2014 machetes review of critical care med

Fagenholz, MD Instructor in Surgery, Harvard Medical School Assistant in Surgery, Department of Surgery Division of Trauma Emergency Surgery, and Critical Care Massachusetts General Hosp

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THE MASSACHUSETTS GENERAL HOSPITAL REVIEW OF CRITICAL CARE MEDICINE

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Section Editors

Peter J Fagenholz, MD

Instructor in Surgery, Harvard Medical School

Assistant in Surgery, Department of Surgery

Division of Trauma Emergency Surgery, and Critical Care

Massachusetts General Hospital

Boston, Massachusetts

Jarone Lee, MD MPH

Trauma, Emergency Surgery, Surgical Critical Care

Ala Nozari, MD, PhD

Assistant Professor of Anaesthesia, Harvard Medical School

Team Leader, Neurosurgical Anesthesia; Attending

Physician, Neuroscience Intensive Care Unit,

Co-Director, Massachusetts General Hospital and Brigham and Women’s Hospital Training Program in Neurosurgical Anesthesia Assistant Anaesthetist, Department of Anesthesia, Critical

Care and Pain Medicine

Ulrich Schmidt, MD, PhD, FCCM

Associate Professor

Department of Anesthesia Critical Care, Pain Medicine

Harvard Medical School

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THE MASSACHUSETTS GENERAL HOSPITAL REVIEW OF CRITICAL CARE MEDICINE

Editors:

Sheri M Berg, MD

Instructor of Anaesthesia, Harvard Medical School

Edward A Bittner, MD, PhD

Assistant Professor of Anaesthesia, Harvard Medical School

Program Director, Critical Care Medicine Fellowship

Associate Director, Surgical Intensive Care Unit

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Product Manager: Nicole T Dernoski

Production Editor: Alicia Jackson

Manufacturing Manager: Beth Welsh

Design Coordinator: Joan Wendt

Compositor: Integra Software Services Pvt Ltd.

Two Commerce Square

as part of their official duties as U.S government employees are not covered by the above-mentioned copyright.

Printed in China

Library of Congress Cataloging-in-Publication Data

Massachusetts General Hospital critical care board review / Sheri M Berg, MD, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts, Edward A Bittner, MD, PhD, associate director for education, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts, editors; Massachusetts General Hospital critical care board review, section editors, Jarone Lee, MD, MPH, Instructor in Surgery, Harvard Medical School, Trauma, Emergency Surgery, Surgical Critical Care, Massachusetts General Hospital, Boston, Massachusetts [and three others].

The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions This is particularly important when the recommended agent is a new or infrequently employed drug.

Some drugs and medical devices presented in this publication have Food and Drug Administration (FDA) clearance for limited use

in restricted research settings It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice.

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10 9 8 7 6 5 4 3 2 1

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To our fellows: past, present, and future

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Young K Ahn, MD

Assistant Clinical Professor

Division of Critical Care

Department of Anesthesia

University of California Los Angeles

Los Angeles, California

Hasan B Alam, MD

Norman Thompson Professor of Surgery

Section Head, General Surgery

University of Michigan Hospital

Ann Arbor, Michigan

Rebecca Aslakson, MD

Assistant Professor

The Johns Hopkins University School of Medicine

Department of Anesthesiology and Critical Care Medicine

The Johns Hopkins University School of Medicine

Baltimore, Maryland

Aranya Bagchi, MBBS

Instructor in Anesthesia,

Department of Anesthesia, Critical Care and Pain Medicine

Lorenzo Berra, MD

Assistant Professor of Anaesthesia,

Assistant Anaesthetist, Department of Anesthesia, Critical

Care and Pain Medicine

Edward A Bittner, MD, PhD

Associate Director for Education

Torrey Boland, MD

Fellow, Neurocritical Care

Massachusetts General Hospital and Brigham & Women’s Hospital

Centennial, Colorado

David Boldt, MD

Assistant Professor

Department of Anesthesiology

University of California, Los Angeles

Kathryn L Butler, MD

Instructor in Surgery

Division of Acute Care Surgery and Critical Care

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Beth Israel Deaconess Medical Center

Mark Caridi-Scheible, MD

Emory University School of Medicine

Department of Emergency Medicine

Instructor, Harvard Medical School

Anesthetist and Staff Intensivist Department of Anesthesia, Critical Care and Pain Medicine

George Z Cheng, MD, PhD

Department of Medicine

Division of Pulmonary & Critical Care

Daniel Chipman

Assistant Director

Respiratory Care Services

Jason Chua, MD

Assistant Professor

Robert S Crawford, MD

Assistant Professor

Division of Vascular Surgery

University of Maryland Medical Center

Baltimore, Maryland

Marc A de Moya, MD, FACS

Assistant Professor of Surgery, Harvard Medical School, Surgical Critical Care Fellowship Director

Medical Director, Blake 12 ICU

Surgical Clerkship Director, Harvard Medical School Associate Program Director, Surgical Residency

Yale University School of Medicine

New Haven, Connecticut

Anahat Dhillon, MD

Assistant Professor

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Assistant Professor of Anesthesiology

Washington University in St Louis

Division of Trauma Emergency Surgery, and Critical Care

Corey R Fehnel, MD

Massachusetts General Hospital and Brigham & Women’s Hospital Boston, Massachusetts

Karim Fikry, MD

Resident

Department of Anesthesia, Critical Care, and Pain Medicine

Robert A Finkelstein, MD

Clinical Fellow, Pediatric Emergency Medicine

Boston Medical Center

Division of Pediatric Emergency Medicine

Graduate Assistant in Pediatrics

Massachusetts General Hospital for Children

Clinical Fellow, Pediatric Emergency Medicine

Division of Pediatric Emergency Medicine

Boston Medical Center

Jonathan Friedstat, MD

Resident, Plastic and Reconstructive Surgery

University of North Carolina

Chapel Hill, North Carolina

Miguel M Gaeta, MD

Trauma Medical Director, Elliot Hospital,

Manchester, New Hampshire

Assistant in Surgery, Massachusetts General Hospital Division of Trauma, Emergency Surgery, and Critical Care

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Baltimore, Maryland

Edward George, MD, PhD

Assistant Professor

Department of Anesthesia,

Critical Care and Pain Medicine

Brandy S Golenia, PharmD, BCPS

Clinical Pharmacy Specialist-Drug Information

Department of Pharmacy Services

Cedars-Sinai Medical Center

Jeremy W Goldfarb, MD

Instructor in Anaesthesia,

Director of Post Anesthesia Care Unit (PACU)

Attending Anesthesiologist, Massachusetts Eye and Ear Infirmary

Steven Greenberg, MD

Director of Critical Care Services, Evanston Hospital

Co-Director for Resident Education

NorthShore University HealthSystem

Assistant Clinical Professor, Department of Anesthesiology Critical Care University of Chicago, Pritzker School of Medicine

Chicago, Illinois

Vadim Gudzenko, MD

Assistant Clinical Professor

Critical Care Division, Department of Anesthesiology

David Geffen School of Medicine at University of California, Los Angeles Los Angeles, California

Jessica Hines

Administrative Coordinator

John O Hwabejire, MD, MPH

Trauma Research Fellow

Division of Trauma, Emergency Surgery, and Critical Care

Critical Care Fellow

University of Nebraska Medical Center

Omaha, Nebraska

Haytham M.A Kaafarani, MD, MPH

Fellow in Trauma, Acute Care Surgery, and Critical Care

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Rebecca Kalman, MD

Clinical Fellow in Anaesthesia, Harvard Medical School

Fellow, Critical Care Medicine

George Kasotakis, MD, MPH

Fellow in Trauma, Acute Care Surgery, and Critical Care

Tariq A Kelker, MD, MSc

Assistant Professor—Trauma/Critical Care Surgery Division

Loma Linda University Medical Center

Diamond Bar, California

Emer Kelly, MD

Pulmonary and Critical Care Fellow

Department of Pulmonary and Critical Care Medicine

Brigham and Women’s Hospital

Erik B Kistler, MD, PhD

Assistant Professor

Department of Anesthesiology & Critical Care

VA San Diego Health Care System/University of California, San Diego San Diego, California

Terrance Kummer, MD, PhD

Jean Kwo, MD

Assistant Medical Director

Ruth Lamm, MD

Assistant Professor of Emergency Medicine

Assistant Professor of Surgery

Atlanta, Georgia

Jarone Lee, MD MPH

Trauma, Emergency Surgery, Surgical Critical Care

Jeanette J Lee, MD

Clinical Instructor of Anesthesia and Critical Care Medicine

Boston University Medical Center

Alexander R Levine, PharmD

Critical Care Pharmacist

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Steven M Lindsey, MD

Atlanta, Georgia

Jakob I McSparron, MD

Clinical Research Fellow

Department of Pulmonary and Critical Care Medicine Massachusetts General Hospital

Daniel C Medina, MD

Fellow, Department of Surgery

University of Maryland Medical Center

Baltimore, Maryland

Kamal Medlej, MD

Assistant Professor of Clinical Emergency Medicine

American University of Beirut Medical Center

Beirut, Lebanon

Angela Meier, MD, PhD

Clinical Critical Care Fellow

Department of Anesthesia, Critical Care and Pain Medicine Massachusetts General Hospital

Andrew D Mihalek, MD

Clinical and Research Fellow

Division of Pulmonary & Critical Care Medicine

Fellow in Critical Care

Division of Burn Surgery

Shamim H Nejad, MD

Assistant Professor of Psychiatry, Harvard Medical School Burns and Trauma Psychiatry Consultation

Attending Physician, Dept of Psychiatry

Crystal M North, MD

Clinical Fellow

Division of Pulmonary and Critical Care Medicine

Massachusetts General Hospital,

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Massachusetts General Hospital and Brigham and Women’s

Hospital Training Program in Neurosurgical Anesthesia

Assistant Anaesthetist

Airadion Omoruan, MD

Clinical Fellow in Cardiothoracic Anesthesiology

Department of Anesthesiology, Critical Care and Pain Medicine Massachusetts General Hospital

Britta Panda, MD, PhD

Assistant Professor

Division of Maternal-Fetal Medicine

Tufts Medical Center

Research Fellow in Anaesthesia

Department of Anesthesia, Critical Care, and Pain Medicine

Paritosh Prasad, MD, DTM&H

Clinical Fellow

Infectious Disease/Critical Care

Massachusetts General Hospital/National Institutes of Health

Sadeq A Quraishi, MD, MHA, MMSc

Assistant Professor of Anaesthesia

Anesthetist and Staff Intensivist

Farbod Nicholas Rahaghi, MD, PhD

Research Fellow

Pulmonary and Critical Care

Brigham and Women’s Hospital

Celine Rahman DeMatteo, MD

Massachusetts General Hospital and Brigham and Women’s Hospital Boston, Massachusetts

Pankajavalli Ramakrishnan, MD, PhD

Robert A Ratzlaff, DO

Assistant Medical Director of the Cardiovascular Intensive

Care Units and Assistant Professor of Anesthesiology

Cleveland Clinic Lerner College of Medicine of Case Western Reserve Anesthesiology Institute, Cardiothoracic Anesthesiology

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Cleveland Clinic

Cleveland, Ohio

Daniel M Rolston, MD, MS

Chief Resident

St Luke’s-Roosevelt Hospital Center

New York, New York

James K Rustad, MD

Core Courtesy Assistant Professor

Department of Psychiatry & Behavioral Medicine

Morsani College of Medicine

University of South Florida

Tampa, Florida

Karim Sadik, MD

Clinical Fellow, Surgical Critical Care

Ulrich Schmidt, MD, PhD, FCCM

Associate Professor

Department of Anesthesia Critical Care, Pain Medicine

Harvard Medical school

William B Schoenfeld, MD

Instructor in Anesthesia, Harvard Medical School

Torin D Shear, MD

Evanston Hospital, NorthShore University HealthSystem

Assistant Clinical Professor, Department of Anesthesiology

Antonios C Sideris, MD

Trauma Research Fellow

Sumit Singh, MD

Assistant Professor

Leigh Ann Slater, MD

Assistant Faculty

Departments of Surgery and Anesthesiology and Critical Care Medicine Trauma/Acute Care Surgery Division of Surgery

Baltimore, Maryland

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David Stahl, MD

Clinical Fellow, Anesthesia Critical Care

John F Burke Professor of Surgery

Chief of Division of Trauma Emergency Surgery

& Surgical Critical Care

Nicholas C Watson, MD

Assistant Professor

Anesthesia Practice Consultants, PC

Grand Rapids, Michigan

Anesthesiology and Critical Care

Michigan State University College of Human Medicine Ada, Michigan

Jean McFall Wheeler, MD, MS

Atlanta, Georgia

Stephanie Whitener, MD

Department of Anesthesia, Division of Cardiothoracic Anesthesia

Duke University Medical Center

Durham, North Carolina

Susan R Wilcox, MD

Staff Physician

Phoebe H Yager, MD

Instructor in Pediatrics, Harvard Medical School

Assistant in Pediatrics, Massachusetts General Hospital Department of Pediatrics

Division of Pediatric Critical Care Medicine

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Hady Latif Zgheib, MD

Resident, Department of Emergency Medicine

American University of Beirut Medical Center

Beirut, Lebanon

George Z Cheng MD, PhD

Department of Medicine

Division of Pulmonary & Critical Care

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Premise:

The field of critical care is constantly expanding and changing, and unfortunately there seems to be alack of great, comprehensive critical care board review books on market A true multidisciplinarybook is needed! We have formatted a concise, although comprehensive review of pertinent criticalcare topics and questions with explanation of answers and selected references for your review Theprimary objective of this book is to provide a text for board certification/recertification, which alsoserves as a refresher/text for rapid reference

Requirements:

At least one author must be a critical care attending/fellow either trained at MGH or work at MGH (toensure consistency in terminology/approach and to provide the “MGH flavor of critical care”) Editorsare drawn from the major specialty areas that encompass adult critical care medicine, anesthesiology,emergency medicine, surgery and neurology The topic list for chapters was developed using thecontent outlines for the subspecialty critical care boards

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2.6 Congenital Heart Disease in Adults

2.7 Noncardiogenic Pulmonary Edema versus Cardiogenic Pulmonary Edema

2.8 Cardiac Arrest and Resuscitation

2.9 Hypertension

2.10 Aneurysms and Dissections

2.11 Implantable Cardiac Devices

3.2 Respiratory Failure, Mechanical Ventilation, and Weaning

3.3 Acute Respiratory Distress Syndrome and Acute Lung Injury

3.4 Ventilator-Induced Lung Injury and Ventilator-Associated Lung Injury

3.5 Pulmonary Embolism

3.6 Pulmonary Hypertension

3.7 Reactive Airway Disease (Asthma)

3.8 Chronic Obstructive Pulmonary Disease (COPD)

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3.9 Restrictive Airway Diseases

3.15 Sleep-Related Breathing Disorders

3.16 Pharmacologic Therapies for Pulmonary Disorders

4.6 Malabsorption in the Critically Ill Patient

4.7 Ileus and Acute Colonic Pseudoobstruction (Ogilvie Syndrome)

4.8 Clostridium Difficile and Toxic Megacolon

4.9 Inflammatory Bowel Disease

4.10 Vascular Diseases of Small Bowel

4.11 Obesity

4.12 Pharmacologic Therapies for Gastrointestinal Disorders

SECTION 5

Renal

5.1 Acute Kidney Injury (AKI)

5.2 Infections of the Urinary Tract

5.3 Acid-Base Physiology and Disorders

5.4 Renal Replacement Therapy

5.5 Pharmacologic Therapies for Renal Disorders

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7.5 Hemoglobinopathies

7.6 Bone Marrow and Stem Cell Transplants

7.7 Tumor Lysis Syndrome

9.4 Central Nervous System Infections

9.5 Traumatic Brain Injury and Intracranial Hypertension9.6 Spinal Cord Injury

9.7 Ischemic Stroke

9.8 Hemorrhagic Stroke

9.9 Subarachnoid Hemorrhage

9.10 Vascular Malformations

9.11 Cerebral Venous Thrombosis

9.12 Demyelinating Syndromes and Prion Disease

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14.1 Pre-eclampsia/Eclampsia and HELLP Syndrome

14.2 Acute Fatty Liver of Pregnancy

14.3 Amniotic Fluid Embolism

14.4 Postpartum Hemorrhage

SECTION 15

Fluids and Electrolytes

15.1 Fluids and Electrolytes

16.1 Basal and Stress Energy Requirements

16.2 Stress Hormone Response

16.3 Nutritional Deficiency States

16.4 Nutrition Support

16.5 Refeeding Syndrome

SECTION 17

Pharmacokinetics and Pharmacodynamics of Drugs

17.1 Basic Pharmacokinetics and Pharmacodynamics

SECTION 18

Transfusion Therapy

18.1 Transfusion Therapy

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Point-of-Care Ultrasound in the ICU

23.1 Point-of-Care Ultrasound in the ICU

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27.1 Tracheostomy

27.2 Cricothyroidotomy

27.3 Bronchoscopy

27.4 Tube Thoracostomy (Chest Tube)

27.5 Thoracentesis, Paracentesis, and Pericardiocentesis27.6 Feeding Tube Placement

SECTION 28

ICU Transport

28.1 ICU Transport

SECTION 29

Epidemiology and Biostatistics

29.1 Epidemiology and Biostatistics

Ethics and Palliative Medicine

32.1 Ethics and Palliative Medicine

SECTION 33

Emergent Airway Management

33.1 Emergent Airway Management

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WBC > 12,000 or < 4,000 or normal with >10% immature forms

C-reactive protein (CRP) > 2 SD normal value, procalcitonin > 2 SD above normal value

Keep in mind other indirect indicators of infection such as altered mental status andhyperglycemia

Severe sepsis = sepsis-induced hypoperfusion or organ dysfunction indicated by one or more of: Septic shock: arterial hypotension = acute systolic blood pressure (SBP) < 90, mean arterialpressure (MAP) < 70, or SBP decrease > 40 from baseline

Arterial hypoxemia (PaO2/FiO2 < 300)

Acute lung injury (ALI) with PaO2/FiO2 < 250 in the absence of pneumonia

ALI with PaO2/FiO2 < 200 in the presence of pneumonia

Elevated lactate (>1.2 mmol/L)

Acute oliguria (UOP < 0.5 mL/kg for 2 hours despite fluid resuscitation)

Creatinine increase (>0.5 mg/dL or 2× baseline)

Hyperbilirubinemia (Tbili > 4 mg/dL acutely)

Thrombocytopenia (platelets < 100,000 acutely)

Acute coagulopathy (INR > 1.5 or aPTT > 60 s)

Mixed venous saturation > 80% (likely sepsis) or < 65% (rule out cardiogenic source)

Severe acute ileus

Decreased capillary refill or mottling

Common Causes to Remember

ANY infection can be complicated by sepsis!

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Examples include:

Gram-positive bacteremia (i.e., Staphylococcus, Streptococcus, Clostridium) via exposed

peptidoglycan in their cell walls, exotoxins

Gram-negative bacteremia (Escherichia coli, Pseudomonas, Acinetobacter) via endotoxins

28-day mortality rate of more than 30%

Associated with an increased risk of death in the ICU

Approximately 100,000 deaths per year in the United States

National incidence ~750,000 cases

Can occur at any age, but there is a correlation with advanced age and not only incidence of septicshock, but also increased mortality

Key Pathophysiology

The pathogenesis of sepsis is a complicated process that occurs as a result of the interaction ofseveral factors including the infectious organism, the patient’s concomitant medical problems, andhis/her immune system

The type of infectious source, the duration of exposure, and the patient’s underlying medicalcomorbidities are factors addressed with early goal-directed therapy and initiation of appropriateantibiotics

Immune response

Pro-inflammatory response mediated by cytokines

Interleukin-1 (IL-1) and IL-6; tumor necrosis factor-α (TNF-α)

Activated by antigen–antibody complexes

The complement system is activated by bacterial wall sugars and endotoxin

Activates neutrophils, lymphocytes, prostaglandins, and acute phase reactant proteins

Pro-inflammatory mediators are counteracted by anti-inflammatory mediators

IL-4 andIL-10

Anti-inflammatory mediators can limit the effects of pro-inflammatory mediators, leading to

a state of “relative” immunosuppression, which is referred to as immunoparalysis

Leads to a reduction of HLA proteins on monocytes

Contributes to increased morbidity and mortality

Cellular dysfunction

Disturbance of mitochondrial oxygen utilization

Results in cytopathic hypoxia: low ATP production in the setting of adequate oxygendelivery

Pathogenic activation of apoptosis

Endothelial dysfunction and loss of hemostatic balance

Endothelial cells assist in regulation of vascular tone and coagulation (via expression ofheparin sulfate)

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Inflammation is a known procoagulant state.

Nitric oxide (NO) is a potent vasodilator produced by NO synthase

In sepsis, inducible NO synthase is stimulated by IL-6 and TNF-α, leading to an increasedproduction of NO and subsequent profound vasodilatation

Endothelial surfaces normally have anticoagulant properties

In sepsis, this anticoagulant balance is disturbed by procoagulant inducers (CRP), leading tointravascular thrombosis

Tissue edema develops secondary to capillary leakage

Fluids are subsequently shifted into the third space

Central nervous system dysfunction

Decreased oxygen delivery to the brain can lead to sepsis-induced encephalopathy (confusion,delirium, obtundation)

Cardiac and circulatory dysfunction

Tachycardia initially compensates for the arterial hypotension caused by severe systemicvasodilatation to maintain stroke volume

Myocardial contractility will eventually decrease and further contribute to the markedhypotension

Impaired oxygen delivery combined with increased oxygen consumption and cardiac work canlead to cardiac dysfunction

Respiratory dysfunction

Sepsis is accompanied by an increased work of breathing

Capillary leak within the lungs leads to oxygenation difficulties

Over time some patients with severe sepsis can develop ALI or acute respiratory distresssyndrome (ARDS)

Renal dysfunction

Hypotension can lead to impaired perfusion, causing oliguria

Can also see acute tubular necrosis (ATN), which can further precipitate renal failure

In severe cases, patients may require renal replacement therapy:

Can be a transient requirement that resolves in weeks to months

Other times permanent dialysis is needed

Hepatic dysfunction

Hypoperfusion can cause “shock liver,” characterized by transaminitis

Cholestasis and hyperbilirubinemia may be present

Endocrine dysfunction

Adrenal insufficiency

Sepsis can impair the normal stress response

Results in inadequate increase in serum cortisol levels

Insulin deficiency

Impaired function of pancreatic β cells

Results in hyperglycemia that can be detrimental secondary to increased frequency ofinfections, delayed wound healing, and reduced granulocyte function

Vasopressin deficiency

Usually secreted in response to hypotension and hypovolemia

Given that these are hallmarks in sepsis, one would predict that vasopressin secretion wouldincrease

However, vasopressin levels are actually decreased in patients with septic shock

Possibly due to depletion of stored vasopressin in the pituitary and/or depression of the

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Always try to rule out other causes of shock.

The mainstay of diagnosing sepsis and septic shock is the early identification of the etiology

This begins by obtaining cultures: blood, urine, sputum, cerebrospinal fluid, and any other fluidsample (e.g., abdominal drains) appropriate to the clinical situation

Diagnostic imaging may also be helpful with tools such as plain films, ultrasounds, and CTscans

Management and Treatment

The combined work of multiple groups has resulted in the development of The Surviving SepsisCampaign

This effort brought evidence-based guidelines to the treatment of sepsis

The most recent guidelines (2012) can be found at www.survivingsepsis.org

Campaign bundles

In the first 3 hours

Obtain lactate levels, blood cultures before administration of broad-spectrum antibiotics, andbolus crystalloid (30 cc/kg) for hypotension or lactate >4

In the first 6 hours

Vasopressor therapy if MAP < 65 and not responding to initial fluid resuscitation, measure CVPand Scvo2, and recheck lactate if the initial lactate level was elevated

Source control is KEY!

Identification of the causative agent and controlling the infection

Timely administration of antimicrobial therapy is a key component in treating sepsis

The goal is to begin therapy within 1 hour of the presumptive diagnosis

Ideally cultures are obtained prior to starting antimicrobial therapy

Therapy is broad spectrum based on the presumed source and is narrowed once culture resultsare reported

Fluid resuscitation plays a key role in ensuring adequate intravascular volume and maintainingperfusion

Resuscitate within the first 6 hours of recognition of the shock state

Can consider colloids (albumin) when the patient continues to require a significant amount ofcrystalloid to maintain MAP

Avoid hetastarches!

Typically, a central venous catheter is inserted to measure central venous pressure (CVP) andresuscitation is continued until a CVP of 8 to 12 is reached

If MAP is < 65 mmHg or SBP is < 90 mmHg, vasopressors are initiated:

Norepinephrine is the first drug of choice

Vasopressin (0.01–0.04 U/min) can also be administered as a second vasopressor

Vasopressin levels are decreased in septic shock

Dopamine should only be used in patients with very low risk for arrhythmias, low heart rateand/or cardiac output Dobutamine can be considered for patients with cardiac dysfunction,

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i.e those with high filling pressures and low cardiac output, or those with clinical signs ofhypoperfusion despite restoration of systemic blood pressure.

Epinephrine is a second-line agent for patients that do not respond to norepinephrine

When blood pressure goals are achieved, a mixed venous (>65%) or central venous saturation(>70%) may be obtained to assess oxygen delivery and extraction

Hemoglobin (Hb) target of 7 to 9 is fine, as long as there are NO signs of coronary artery disease(CAD), tissue hypoperfusion, or hemorrhage

If oxygen delivery goals are not met, then consideration is given to transfusion if Hb is not 10.0

or initiation of inotropic therapy

Dobutamine or milrinone are agents that are typically used

Dobutamine is helpful when there is evidence of myocardial dysfunction

In this situation, one would observe high filling pressures with a low cardiac output

Can also be used when there are ongoing signs of hypoperfusion despite adequateintravascular volume status and MAP

Examples include:

Low cardiac output

Low CVP

Elevated filling pressures

Ultrasound evidence of a low ejection fraction

Ensure patients are well oxygenated and correct hypoxemia

Hemodynamically unstable patients will often require endotracheal intubation

Given that up to 40% of patients with septic shock will develop ALI, consider using ventilationwith lung protective strategies (TV 6 cc/kg of ideal body weight and maintain plateau pressures

<30 cm H2O)

Avoid muscle relaxation in sepsis WITHOUT ARDS

A short trial (˜48 hours) may be used for patients with early ARDS (PaO2/FiO2 < 150)

Corticosteroid administration

Remains controversial, but consider using in patients who remain hypotensive despite presumedadequate fluid resuscitation and/or those on escalating doses of vasopressor therapy

Dosing = 50 mg hydrocortisone every 6 hours

Discontinue as soon as the patient is no longer on vasopressors

Do not use for >7 days

Glucose control

110 to 150

Hyperglycemia and hypoglycemia are associated with worse outcomes

Ensure the patient receives a sugar source (D5W, D10) if he/she requires an insulin infusion Nutritional support

Adequate nutrition is key, as malnutrition can lengthen the course of sepsis and further increasecomplications

Enteral nutrition is always preferred

Do not initiate during the resuscitation phase

Begin as soon as the patient has entered a phase of relative hemodynamic stability(vasopressor requirement is not increasing)

Stress ulcer prophylaxis

Outcomes

Early goal-directed therapy is key!

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APACHE II scores aid in prediction of mortality.

SUGGESTED READINGS

Angus DC, Linde-Zwirble WT, Lidicker J, et al Epidemiology of severe sepsis in the United States: analysis of incidence, outcome,

and associated costs of care Crit Care Med 2001;29(7):1303-1310.

Annane D, Sébille V, Charpentier C, et al Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in

patients with septic shock JAMA 2002;288(7):862-871.

Bernard GR, Vincent JL, Laterre PF, et al Efficacy and safety of recombinant human activated protein C for severe sepsis N Engl J

Med 2001;344(10):699-709.

Dellinger RP, Levy MM, Rhodes A, et al Surviving sepsis campaign: international guidelines for management of severe sepsis and

shock: 2012 Crit Care Med 2013;41(2):580-637.

Desai KH, Tan CS, Leek JT, et al Dissecting inflammatory complications in critically injured patients by within-patient gene

expression changes: a longitudinal clinical genomics study PLoS Med 2011;8(9):e1001093.

Hotchkiss RS, Karl IE The pathophysiology and treatment of sepsis N Engl J Med 2003;348(2):138-150.

Kumar A, Roberts D, Wood KE, et al Duration of hypotension before initiation of effective antimicrobial therapy is the critical

determinant of survival in human septic shock Crit Care Med 2006;34(6): 1589-1596.

The approach to any patient in shock is to first rule out hypovolemia as a potential cause

The most common types of shock identified in surgical, trauma, and burn patients

Hemorrhage (Table 1.2.1)

Dehydration (due to gastrointestinal [GI] losses)

Third spacing (due to burns)

Epidemiology

Hypovolemia and hemorrhage are responsible for over half of deaths in trauma cases

Approximately one third of these deaths occur out of the hospital

Hemorrhage and resulting hypovolemic shock are major causes of mortality within 4 hours ofinjury

The mechanism of injury and immediate availability of a trauma center play a role in the mortality

of these afflicted patients

Total body water in the average adult male is equal to 60% of lean body weight (versus 50% infemales)

Two thirds of the total body water is intracellular fluid (ICF)

The remaining extracellular fluid (ECF) is further divided into interstitial fluid and plasma

The average adult has approximately 5 to 6 L of blood, which is equivalent to about 8% of the totalbody water

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An example of this calculation is shown below for an 80-kg male:

0.6 × 80 kg = 48 L of total body water

2/3 × 48 L = 32 L ICFTBW – ICF = ECF

48 L – 32 L = 16 L ECF3/4 × 16 L= 12 L of interstitial fluid1/4 × 16 = 4 L of plasma

When the body is hypovolemic, the earliest response is the movement of interstitial fluid into thecapillaries

This transcapillary fluid shift is able to replace up to 15% of the intravascular volume, thusproviding the mechanism for compensation in stage I shock

Acute blood loss results in the activation of the renin–angiotensin–aldosterone (RAA) system

Hypovolemic shock is classified into four stages based on the volume of blood loss and the

patient’s physiologic response.

Stage I shock results from a decrease of up to 15% of the circulating volume, or 750 mL to1,000 mL

Referred to as “compensated shock” because the body is able to physiologically adjustwithout showing clinical evidence of hypovolemia

Tachycardia, decreased systolic blood pressure, decreased pulse pressure, and decreased urineoutput do not occur

Routine blood donation is an example of stage I shock

Stage II shock is associated with a 15% to 30% decrease in intravascular volume, or 1,000 mL

to 1,500 mL

Referred to as “mild shock”

The hallmark of this stage is mild tachycardia accompanied by normal systolic blood pressureand decreased pulse pressure

Stage III shock is characterized by decreased systolic blood pressure, decreased urine output,and mental status changes

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Referred to as “decompensated shock”

Stage IV shock results from the loss of > 2 L of circulating fluid

Referred to as “severe shock”

Patients present with respiratory failure, anuria, and obtundation

Trauma patients that present in decompensated and severe shock have a markedly increasedmortality

Differential Diagnosis

Hypovolemic shock occurs after a loss of at least 20% of the body’s intravascular volume

The most dramatic cause of hypovolemia is rapid blood loss, referred to as hemorrhagic shock Liver and splenic injuries are the most common sources of hemorrhage following bothpenetrating and blunt abdominal trauma

Orthopedic injuries such as pelvic and femur fractures can also be associated with massiveblood loss

The most common causes of nontraumatic hemorrhage include ruptured aneurysms and GIbleeds

Peptic ulcers and diverticulosis are responsible for most cases of upper and lower GI bleeds,respectively

Hypovolemic shock also results from nonhemorrhagic intravascular volume loss

Dehydration from poor oral intake, vomiting, or diarrhea can lead to hypovolemia

Additional sources of GI fluid loss include high output fistulas and stomas

Insensible fluid losses also contribute to total body fluid balance

Examples of increased insensible losses leading to hypovolemia include burns, open wounds,excessive sweating, and heat stroke

The kidneys are another potential source of volume depletion: uncontrolled urine output, such asthe recovery phase of acute tubular necrosis, or diabetic ketoacidosis, can lead to hypovolemia Rule out other causes of shock

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Resuscitation is complete when the oxygen debt has been repaid, tissue acidosis eliminated, and normal aerobic metabolism restored in all tissue beds.

–– EAST Practice Management Guideline Committee

The treatment of hypovolemic shock centers on rapid hemostasis and fluid resuscitation

In order to maintain end-organ function, oxygen delivery and consumption must be optimized Traditional endpoints of resuscitation include the restoration of blood pressure and pulse, as well asurine output and central venous pressure

However, the normalization of these parameters does not necessarily indicate that tissuehypoperfusion has ceased

For this reason, additional endpoints must be utilized

Newer parameters of resuscitation include arterial pH, base deficit, lactate, serum bicarbonate, andcentral venous oxygen saturation

These laboratory values not only guide appropriate fluid resuscitation, but the time tonormalization of pH, lactate, and base deficit has prognostic ramifications In the traumapopulation, patients whose pH and lactate levels have returned to baseline within 24 hours havemarkedly improved survival rate

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Management Guidelines J Trauma 2004;57(4):898-912 endpoints

http://www.east.org/resources/treatment-guidelines/resuscitation-1.3

Cardiogenic Shock

Robert Ratzlaff

Definitions

End-organ hypoperfusion due to cardiac failure is typically characterized by

Persistent systolic blood pressure <90 mmHg or mean arterial pressure 30 mmHg lower thanbaseline

Low cardiac index (<1.8 L min−1 m−2 without support or <2.0 L min−1 m−2 with support

Left ventricular end-diastolic pressure >18 mmHg or right ventricular end-diastolic pressure >10 to

15 mmHg

High systemic vascular resistance

Low venous oxygen saturation

High lactate level

Early recognition and reperfusion of myocardial infarction (MI) reduces cardiogenic shockincidence

Acute MI with left ventricular failure

Acute, severe left ventricular or right ventricular dysfunction

Acute valvular regurgitation

Epidemiology

Acute MI involving 40% or more of the ventricular mass is the most common cause of cardiogenicshock

Occurs in 5% to 8% of patients hospitalized with STEMI

Occurs in 2.5% of patients hospitalized with non-STEMI

Risk factors are HTN, DM, prior MI, angina or heart failure, CAD, LBBB, older age, STEMI

Myocardial injury causes systolic and diastolic dysfunction

Decrease in cardiac output leads to decrease in systemic and coronary perfusion in other vitalorgans

Hypoperfusion is a hallmark of cardiogenic shock

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Hypoperfusion leads to release of catecholamines increasing myocardial oxygen demand, makingmyocardium more prone to arrhythmias.

Vasoconstriction ensues leading to progressive myocardial dysfunction

MI can cause systemic inflammatory response syndrome which can lead to increased levels of

IL-6, TNF, and nitric oxide all of which have myocardial depressant actions and create a low perfusionstate

Differential Diagnosis

MI

Mechanical complications from an MI

Ventricular septal wall rupture

Contained free wall rupture

Papillary muscle rupture

Early recognition and reperfusion of MI

Acetylsalicylic acid (ASA) and heparin as recommended for MI

Clopidrogrel in patients who undergo percutaneous coronary intervention (PCI)

Controlling ventilation via noninvasive or by intubation

Early echocardiography to rule out mechanical causes of cardiogenic shock (rupture of theventricular septum, free wall or papillary muscles)

Early surgical repair of mechanical causes of cardiogenic shock

Optimize oxygenation and pH—mechanical ventilation may be needed

Pulmonary artery catheter or Doppler echocardiography for guiding hemodynamic management Use of inotropic and vasopressors agents to maintain coronary and systemic perfusion(norepinephrine first line per American College of Cardiology/American Heart Associationguidelines)

Early cardiac catheterization, coronary angiography, and intraaortic balloon pump to assist incoronary and peripheral perfusion

Early revascularization—1 or 2 vessel CAD or moderate 3-vessel CAD increases survival

Thrombolytic therapy is an option when PCI is not possible

Immediate coronary artery bypass graft (CABG)—severe 3-vessel CAD or left main CAD

Left ventricular assist device or extracorporeal life support may be needed

Appropriate treatment of cardiogenic shock due to mechanical complications (rupture of

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ventricular septum, free wall or papillary muscles)

Outcomes

Aggressive early revascularization is associated with survival benefit (SHOCK trial)

Quality of life studies have shown functional class improvement with early revascularization

Antman EM, Anbe DT, Armstrong, PW, et al ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice

Guidelines Circulation 2004;110:588-636.

Babaev A, Frederick PD, Pasta DJ, et al Trends in management and outcomes of patients with acute myocardial infarction

complicated by cardiogenic shock JAMA 2005;294:448-454.

Beyersdorf F, Buckberg GD, Acar C, et al Cardiogenic shock after acute coronary occlusion: pathogenesis, early diagnosis, and

treatment Thorac Cardiovasc Surg 1989;37:28-36.

Fox KA, Anderson FA, Dabbous OH, et al Intervention in acute coronary syndromes: do patients undergo intervention on the basis

of their risk characteristics? The Global Registry of Acute Coronary Events (GRACE) Heart 2007;93:177-182.

Goldberg RJ, Spencer FA, Gore JM, et al Thirty-Year trends (1975–2005) in the magnitude of, management of, and hospital death

rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective Circulation.

2009;119:1211-1219.

Hasdai D, Harrington RA, Hochman JS, et al Platelet glycoprotein IIb/IIIa blockade and outcome of cardiogenic shock complicating

acute coronary syndromes without persistent ST-segment elevation J Am Coll Cardiol 2000;36:685-692.

Hochman JS, Sleeper JA, Webb JG, et al Early revascularization in acute myocardial infarction complicated by cardiogenic shock:

SHOCK Investigators: should we emergently revascularize occluded coronaries for cardiogenic shock N Engl J Med.

1999;341:625-634.

Hochman JS, Sleeper LA, Webb JG, et al Early revascularization and long-term survival in cardiogenic shock complicating acute

myocardial infarction JAMA 2006;295:2511-2515.

Jacobs AK, Leopold JA, Bates E, et al Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry J

Am Coll Cardiol 2003;41:1273-1279.

Kohsaka S, Menon V, Lowe AM, et al Systemic inflammatory response syndrome after acute myocardial infarction complicated by

cardiogenic shock Arch Intern Med 2005;165:1643-1650.

Mann HJ, Nolan PE Update on the management of cardiogenic shock Curr Opin Crit Care 2006;12:431-436.

Reynolds HR, Hochman JS Cardiogenic shock: current concepts and improving outcomes Circulation 2008;117:686-697.

Sleeper LA, Ramanathan K, Picard MH, et al Functional status and quality of life after emergency revascularization for cardiogenic

shock complicating acute myocardial infarction J Am Coll Cardiol 2005;46:266-273.

Stevenson LW, Miller LW, Desvigne-Nickens P, et al Left ventricular assist device as destination for patients undergoing intravenous inotropic therapy: a subset analysis from REMATCH (Randomized Evaluation of Mechanical Assistance in Treatment of Chronic

Heart Failure) Circulation 2004;110:975-981.

Yehudai L, Reynolds HR, Schwarz SA, et al Serial echocardiograms in patients with cardiogenic shock: analysis of the SHOCK

Trial J Am Coll Cardiol 2006;479(suppl A):111A.

Decreased blood pressure or symptoms of end-organ dysfunction

Two or more of the following rapidly occurring symptoms following exposure to a likely

allergen for the patient in question:

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Involvement of skin or mucosal tissue

Respiratory compromise

Decreased blood pressure or associated symptoms

Persistent gastrointestinal (GI) symptoms

Decreased blood pressure after exposure to known allergen for the patient in question

While the WAO recommends that anaphylaxis be divided into immunologic and nonimmunologicreactions (with elimination of the term “anaphylactoid”), the American Academy of Allergy, Asthma,and Immunology continues to use the term anaphylactoid to refer to non–IgE-mediated reactions thatproduce the same clinical response as anaphylaxis

(Note: Some agents can cause anaphylaxis via multiple mechanisms)

The IgE binds to high-affinity IgE receptors on the surface of mast cells and basophils

Subsequent exposure to the allergen allows surface-bound IgE to cross-link, leading to theactivation and degranulation of mast cells and basophils

This results in the release of preformed chemical mediators of anaphylaxis (e.g., histamine,tryptase, platelet-activating factor, prostaglandins, leukotrienes, cytokines, chemokines)

Other mediator cascades, such as the complement, coagulation, and kallikrein–kinin contactsystem, are also activated

Anaphylaxis is primarily categorized as a distributive shock syndrome characterized by profoundvasodilation

However, increased vascular permeability can cause massive amounts of fluid to move

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extravascularly, leading to concomitant hypovolemic shock.

Direct myocardial depression may also occur

Capillary leak syndrome

Diagnosis of anaphylaxis can be made by history and physical examination alone althoughlaboratory studies may be helpful in confirming the diagnosis

Plasma histamine levels peak 5 to 10 minutes after the onset of symptoms and remain elevatedfor 30 to 60 minutes; histamine should be measured in blood samples obtained within 30minutes of onset

Serum tryptase levels peak at 60 to 90 minutes after the onset of symptoms and persist for aslong as 5 hours; ideally, serum tryptase should be measured 30 minutes to 3 hours aftersymptom onset

Serial histamine and tryptase measurements increase the sensitivity of the tests to diagnoseanaphylaxis; comparison to baseline levels (obtained after resolution of symptoms) is helpful

A normal tryptase level does not rule out anaphylaxis For example, in food-inducedanaphylaxis, basophil involvement may predominate over mast cell involvement; so anelevation in tryptase may not be seen

Skin tests or in vitro tests can determine the presence of specific IgE antibodies to foods,medications, or stinging insects; for the majority of allergens, however, standardized skin testing isnot available

Challenge testing with the suspected agent can be considered in instances in which skin tests or invitro tests have been inconclusive or in patients who develop non–IgE-mediated reactions

Initial management of anaphylaxis:

Assess airway, breathing, and circulation Remove offending allergen

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Epinephrine is the mainstay of management and should be administered as soon as possible Aqueous epinephrine 1:1000 dilution (1 mg/mL), 0.2–0.5 mL (0.01 mg/kg in children) should beadministered IM in the anterolateral thigh every 5 minutes as necessary to control symptomsand increase blood pressure.

Clinicians should not wait for overt signs of shock to develop before administering epinephrine

as delays in epinephrine administration are associated with fatal anaphylaxis

Epinephrine should be administered even when systemic symptoms are judged to be mild

Ameliorates the clinical symptoms of anaphylaxis via its action on adrenergic receptors:alpha-1 agonist effects include vasoconstriction, increased peripheral vascular resistance, anddecreased mucosal edema; beta-1 agonist effects include increased inotropy and chronotropy;beta-2 agonist effects include bronchodilation and decreased mediator release from mast cellsand basophils

In patients who remain hypotensive, intravenous epinephrine may be required

Continuous infusions of epinephrine are superior to bolus intravenous dosing

Infusion rates should be started at a rate of 2 to 10 mcg/minute (0.1 to 1 mcg/kg/min inchildren) and titrated to hemodynamic data

Fluid management is extremely important because increases in vascular permeability can cause

as much as 35% of the intravascular volume to move extravascularly

Rapid intravenous fluid replacement should be initiated immediately

Consider H1 blockers (diphenhydramine) and H2 blockers (ranitidine or cimetidine)

These agents primarily treat the cutaneous manifestations of anaphylaxis and should never beused alone without epinephrine

Consider inhaled B-agonist (albuterol) for bronchoconstriction resistant to epinephrine

Although there is no consistent high-quality evidence supporting the role of glucocorticoids inthe management of anaphylaxis, the WAO continues to recommend their use

Glucocorticoids act too slowly to acutely improve shock, but theoretically help to preventbiphasic or protracted anaphylaxis

Other possible adjunctive therapies include glucagon (in patients being treated with blockers), vasopressin, methylene blue, and tranexamic acid

beta-Outcomes

Recurrent or biphasic anaphylaxis, which occurs when symptoms reappear following apparentresolution of the initial event, can occur up to 72 hours (mean of 10 hours) after the initialpresentation in up to 20% of patients

Protracted anaphylaxis, in which symptoms last up to 32 hours, can also occur

Biphasic or protracted anaphylaxis cannot be predicted by the severity of initial presentation, so aperiod of subsequent observation is recommended following an anaphylactic episode

There is no consensus on the optimal length of this observation period

Upon discharge, patients should be provided with an epinephrine autoinjector

Kemp SF and Lockey RF Anaphylaxis: a review of causes and mechanisms Curr Rev Allergy Clin Immunol 2002;110:341-348 Koplin JJ, Martin PE, and Allen KJ An update on epidemiology of anaphylaxis in children and adults Curr Opin Allergy Clin

immunol 2011;11:492-496.

Lee JK and Vadas P Anaphylaxis: mechanisms and management Clin Exp Allergy 2011;41:923-938.

Lieberman P, Nicklas RA, Oppenheimer J, et al The diagnosis and management of anaphylaxis practice parameter: 2010 update J

Allergy Clin Immunol 2010;126:477, e1-42.

Simons FE, Ardusso LR, World Allergy Organization, et al World Allergy Organization anaphylaxis guideline: summary J Allergy

Clin Immunol 2011;127:587-593, e1-22.

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SECTION 2

Cardiology

2.1

Coronary Artery Disease

Kenneth Shelton and Airadion Omoruan

Cigarette smoking, diabetes mellitus (DM), hypertension (HTN), hyperlipidemia, obesity, and afamily history of premature CAD are risk factors for CAD

Many of the common symptoms such as chest pain, shortness of breath, diaphoresis, and nauseathat physicians use in the outpatient setting to determine which patients are likely suffering anacute coronary event may not be routinely available to the intensivist when attempting to assessacute coronary syndrome (ACS) in the ICU patient

Classic symptoms in an awake and alert patient often include chest pressure with radiation to theleft arm/neck, diaphoresis, and nausea/vomiting These symptoms may often be masked or altered

in patients with diabetes mellitus and in female patients, with many of them presenting with little

to no classic symptoms

In an intubated patient under general anesthesia or an intensive care patient coming out of majorsurgery, the intensivist must look for other signs that ischemia is taking place, such ashemodynamic changes, difficulty weaning from the ventilator, and ECG changes Other potentialsigns include new wall motion abnormalities on echocardiography, unexplained tachycardia,increasing vasopressor requirement, or a sudden increase in pulmonary artery pressure/centralvenous pressure

Epidemiology

CAD continues to be the leading cause of death in the world and in the United States according tothe World Health Organization and the American Health Association and American StrokeAssociation’s 2006 publication on heart disease

It accounts for 7.25 million deaths a year worldwide

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CAD has been linked to the combination of several complex modifiable and nonmodifiable riskfactors—most notably high levels of LDL cholesterol, low HDL cholesterol, HTN, DM, familyhistory of CAD, and smoking Other factors such as obesity and age also serve as additional riskfactors for CAD But bear in mind that these classic risk factors might not be present in all cases Many of these risk factors are at the front of a cascade of molecular mechanisms that work together

to create disease

Biochemical markers linked to vascular inflammation as well as the upregulation/downregulation

of certain transcription pathways will likely play a key role in how we think about the process ofcoronary disease and the future of treatment options

Familiarity with the anatomy of the coronary vessels is crucial to understanding the relationshipbetween the path of each coronary vessel and the territory of the heart for which it is responsiblefor supplying blood, oxygen, and nutrients This can be extremely useful when wall motionabnormalities are identified by the intensivist who utilizes point of care echocardiography

The branches of the left circumflex coronary artery include the left obtuse marginal

The right coronary artery as previously mentioned typically supplies the posterior descendingartery

It also supplies the sinus node and is therefore responsible for dysrhythmias during ischemicevents

The right marginal branch comes off of the right coronary artery and supplies the rightventricle

Cardiac troponin I is a regulatory protein frequently used as a marker for cardiac ischemia While

it has become the standard cardiac marker it is still not a perfect test

The sensitivity of the test continues to increase without a clear understanding of how to interpretpositive results

For example, in the trauma patient anything from blunt chest trauma to demand ischemia canlead to a positive test

Elevated troponins can occur in conditions other than cardiac ischemia including sepsis,congestive heart failure (CHF) renal failure, cardiac trauma/contusion, acute pulmonaryembolism, acute pericarditis/myocarditis, and certain infiltrative cardiac disorders

Elevated troponins are often used with the ECG/echo in addition to the overall clinical picture(vasopressor changes, dysrhythmias) to guide management rather than being used as a single test

to make clinical decisions

Management of CAD can be divided into prevention and acute management

Prevention: lifestyle changes including weight loss and quitting smoking are some of the

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