical School, Bos-
ton, MA, USA
CamilleR.Petri Division of Pulmonary and Critical Care, Department of Medi-
cine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
Kayla Popova University of Michigan Health—Michigan Medicine, Ann
Arbor, MI, USA
AndrewPosen Department of Pharmacy Practice, University of Illinois Chicago
College of Pharmacy, Chicago, IL, USA
LeandroLuis Pozzer Section of Cardiac Electrophysiology, Buenos Aires Car-
diovascular Institute, Buenos Aires, Argentina
EliasH.Pratt Division of Pulmonary Allergy, and Critical Care Medicine, Duke
University School of Medicine, Durham, NC, USA
MaleriePratt Brigham and Women’s Hospital, Boston, MA, USA
Craig R. Rackley Division of Pulmonary Allergy, and Critical Care Medicine,
Duke University School of Medicine, Durham, NC, USA
Lance Ray Department of Pharmacy, Denver Health Medical Center, Den-
ver, CO, USA
ErinReichert Department of Pharmacy, The Ohio State University, Wexner Med-
ical Center, Columbus, OH, USA
AlyseReichheld Department of Medicine, Beth Israel Deaconess Medical Center,
Boston, MA, USA
Danilo Weir Restrepo Internal Medicine Resident, CES University, Medellín,
Colombia
Adele Robbins Advanced Heart Failure and Transplant, Piedmont Hospital,
Atlanta, GA, USA

xxvi
Contributors
Francisco Machiavello Roman Section of Infectious Diseases, Yale University
School of Medicine, New Haven, CT, USA
Claudio Ronco International Renal research Institute of Vicenza (IRRIV),
Vicenza, Italy
MahmoudM.Sabawi Houston Methodist Hospital, Houston, TX, USA
MehrnazSadrolashra Beth Israel Deaconess Medical Center, Boston, MA, USA
Ruben Santiago
Department of Pharmacy, Jackson Memorial Hospital,
Miami, FL, USA
CinaSasannejad Department of Neurology, Duke University School of Medicine,
Durham, NC, USA
RichardM.Schwartzstein Beth Israel Deaconess Medical Center, Harvard Med-
ical School, Boston, MA, USA
KristineN.Schwietz Department of Pharmacy, Massachusetts General Hospital,
Boston, MA, USA
YahyaShehabi Department of Intensive Care Medicine, Victorian Heart Hospital,
Monash Health, Clayton, VIC, Australia
School of Clinical Sciences, Monash University, Clayton, VIC, Australia
Prince of Wales Clinical School of Medicine, University of New South Wales,
Randwick, Sydney, NSW, Australia
Sheela V. Shenoi Yale University School of Medicine, Veterans Administration
Connecticut Healthcare System, West Haven, CT, USA
Bethany R. Shoulders University of Florida College of Pharmacy, Gaines-
ville, FL, USA
SarahMatuszak Barnes-Jewish Hospital Plaza, St Louis, MO, USA
ChelseySong University of Maryland Medical Center, Baltimore, MD, USA
Andrej Spec Washington University in St. Louis, Barnes Jewish Hospital, St.
Louis, MO, USA
KatherineSpezzano University of Kentucky HealthCare, Lexington, KY, USA
JoannaL.Stollings Department of Pharmaceutical Services, Vanderbilt Univer-
sity Medical Center, Nashville, TN, USA
Critical Illness, Brain Dysfunction, and Survivorship (CIBS) Center, Vanderbilt
University Medical Center, Nashville, TN, USA
DavidSugrue Department of Pharmacy, UW Health, Madison, WI, USA
LaurenSutton Barnes-Jewish Hospital Plaza, St Louis, MO, USA

Contributors
xxvii
PoornimaLakshmiTamma New York-Presbyterian Hospital, Columbia Univer-
sity Irving Medical Center, New York, NY, USA
Erica Tavares Department of Pharmacy, Massachusetts General Hospital, Bos-
ton, MA, USA
FernandaTavares-Da-Silva Drug Safety, Organon BV, Brussels, Belgium
SeemaS.Tekwani Division of Pulmonary, Allergy, Critical Care, and Sleep Med-
icine, Emory University School of Medicine, Atlanta, GA, USA
HaileyA.Thompson
Department of Pharmacy, UW Health, Madison, WI, USA
Beverly Tomita Carle Illinois College of Medicine, University of Illinois,
Urbana, IL, USA
Morgan Trammel Department of Pharmacy, Duke University Hospital,
Durham, USA
MiguelH.Vicco Drug Safety Lead, Organon BV, Brussels, Belgium
SybilE.Watkins Department of Internal Medicine, Vanderbilt University Medical
Center, Nashville, TN, USA
AndrewJ.Webb Massachusetts General Hospital, Boston, MA, USA
DexterWimer Departments of Clinical Pharmacy and Pharmaceutical Services,
University of California, San Francisco Health, San Francisco, CA, USA
AdrianWong Beth Israel Deaconess Medical Center, Boston, MA, USA
NikithaYagnala Department of Pharmacy, Hospital of University of Pennsylva-
nia, Philadelphia, PA, USA
GiacomoZaccherini Department of Medical and Surgical Sciences, Alma Mater
Studiorum—University of Bologna, Bologna, Italy
Alberto Zanella Anestesia e Terapia Intensiva Adulti, Fondazione IRCCS Ca’
Granda—Ospedale Maggiore Policlinico, Milan, Italy
Department of Pathophysiology and Transplantation, University of Milan,
Milan, Italy

Part I
Clinical and Diagnostic Approach

Chapter 1
Approach toClinical Reasoning inCritical
Care
YasirAlzaidi
1.1 Introduction
The diagnostic possibilities entertained in the critical care unit are limited in number versus other noncritical care settings. However, diagnostic errors are common.
A study by Winters etal. identied 28% of autopsies as having at least one misdiagnosis, with potentially lethal misdiagnoses quantied at 6.3% [44]. A more recent
study by Auerbach etal. reported similar ndings, in which 23% of adult patients,
who were transferred to the intensive care unit (ICU) or died in the hospital, had
missed or delayed diagnoses [4]. In addition to being common, the unifying theme
among all diagnostic errors is that they are largely preventable [45]. A major cause
leading to diagnostic errors implicates cognitive bias, a aw in judgment and
decision- making [36]. Graber etal. in a study of diagnostic errors in internal medicine identied cognitive factors as being the leading cause of diagnostic errors,
exceeding system-related factors [22]. More amenable environments to cognitive
diagnostic errors are high-stress areas, including critical care units (CCUs).
Accordingly, and in response to diagnostic errors being an urgent patient safety
concern, the National Academy of Medicine’s report, “Improving Diagnosis in
Health Care,” outlined a set of recommendations to “improve diagnosis and reduce
diagnostic errors,” emphasizing the implementation of a collaborative, team-based
approach to diagnosis, and the education and training of all healthcare professionals
in the diagnostic process [5].
While pharmacists endeavor to ensure appropriate drug therapy in the ICU, it
should be recognized that drug therapy cannot be appropriate unless related to the
correct diagnosis.It has been said, and I agree, that “the two major products of clinical decision making are diagnoses and treatment plans. If the rst is correct, the
second has a greater chance of being correct too” [8]. Diagnostic errors, therefore,
Y. Alzaidi (*)
Department of Pharmacy, Al Hada Armed Forces Hospital, Taif, Saudi Arabia
Switzerland AG 2025
Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical
Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_1
3© The Author(s), under exclusive license to Springer Nature

4
Fig. 1.1 A collaborative
approach to diagnosis and
the role of the pharmacist
clinician
Pharmacist clinicians
who support the diagnostic process
Physicians
The patient
Y. Alz a i d i
defy the best-intended efforts to improvedrug therapy outcomes. Moreover, while
misdiagnosis leads to wasteful or unnecessary treatments, it exposes patients to
toxic medications, causes delay in treatment, and leads to failure in treating the correct underlying condition. The safe and effective use of drug therapy, therefore,
mandates a collaborative, team-based approach to diagnosis, in which the pharma-
cist clinician plays an active role (Fig.1.1). Graber etal. best described the collab-
orative approach to diagnosis as being a matter of “distributed cognition,” to which
pharmacist clinicians, I argue, contribute unique knowledge and perspective [23].
Specically, pharmacists excel at checking for errors and would prove indispensable in preventing lapses in clinical reasoning. This “expanded role of the pharmacist” should not be perceived as nonessential or noncore to the pharmacy profession.
In fact, the full potential of pharmacists’involvement in diagnostic safety has yet to
be realized.
1.2 Cognitive Bias inCritical Care
Among important areas that are amenable to improvement in the ICU are the recognition and avoidance of diagnostic errors, of which cognitive biases constitute a
principal cause [8]. In essence, what is referred to as cognitive biases are thought
patterns that inuence decision-making and subsequently set the stage for erroneous
clinical judgment. Many types of cognitive biases are now appreciated, with the
most commonly encountered types in the ICU are availability bias, conrmation

Ap
1
proach toClinical Reasoning inCritical Care
5
bias, anchoring bias, framing effect, diagnostic momentum, and premature closure
(Table1.1; [26]).
Prevention of diagnostic errors due to cognitive factors relies on understanding
how these errors occur.Flaws in clinical diagnostic reasoning contribute largely to
diagnostic errors with knowledge decits being less contributory [22]. One of the
theories that explain diagnostic reasoning is the dual-process model, which theorizes two systems of thinking: the automatic thinking (System I) versus nonintuitive
deliberate thinking (System II; [28]). These two systems of clinical reasoning markedly differ. System I thinking is fast and intuitive, relies on pattern recognition, and
is automatic. In contrast, System II thinking is slow, effortful, analytical, and voluntary[28]. The majority of cognitive biases originate from the fast intuitive thinking
of System I [9]. While System I thinking is error-prone, System II thinking—albeit
imperfect—is error-resistant and less vulnerable to bias.Accordingly, it should be
appreciated that clinical experience, per se, does not protect from cognitive bias.
Expert clinicians are not immune from making cognitive errors, primarily because
of their tendency to resort to System I thinking, opting for short-cuts, reex assumptions, rules of thumb, and decision-making based on incomplete data. Notably, novices are not more likely to make diagnostic errors compared to expert clinicians
[29].All too often, novices default to the slow and deliberate System II thinking,
and only make a ‘working diagnosis’ after having carefully analyzed all related
data. It should be noted, however, that in the complex and fast-paced environment
of critical care, it may be more difcult to resist System I thinking, mandating effective preventative strategies.
Strategies to prevent cognitive diagnostic errors include debiasing strategies and
cognitive bias awareness, also known as metacognition [36]. Metacognition is
increasingly adopted and involves self-reection on the process of reasoning,
employing System II problem-solving [36]. However, metacognition alone is likely
to be insufcient and merits a synergistic approach. In addition to metacognition,
external scrutiny of one’s clinical diagnostic reasoning is proposed. A multidisciplinary approach to diagnosis, in which pharmacists play an active role, ensures
Table 1.1 Common cognitive biases in the ICU
Biases Description
Anchoring bias The tendency to xate on initial impressions without adjusting
Availability bias The tendency to judge a diagnosis as more likely if it readily
Conrmation bias The selective search for evidence that supports the diagnosis
Diagnostic momentum A diagnosis is accepted and passed on without supporting
Base rate neglect The tendency to neglect the true prevalence of a disease
Framing effect The diagnosis is inuenced by how the information is presented
Premature closure (or search
satiscing)
Commission bias The tendency towards action in preference to inaction
to additional new information
comes to mind
evidence
The tendency to stop the search once the rst plausible cause is
identied

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Y. Alz a i d i
sound clinical reasoning and prevents cognitive lapses leading to diagnostic errors.
With the proper education on diagnostic reasoning, pharmacists are able to assist
diagnosticians in avoiding diagnostic pitfalls, thus reducing diagnostic errors and
improving drugtherapy outcomes (Fig.1.1).
1.3 The Art ofClinical Assessment intheICU
The clinical assessment of a critically ill patient should follow a structured, systematic approach with careful attention to detail.The systematic approach should, preferably, begin with an independent review of systems—for example, the central
nervous, respiratory, cardiovascular, gastrointestinal, genitourinary, and musculoskeletal systems (Table1.2). The use of a mnemonic checklistas a supplementis of
particular value. One of the most commonly usedcare bundle checklists in the ICU
is the FASTHUG mnemonic [39]. Subsequently, the independent review of systems
is then complemented by the documented patient-specic information, includinghistory of present illness, past medical history, progress notes,clinical examinations, laboratory ndings, medication history, etc. This sequential approach to
patient assessment is proposed to ensure unbiased evaluation and to reconcilemissing, discordant, or conicting ndings from the independent review of systems with
that obtained from thedocumentedpatient-specicinformation. Drug therapy decisions can then be decided on the basis of ndings from this assessmentapproach
(Fig.1.2).
Notably, an important element of clinical assessment in the ICU is sound clinical
reasoning. As previously noted,a majorcause of diagnostic errors implicates faulty
clinical reasoning due to cognitive bias. Accordingly, sound clinical reasoning
should incorporate debiasing strategies to counteract cognitive bias. For example,instead of searching for evidence that conrms the diagnosis, a sound clinical
reasoning involves the search for evidence that is inconsistent with the diagnosis
and always considers plausible alternative diagnoses. Specic questions to ask
when evaluating the grounds for the initial diagnosis include the following:What
nding does not t with the proposeddiagnosis? Is there an alternate cause that
could satisfactorily explain the clinical presentation?If so, what additional causes
might account for the clinical presentation, etc.? Importantly, wheninvestigating
severalcauses, a higher “diagnostic weight” should be assigned to the relatively
more common cause (Table1.3). “Common things occur commonly,” and“uncommon presentations of common diseases are more common than common presentations of uncommon diseases.” Failure to consider the base rate can result in
diagnostic errors [3].
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