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American Association of Anesthesia Assistants AAA_09_Syllabus

American Association of Anesthesia Assistants AAA_09_Syllabus

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American Association of Anesthesia Assistants CME
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cademy of A n a c i r e Am

Anesthesiologist A

ssistan ts

The Hilton Clearwater Beach Resort Clearwater, Florida

April 18 - 22, 2009

Syllabus

Message from the President

Welcome to the 33rd Annual Meeting of the American Academy of Anesthesiologist Assistants! Just as in years past, this week promises to be the biggest annual meeting in our history. Interest in the AA profession continues to grow more rapidly every year, and the best place to connect with AAs, whether in practice or in training, is at the biggest gathering of AAs in the nation, the AAAA Annual Meeting. Take advantage of the following: • • Informative lectures on a variety of topics to meet your CME needs. Access to the leadership of the AAAA, the growing number of your colleagues dedicated to getting AAs the recognition they deserve. Insights on the state of the specialty of anesthesia and the development of the relationship between the ASA and AAAA, from the perspective of keynote speaker Alex Hannenberg, ASA President-Elect. Opportunities to meet with prospective employers Information about the growing number of ways you can make a difference – Clinical instruction enrichment – Profession advocacy at the local, state, and federal level – Charitable donations – Committee involvement Conversation with AAs from student to near retirement, from every corner of the AA map.

Deborah Lawson, AA-C AAAA President

• • •

Reach out and thank our supporters, without whom our meetings would not be nearly as rich an event. Meet the AAAA office and management team from Ruggles. Join the effort to gain wider acceptance of your chosen profession. There’s no better place to do all of this than the AAAA Annual Meeting. Together we can accomplish great things, and this is our best opportunity to become the team that can deliver. Welcome!

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Table of Contents
AAAA Officers, Directors & Committees. ....................................................................................................................................................4 Course Objectives. ........................................................................................................................................................................................................5 Faculty & Disclosures..................................................................................................................................................................................................6 33rd Annual Conference Program.....................................................................................................................................................................7

Saturday April 18, 2009
8:00 am-9:00 am 9:00 am-10:00 am 10:30 am-11:30 am 11:30 am-12:30 pm 2:00 pm-3:00 pm 3:00 pm-4:00 pm Perspectives on Clinical Education.....................................................................................................................................10 Malpractice Lawsuit..........................................................................................................................................................13 The Critically Ill Obstetric Patient.......................................................................................................................................26 ASA Update.......................................................................................................................................................................36 Risk Management/Management of Adverse Events..........................................................................................................46 Perioperative Positioning Injuries and Their Prevention....................................................................................................56

Sunday April 19, 2009
12:00 pm-1:00 pm 1:00 pm-2:00 pm 2:30 pm-4:30 pm 2:30 pm-3:30 pm 3:30 pm-4:30 pm Update on Pediatric Inductions.........................................................................................................................................67 Post-Operative Nausea and Vomiting................................................................................................................................72 Clinical Instructors’ Educational Workshop........................................................................................................................76 Pediatric PACU...................................................................................................................................................................83 Medication Safety in the Operating Room........................................................................................................................88

Monday April 20, 2009
8:00 am-9:00 am 9:00 am-10:00 am 10:30 am-11:30 am 11:30 am-12:30 pm Trauma Anesthesia............................................................................................................................................................93 Can/Should Simulation Be Used for Certification Assessment of AA Students.................................................................101 Alpha-2 Agonists for Sedation and General Anesthesia...................................................................................................110 Cardiac Output after the Pulmonary Artery Catheter.......................................................................................................114

Tuesday April 21, 2009
8:00 am-9:00 am 9:00 am-10:00 am 10:30 am-11:30 am 11:30 am-12:30 pm Future Directions in Anesthetic Pharmacology................................................................................................................116 Intraoperative Fluid Management..................................................................................................................................139 Perioperative Temperature Management........................................................................................................................164 Lipid Rescue for Local Anesthetic Toxicity........................................................................................................................180

Wednesday April 22, 2009
8:00 am-9:00 am 9:00 am-10:00 am 10:30 am-11:30 am Myocardial Ischemia and Postoperative Monitoring........................................................................................................193 CAAHEP/ARC-AA Update.......................................................................................................................................................... 200 Preoperative Cardiac Evaluation............................................................................................................................................... 201

Product Descriptions..............................................................................................................................................................................................248 Exhibitor Floor Plan & Hours............................................................................................................................................................................250 Conference Supporters & Exhibitors.........................................................................................................................................................251
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Annual Conference Committee
Chris Caldwell, AA-C
Committee Chair

Carie Twichell, AA-C
Committee Vice Chair

AAAA Officers & Directors
PRESIDENT Deborah Lawson, AA-C PRESIDENT-ELECT Pete Kaluszyk, AA-C SECRETARY Ellen Allinger, AA-C TREASURER Barry Hunt, AA-C IMMEDIATE PAST PRESIDENT Mike Nichols, AA-C DIRECTOR #1 Joe Rifici, AA-C DIRECTOR #2 Saral Patel, AA-C DIRECTOR #3 Bradley J. Maxwell, AA-C DIRECTOR #4 Lance Franklin, AA-C DIRECTOR #5 Len Boras, AA-C DIRECTOR #6 Rob Wagner, AA-C, RRT DIRECTOR #7 Carie Twichell, AA-C

AAAA Committees
Executive Committee President, Chair.............................................................Deborah Lawson President-Elect.................................................................. Pete Kaluszyk Treasurer.................................................................................Barry Hunt Secretary............................................................................Ellen Allinger Immediate Past President....................................................Mike Nichols By-laws and Ethics Committee Chair....................................................................................... Saral Patel Vice-Chair........................................................................ Claire Chandler Communications Committee Chair................................................................................... Sarah Russell Vice-Chair (External)........................................................Lauren Hojdila Vice-Chair (Internal)..............................................................Leslie Dean Newsletter Co-Editors................................Tiffany Lewis-Roberts and Alyson Finamore Committee on Education and Practice Chair....................................................................................Mike Nichols Vice-Chair for Practical & Clinical Instruction...........................Joe Mader Vice-Chair for Education............................................................ Joe Rifici Finance Committee Chair.......................................................................................Barry Hunt Vice-Chair............................................................................Mike Nichols
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Membership Committee Chair................................................................................. Amie Schilling Vice-Chair.........................................................................Lauren Hojdila National Affairs Committee Chair...................................................................................Ellen Allinger Vice-Chair............................................................................Mike Nichols Nomination and Elections Committee Chair....................................................................................Mike Nichols Student Committee Chair..................................................................... Gudron Henry (South) Website Committee Chair............................................................................................. vacant Delegate Assembly Co-Speakers.................................................. Dave Biel and Shane Angus Leadership Development Council Director........................................................................... Claire Chandler Committee for Community Initiatives Chair.................................................................................. Carie Twichell Vice-Chair..............................................................................Jen Jackson Data Collection Taskforce Chair................................................................................Megan Varellas

American Academy of Anesthesiologist Assistants

33rd Annual Conference
Target Audience
Certified anesthesiologist assistants, anesthesiologist assistant educational program directors, and students in an accredited anesthesiologist assistant educational program will benefit from attending this meeting.

Overall Conference Objective
This conference is designed to update those who care for patients whose surgery or procedure requires the participation of the anesthesia care team. Based on comments from past conference participants, this year’s sessions are devoted to various aspects of anesthesia practice, including perioperative and postoperative issues, pediatrics, medication safety, risk management, and updates from ASA, CAAHEP and the ARC-AA. Upon completion of this course, the attendee will have a better understanding of the topics presented, have the most up to date information from the ASA, CAAHEP, and the ARC-AA, and have seen what the AAAA has done, and is continuing to do, to advance and improve the AA profession.

Statement of Need
The successful outcome of each surgery or procedure requiring anesthesia is dependent upon the knowledge and teamwork of the anesthesia care team. Ultimately, the purpose of this course is to enhance the care of the patient that requires the services of the anesthesia care team. This program is also designed to enhance the educational and professional growth of anesthesiologist assistant students.

Hilton Clearwater Beach Resort Resort Hilton Clearwater Beach

Accreditation by the American Academy of Physician Assistants
This program has been reviewed and is approved for a maximum of 21 hours of AAPA Category I CME credit by the Physician Assistant Review Panel. Physician assistants should claim only those hours actually spent participating in the CME activity. This program was planned in accordance with AAPA’s CME Standards for Live Programs and for Commercial Support of Live Programs. Participants attending the Certification Review Course may claim a maximum of 3 hours of AAPA Category I CME credit by the Physician Assistant Review Panel.
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AAAA 33rd Annual Conference Faculty
Ellen Allinger, AA-C, MMSc Secretary, AAAA; National Affairs Committee Chair Anesthesia Associates of Rock Hill Rock Hill, NC Shane Angus, MS, AA-C Assistant Program Director Assistant Professor Anesthesiologist Assistant Program Nova Southeastern University Fort Lauderdale, FL Ann Bailey, MD Professor of Anesthesiology and Pediatrics University of North Carolina Chapel Hill Chapel Hill, NC Claire Chandler, AA-C Faculty Physician Assistant Education Program University of Manitoba Winnipeg, MB, Canada John E. Ellis, MD Adjunct Professor, Department of Anesthesiology and Critical Care University of Pennsylvania School of Medicine Philadelphia, PA Tong J. Gan, MB, BS, MHS, FRCA Professor and Vice Chair Duke University Medical Center Durham, NC Alexander A. Hannenberg, MD President-Elect, ASA Newton-Wellesley Hospital Newton, MA Gerald A. Maccioli, MD, FCCM ASA Director (NC), Chair ASA Section on Education & Research Critical Health Systems of North Carolina Raleigh, NC Joseph P. Mader, RN, AA-C Vice Chair, Education & Practice Committee Staff Anesthetist Mercy Anesthesiologists Springfield, OH Tricia A. Meyer, PharmD Director of Pharmacy, Assistant Professor of Anesthesiology Scott and White Healthcare System Temple, TX Robert C. Morell, MD Editor, APSF Newsletter Clinical Associate Professor of Anesthesiology Wake Forest University School of Medicine Adjunct Clinical Associate Professor of Anesthesia University of Florida College of Medicine Staff Anesthesiologist-Twin Cities Hospital Niceville, FL Michael S. Nichols, AA-C, MSA Immediate Past President; Chair, Education & Practice Committee; Vice Chair, National Affairs Committee Assistant Program Director & Assistant Professor Anesthesiologist Assistant Program Nova Southeastern University Fort Lauderdale, FL Roy G. Soto, MD Director of Anesthesiology Education Beaumont Hospitals Royal Oak, MI Matthew W. Zeleznik, MD Anesthesiologist Physician Specialists in Anesthesia Atlanta, GA Joel Zivot, MD Associate Professor, The University of Manitoba, Department of Anesthesiology; Director, Intensive Care Unit, Cardiac Sciences Program, Winnipeg Regional Health Authority; Medical Director, ICCS Cardiac Sciences Program St. Boniface General Hospital Winnipeg, MB, Canada

Disclosure Key
1. Honorarium 2. Consultant 3. Grants/Research Support 4. Stock Shareholder 5. Other Financial or Material Support 6. Speakers’ Bureau 7. No Relationship with Commercial Supporters 8. Employee

Disclosures
Shane Angus, AA-C...........................................7 Ann Bailey, MD..................................................7 Chris Caldwell, AA-C..........................................7 Claire Chandler, AA-C............. No Disclosure Provided John E. Ellis, MD Baxter, The Medicines Company..................6 Tong J. Gan, MD Baxter.........................................................1 Schering Plough, MGI, Baxter, Edwards Lifescience....................................3 Alexander A. Hannenberg, MD..........................7 Gerald A. Maccioli, MD, FCCM............................7 Joseph P. Mader, RN, AA-C.................................7 Patricia Meyer, PharmD Merck..........................................................3 Abbott........................................................6 Robert C. Morell, MD.........................................7 Michael S. Nichols, AA-C Advance Education Solutions, LLC...............8 Roy Soto, MD.....................................................7 Carie M. Twichell, AA-C......................................7 Matt Zeleznik, MD.............................................7 Joel Zivot, MD....................................................7

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33rd Annual Conference Program
Friday April 17, 2009
3:00 pm-5:00 pm 5:00 pm-8:00 pm Early Registration Board of Directors Meeting

Saturday April 18, 2009
7:00 am-4:30 pm 7:30 am-8:00 am 8:00 am-9:00 am 9:00 am-10:00 am 10:00 am-10:30 am 10:30 am-11:30 am 11:30 am-12:30 pm 12:30 pm-1:00 pm 1:00 pm-2:00 pm 1:00 pm-3:00 pm 2:00 pm-5:00 pm 2:00 pm-3:00 pm 3:00 pm-4:00 pm 4:30 pm-5:30 pm 6:00 pm-8:00 pm
concurrent sessions

Registration Continental Breakfast with Exhibitors Perspectives on Clinical Education Shane Angus, AA-C / Joseph P. Mader, RN, AA-C Malpractice Lawsuit Gerald A. Maccioli, MD Coffee Break and Committee Meet and Greet with Exhibitors The Critically Ill Obstetric Patient Gerald A. Maccioli, MD ASA Update Alexander A. Hannenberg, MD Honor Awards Presentation Lunch with Exhibitors Leadership Lunch Certification Review Course Carrie Twichell, AA-C / Joel Zivot, MD Risk Management/Management of Adverse Events Robert Morell, MD Perioperative Positioning Injuries and Their Prevention Robert Morell, MD President’s Reception (For distinguished guests and President’s Club members) Welcome Reception

Blood Drive
Saturday, April 18 8 am – 5 pm Sunday, April 19 11 am – 5 pm Mandalay Room

Sunday April 19, 2009
7:00 am-5:00 pm 8:00 am-11:00 am 11:00 am-12:00 pm 12:00 pm-1:00 pm 1:00 pm-2:00 pm 2:00 pm-2:30 pm 2:30 pm-4:30 pm 2:30 pm-3:30 pm 3:30 pm-4:30 pm
concurrent sessions

Registration Breakfast, Annual Business Meeting, Delegate Assembly Break with Exhibitors Update on Pediatric Inductions Ann Bailey, MD Post-Operative Nausea and Vomiting Tricia A. Meyer, PharmD Coffee Break with Exhibitors Clinical Instructors’ Educational Workshop Shane Angus, AA-C Pediatric PACU Ann Bailey, MD Medication Safety in the Operating Room Tricia A. Meyer, PharmD

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4:30 pm-5:00 pm 5:00 pm-6:00 pm 6:00 pm-8:00 pm

Break with Exhibitors Jeopardy—No CME credit awarded Student Social and Job Fair in Exhibit Area

Monday April 20, 2009
7:00 am-5:30 pm 7:30 am-8:00 am 8:00 am-9:00 am 9:00 am-10:00 am 10:00 am-10:30 am 10:30 am-11:30 am 11:30 am-12:30 pm 11:30 am-12:30 pm 12:30 pm-2:00 pm 2:00 pm-4:00 pm 4:00 pm-5:00 pm
concurrent sessions

Registration Continental Breakfast Trauma Anesthesia Roy Soto, MD Can/Should Simulation Be Used for Certification Assessment of AA Students Michael S. Nichols, AA-C Coffee Break Alpha-2 Agonists for Sedation and General Anesthesia Roy Soto, MD Cardiac Output after the Pulmonary Artery Catheter Joel Zivot, MD AA Spokesperson Training/Mock Legislative Committee Hearing (Leadership)—No CME credit awarded Ellen Allinger, AA-C, MMSc Lunch on Own Student Forum Student Spokesperson Training Shane Angus, AA-C

Tuesday April 21, 2009
7:00 am-12:00 n 7:30 am-8:00 am 8:00 am-9:00 am 9:00 am-10:00 am 10:00 am-10:30 am 10:30 am-11:30 am 11:30 am-12:30 pm 2:00 pm Registration Continental Breakfast Future Directions in Anesthetic Pharmacology Tong J. Gan, MD Intraoperative Fluid Management Tong J. Gan, MD Coffee Break and Committee Meet and Greet Perioperative Temperature Management Matt Zeleznik, MD Lipid Rescue for Local Anesthetic Toxicity Matt Zeleznik, MD 2nd Annual AAAA Golf Scramble

Wednesday April 22, 2009
7:00 am-12:00 n 7:30 am-8:00 am 8:00 am-9:00 am 9:00 am-10:00 am 10:00 am-10:30 am 10:30 am-11:30 am Registration Continental Breakfast Myocardial Ischemia and Postoperative Monitoring John Ellis, MD CAAHEP/ARC-AA Update Claire Chandler, AA-C Coffee Break Preoperative Cardiac Evaluation John Ellis, MD

8

Saturday, April 18

Saturday April 18, 2009
7:00 am-4:30 pm 7:30 am-8:00 am Registration Continental Breakfast with Exhibitors Perspectives on Clinical Education Shane Angus, AA-C / Joseph P. Mader, RN, AA-C Malpractice Lawsuit Gerald A. Maccioli, MD Coffee Break and Committee Meet and Greet with Exhibitors The Critically Ill Obstetric Patient Gerald A. Maccioli, MD ASA Update Alexander A. Hannenberg, MD Honor Awards Presentation Lunch with Exhibitors Leadership Lunch (by invitation only) Certification Review Course Carrie Twichell, AA-C / Joel Zivot, MD Risk Management/Management of Adverse Events Robert Morell, MD Perioperative Positioning Injuries and Their Prevention Robert Morell, MD President’s Reception (For distinguished guests and President’s Club members) Welcome Reception

8:00 am-9:00 am 9:00 am-10:00 am 10:00 am-10:30 am

10:30 am-11:30 am 11:30 am-12:30 pm
concurrent sessions

12:30 pm-1:00 pm 1:00 pm-2:00 pm 1:00 pm-3:00 pm

2:00 pm-5:00 pm 2:00 pm-3:00 pm 3:00 pm-4:00 pm 4:30 pm-5:30 pm 6:00 pm-8:00 pm

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Perspectives on Clinical Education
Shane Angus, AA-C / Joseph P. Mader, RN, AA-C
Objective: At the conclusion of this course, the participant will 1) comprehend the significance of clinical education; 2) recognize differing student learning approaches; 3) understand the distinct clinical preceptor types; and 4) appreciate clinical feedback methods.

10

1 2 3

Approaches to and Styles of Learning Approach to Learning Approach to Learning
Outcome Surface Superficial level of understanding May have knowledge of factual information Strategic Verbal level of understanding Depends on course requirements and methods of assessment

4

Approach to Learning
Outcome Deep Integrates principles with facts Uses evidence to develop arguments Deep level of understanding

5 6

What are learning styles? Different Learning Styles
There are more than 50 different learning styles. The following are the 4 main learning styles that have been identified by Honey & Mumford:

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Active Learners
Activists… Are open minded and enthusiastic about new ideas Enjoy doing things Like to be involved Active learners learn more effectively when… They get involved in new experiences They work with others in groups and role play Chairing meetings and leading discussions Active learners learn less effectively when… Listening to lectures Following precise instructions They are reading, writing or thinking on their own

11

8

Reflective Learners
Reflectors…. Like to look at a situation from different perspectives Prefer to listen to the views of others before offering their own Think carefully before coming to a conclusion Reflective learners learn more effectively when… They have had chance to think about what they have learned They have the opportunity to observe individuals or groups at work They produce work without deadlines to meet Reflective learners learn less effectively when… They are performing in front of others They have no time to prepare

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Theoretical Learners
Theorists… Are analytical rather than subjective in their thinking Like to think things through in a logical order Tend to be perfectionists Theoretical Learners learn more effectively when… They have to use their skills and know how They have a clear purpose They are given the opportunity to question what they are learning Theoretical Learners learn less effectively when… They have to express emotions and feelings (i.e. role play) Instructions are poor

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Pragmatic Learners
Pragmatists… Like to try things out Can be impatient, practical and down to earth Pragmatic learners learn most effectively when… They can try out techniques and get feedback Advantages of differing techniques are made obvious There is a link between what they are learning and the task in hand Pragmatic learners learn less effectively when… They cannot see how they will benefit from what they are learning Learning is all ‘theory’ There are no instructions on how to do something

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Malpractice Lawsuit
Gerald A. Maccioli, MD
Objective: At the conclusion of this course, the participant will be able to have a more complete understanding of the medical-legal interface and how to more actively participate if they are named in a lawsuit.

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Being on Trial:
Analysis of a lawsuit from the perspective of the defendant Gerald A. Maccioli, MD, FCCM
ASA Director, North Carolina ASA Section Chair, Education & Research

November 29, 2001

Case posted by Orthopaedics
  

Estimated 4 hours Autologous: 2 units Cell saver requested

Proper Consent

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PrePre -Op Workup

Intraoperative Record: Documentation?

15

10:05 Cellsaver started

Timing of fluids

Documentation during Code

Code Sheet

16

 

Meeting with family Late notes

Lawsuit is filed November 26, 2003

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Deposition Process
49 depositions total between May 19, 2004 and February 24, 2006

Gerald A. Maccioli, MD
June 22, 2004 12:1012:10-2:15 p.m. (2 hours 5 minutes)

Michele Weaver, CRNA
June 21, 2004 3:353:35-5:42 p.m. (2 hours 7 minutes)

Mediation
   

Bill Faison asked for 8 million dollars. Decedents spouse present. Defendants required to be there. Themes:
– “Textbook case of negligence” – Failure to report case to FDA – Husband’s search for the truth

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Trial
 

Set for August 28, 2006. 5 weeks long (6 weeks with Judge’s vacation) vacation). Surgeon [dismissed] and hospital [financial settlement], not at trial.

Jury Selection

Jurors’ Occupations
             

Captain American Eagles Internet Book seller SAS Tech Support Analyst Retired GE software engineer Siemens Medical software integration Medical Tech for French lab equipt equipt. Nuclear Engineer Retired NCSU secretary Progress Energy Engineer Manager Web Application Developer Watson Electric supervisor commercial construction 401k/Pension Administrator Bayer Crop Science Food Lion Customer Service Manager

Plaintiff’s Case

Plaintiffs Experts

David Eckmann, MD, PhD - University of Pennsylvania Armen Bogosian, MD - retired anesthsiologist from Seattle [frequent flyer on the Med Mal circuit] Jonathan Benumof, MD - UC San Diego [million dollar earning med mal expert]

19

Eckmann

20

Bogosian

21

22

Benumof

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Judge’s Instructions
I instruct you that negligence is not to be presumed from the mere fact of injury. j y

On this issue the burden of proof is on the plaintiff. This means that the plaintiff must prove, by the greater weight of the evidence, that the defendants were negligent and that such negligence g g was a proximate cause of the death of Patricia Scott. Negligence refers to a person's failure to follow a duty of conduct imposed by law.

Every health care provider is under a duty
 

1. to use his or her best judgment in the treatment and care of their patient; 2. to use reasonable care and diligence in the application of his or her knowledge and skill to their patient's care; and, 3 to provide health care in accordance 3. with the standards of practice among members of the same health care profession with similar training and experience situated in the same or similar communities at the time the health care is rendered.

The plaintiff not only has the burden of proving negligence, but also that such negligence was a proximate cause of the injury. Proximate cause is a cause which in a natural and continuous sequence produces a person's injury, and is a cause which a reasonable and prudent health care provider could have foreseen would probably produce such injury or some similar injurious result. There may be more than one proximate cause of an injury. Therefore, the plaintiff need not prove that the defendant's negligence was the sole proximate cause of the injury. The plaintiff must prove, by the greater weight of the evidence, only that the defendant's negligence was a proximate cause.

Proximate Cause

There may be more than one proximate cause of [an injury] [damage]. Therefore, the plaintiff need not prove that the defendant’s negligence was the sole proximate cause of the [injury] [damage]. The plaintiff must prove, by the greater weight of the evidence, only that the defendant’s negligence was a proximate cause. – Proximate cause is: – a cause which in a natural and continuous sequence produces a person’s [injury] [damage] and is – a cause which a reasonable and prudent health care provider could have foreseen would probably produce such [injury] [damage] or some similar injurious result.

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1.

Was the death of Patricia Scott caused by negligence of Gerald Maccioli? Answer:

1.

Was the death of Patricia Scott caused by negligence of Gerald Maccioli? Answer:

NO

2.

Was the death of Patricia Scott caused by negligence of Michele Weaver? Answer:

2.

Was the death of Patricia Scott caused by negligence of Michele Weaver? Answer:

NO

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The Critically Ill Obstetric Patient
Gerald A. Maccioli, MD
Objective: At the conclusion of this course, the participant will have a more complete understanding of critical illness in the pregnant patient and the anesthetic implications.

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30

31

32

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ASA Update
Alexander A. Hannenberg, MD
Objective: At the conclusion of this course, the participant will be more informed on the recent initiatives of the American Society of Anesthesiologists in advancing the quality of anesthetic care and the education of anesthesia providers nationwide.

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Achieving Excellence, Providing Value

Alexander A. Hannenberg, M.D.
President Elect American Society of Anesthesiologists Tufts University School of Medicine Newton-Wellesley Hospital Newton, MA

Agenda

 What’s going on at ASA?  Our education & research mission  Advocacy achievements & challenges

Organizational Improvement
 Strategic Plan  Staffing needs assessment  Human Resources Director
 Personnel performance assessment  Compensation/Benefits Policy

 Upgraded Budget & Accounting  Information Technology Assessment  Integrate Park Ridge, Washington activities  Business Model for Subspecialty Support

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Specialty Society Horsepower

2006

John A. Thorner, J.D.
Executive Vice President - Park Ridge

 J.D. (Georgia), M.A.

   

Journalism (Columbia), B.A. (Duke) Washington Post, Associated Press Board of Directors, ASAE Exec Director, Natl Recreation & Parks Assn. Exec Director, Optical Society of America

A Varsity Team

Dawn Glossa, M.P.A. Director of Communications

Robert Fine, J.D. Director of Subspecialty Societies

Jason Byrd, J.D. Associate Director (DC) Practice Mgmt & Quality Initiatives

Tom Conway, M.B.A., C.P.A. Chief Financial Officer

Celeste Kirschner Director of Member Services

Michael E. Parker, M.P.A. Director of Information Services

Karen Buehring, M.B.A. Director of Human Resources

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Non Dues Revenue
 Enhanced Revenue from Existing Programs
 Annual Meeting Exhibitor Contracting  Newsletter Advertising

 New Programs/Services for Members
 Coding Webinar

 Products for Non-Anesthesiologists
 Coding and Billing Instruction  Training in Moderate Sedation

Financial Downturn & ASA
 

2009 Operating Budget: 6.7% from Spendable Account

$2 million

Revenue from Industry at Risk
  

Advertising Meeting Exhibits Foundation support

Member Earnings
   

Unemployment --> Uninsured Decline in Elective Surgical Procedures Hospital Closures Travel/Meeting Restrictions

Anesthesia Quality Institute
 ASA-Related 501c3 Charitable Foundation  Owner & Operator of Anesthesiology’s National

Clinical Registry
 Quality Benchmarking  Integration with Subspecialty and Surgical Registries  Credentialing: Hospital and Health Plan  MOCA  Public Reporting  Clinical Research

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FAER Research Support
1995-2007

Safety Research Funding

Annual Meeting Content Growing

Program Growth 2002-2008

40

Simulation Registry

http://simulation.asahq.org/search/index.asp

Money
 Medicare Payment
 Sustainable Growth Rate  Anesthesia Conversion Factor  Teaching Penalty

Annual Economic Value of Advocacy
Specialty Conversion Factor SGR Relief Teaching Rule Coding Changes $400 M $170 M $50 M $300 M Member $13,000 $5,700 $11,000* $10,000

$920 M

$39,700
30,000 Active Members 4,500 Teaching Anesthesiologists

41

Medicare Physician Payments vs Inflation
Impact of Sustainable Growth Rate Formula

SGR Reform Alternative

Budget Options, Vol. I: Health Care. Congressional Budget Office, Dec 2008

Payment Issues in Pain Medicine
ASA Advocacy  Five Year Review: E&M Increases  Practice Expense Methodology
 Further Update Pending Survey Results

 Imaging Services - ↑ Volume ↓Payments  Work Value Reassessment (Survey Responses)
 High Volume  3rd Five Year Review

 OIG: Facet Coding Incorrect  Pump Refills & Compounded Drugs

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Health Care Reform 2009
Anesthesiology Watch List

 Expanded Health Insurance Coverage

Increase in Government Based Programs

Application of Medicare Payment Formula

 “Innovative” Payment Methodology

Bundled Payments as alternative to Fee-for-Service
  

Episode Treatment Groups Prometheus System Acute Care Episode Demonstration

Health Care Reform 2009
Anesthesiology Watch List

 Newly Insured Seek Elective, Preventive

Services

Massachusetts Universal Coverage Mandate

 Demand for Services > Physician Capacity
 

Primary Care Opportunity Non-Physician Opportunity

Physician Supply & Demand
Primary Care Non-Primary Care

Physician Supply and Demand: Projections to 2020, U.S. Department of Health and Human Services, Health Resources and Services Administration , Bureau of Health Professions October 2006

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Are Primary Care Recruitment Problems Economic in Origin?
Relationship of medical student debt to specialty choice:

Rosenblatt RA, Andrilla HCA
(n=14,240)

Acad Med 2005; 80:815

“the effect was modest” [OR=0.96]

Kahn MJ, Markert RJ et al
(n=2,022)

MedGenMed 2006:8(4)

“…total debt was not a predictor of a primary care residency…”[p=0.64]

Hauer KE, Durning SJ et al
(n=1,177)

JAMA 2008;300(10):1154

“…debt was not related to specialty choice.” [p=0.37]

Annual Graduating Class Size

Point, Click and You’re a Doctor
On-Line Doctor of Nursing Practice Degree

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Who is a Licensed M.D. ?
n=1001

2006

Anesthesiologists: Physicians Providing the Lifeline of Modern Medicine

ahannenberg@partners.org

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Risk Management/Management of Adverse Events
Robert Morell, MD
Objective: At the conclusion of this course, the participant will be able to 1) understand the nature of perioperative risk; 2) appreciate the importance of eliminating the culture of blame and focusing on system approaches; 3) appreciate the importance of audible alarms and 4) become familiar with medication errors, their causes and prevention.

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Risk Management and Management of Adverse Events Robert C. Morell, MD

Key Concepts
Risk Management and Management of Adverse Events
Robert C. Morell, MD Editor: APSF Newsletter Clinical Associate Professor of Anesthesiology Wake Forest University School of Medicine Adjunct Clinical Associate Professor University of Florida College of Medicine Fort Walton Beach Anesthesia

• • • • •

Risk can never be zero Goal is six-sigma Eliminate culture of blame Focus on system fixes Foster teamwork and team training

Six Sigma Perspective
• Would you fly on an airplane with 99% reliability? • Would you fly on an airplane with 99.9% reliability? • Would you fly on an airplane with 99.99% reliability?

99.99% Reliability sounds pretty darn good, doesn’t it?

99.99% reliability
• 1:10,000 • Charlotte Douglas airport has over 500 arrivals and departures per day • 1:10,000 means 1 crash every 20 days 
    

If 99.9% Reliability is OK
We would expect:
500 incorrect surgeries each week 20,000 incorrect prescriptions filled annually 16,000 pieces of mail lost each hour 19,000 babies dropped at birth each year 22,000 paychecks incorrectly posted each hour Your heart will fail to beat 32,000 times per year

UNACCEPTABLE

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HRO: High Reliability Organization
• Failure free operation despite:
– High tempo – Varying conditions – Production pressures – Changing personnel

Flattening the Hierarchy

Flattening the hierarchy
• Anyone on the team can, and should, speak out without fear of reprisal • Input of everyone is valuable and important • Numerous aviation examples

Flattening the hierarchy
• Military plane in flight • Pilot requests permission to climb to 35,000 feet • Tower responds, transmission a bit hard to hear • Pilot believes he is granted permission • Young airman interrupts and says he heard differently

Don’t be afraid to speak up Don’t be too proud to listen • 30 seconds later a 2nd plane flies by 500 feet above the first plane • Airman’s willingness to speak up saved a lot of lives

An Active Process is Needed 
HRO approach to safety requires a top down approach  Production pressures cannot be allowed to erode safety  All participants must “buy in”

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Intensive Training During Routine Operations and In Simulations

HRO Lessons Learned
Teams & Microsystems are critical • Interchangeable parts model (any nurse, any MD) will not always work • Need to create & foster real teams • Train intensively about and/or in teams • Flatten the hierarchy • Enhance Communication Find system fixes, not individual fixes • If one individual “screws up”, others probably will too • System has to be resilient against individual failures

Train the system, not just the individual Over entire career, not just the beginning

Tying this together
– Strive toward 6 Sigma Reliability (HRO) – Eliminate the culture of blame – Enhance communication – Proactively examine processes (FMEA) – Retroactively examine errors (RCA)

Clinical Alarms
• Clinical alarms are often turned off • Do you always have your audible alarms turned on?

Why bother with those pesky alarms? Case #1
• • • • 23 y.o. healthy male for laparoscopic BIHR First such procedure in this hospital – filmed General anesthesia with Isoflurane & Atracurium Anesthesiologist left head of bed to watch film crew and see video monitors • Surgeon switched sides and anesthesiologist returned to HOB

Why bother with those pesky alarms? Case #1 • Disconnect at the Y-piece, full arrest • Visual alarms flashing but audio had been silenced • Severe permanent brain damage

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Isolated occurrence?
Case #2 • 32 y.o. female for laparoscopic chole • Plain film shot during cholangiogram • Ventilator turned off during x-ray to minimize artifact

We have all been there
Case #2
• X-ray tech had trouble removing cassette from under table • Anesthesiologist tried to help, but bed gears became jammed • X-ray finally removed…surgery resumed • Anesthesiologists looks at monitor and sees severe bradycardia • Ventilator had been off for many minutes • Patient died

No one can be vigilant 100% of the time Case #3

Alarms protect our patient and protect us Case #3

• 54 year old for ORIF of ankle under SAB • Patient sedated and snoring loudly • Spinal wearing off, patient became restless and agitated • Additional fentanyl and midazolam given • Patient moving hands and knocking pulse oximeter off of his finger • Alarm silenced

• Anesthesiologist goes to foot of table to ask surgeon how much longer • Engages in chit-chat while watching closure • Case over, drapes removed, patient agonal and cyanotic • Profound brain damage after resuscitation

Can this happen to me?
• All 3 of these cases are real cases • Files of a malpractice carrier • All would have been prevented by audible alarms • No one can be 100% vigilant 100% of the time • When interviewed the anesthesiologists said things like “I just got distracted, it seemed like such a short time.”

It is Now Standard of Care
ASA Standards for Basic Anesthetic Monitoring - October 2005

When the pulse oximeter is utilized, the variable pitch pulse tone and the low threshold alarm shall be audible to the anesthesiologist or the anesthesia care team personnel. When capnography or capnometry is utilized, the end tidal CO2 alarm shall be audible to the anesthesiologist or the anesthesia care team personnel.

You Bet it Can

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Institute of Medicine 
44,000-98,000 annual deaths due to preventable medical error 50% of adverse drug reactions due to error ADR adds 4.6 extra hospital days and costs $5,800 per event

Magnitude of Drug Errors
• 1990 Harvard study of New York hospitals
– 19.4% of errors were medication related

• Analysis of 289,000 medication orders
– Error rate was 3.1/1000 written orders – Significant errors were 1.8/1000 written orders

• Pediatrics = high risk
– 4.9 errors/1000 – 27/479 errors were potentially lethal

How Errors Occur
(wrong drug prescribed) 1st Defense (distracted nurse) 2nd Defense (pharmacy)

How Errors Can Be Prevented
(wrong drug prescribed) 1st Defense (distracted nurse) 2nd Defense (pharmacy)

TRIGGER

TRIGGER

Latent failure (understaffing) Latent failure (no Rx tracking) Latent failure (understaffing)

Latent failure (understaffing) Latent failure (no Rx tracking) Latent failure (understaffing)

Defense (another distracted nurse)

3rd

Defense (vigilant nurse)

3rd

Adverse Event Averted
Sources: Reason J Human error: Models and Management, BMJ, 18 March 2000. Cook R. University of Chicago, 1991-99.

EVENT

Enhanced Communication
• Communication is a two way street • Clarity and accuracy are important for both written and verbal communication • Use repeat back! • COE improves accuracy • Don’t assume – catastrophe can follow

Australian Incident Monitoring Study
• • • • • 2000 incident reports 117 events where wrong drug given 27 events wrong drug nearly given 74% had potential for serious harm 93% involved syringes/50% were correctly labeled

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Common Causes of Medication Errors Miscommunication of Drug Orders
• Written prescriptions - legibility • Look-alike names • Sound-alike names • Misuse of decimal points and zeroes • Inappropriate abbreviations • Misuse of metric and apothecary measures • Ambiguous or incomplete orders

Goals for Drug Safety
• Correct drug • Correct dose (death by decimal - 0.1 vs 1.0) • Correct timing • Correct route of administration • Correct concentration • Correct documentation

Type of Drug Administration Errors
• Misidentification or a vial, ampoule, or prefilled syringe • Mislabeling or a syringe • Syringe swap • Right drug but wrong concentration • Right drug but wrong route of administration

Typical Intraoperative Work Surface

Labels Can Make or Break You

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Look Alike Pitfalls

Visual Clues Can Fail

The Simple Things Can Get You

Read the Label 3 Times
• When you draw up the drug • When you attach the syringe • When you administer the drug

Visual Clues Can Fail

One Must Read the Label

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More Needs to be Done

So what do we do when an error occurs? • • • • Take care of the patient Take care of the family Take care of the providers Take care of the system

Taking care of the patient
• • • • Incident supervisor Immediate care/ resuscitation Follow up care Appropriate consultation

Taking care of the family
• Full Disclosure • OK to say you are sorry • Support
– Clergy – Location – Privacy – Administration

Full disclosure after adverse events
• • • • Recent mandate Old fears loosing credence May actually decrease liability losses Patients and family deserve and need disclosure • Numerous examples support this • • • •

Full disclosure
Beginning to be protected OK to say you are sorry Sorryworks.net Once again, good communication is key!

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Full Disclosure
• Shows respect for the patient, acknowledges the hurt • Re-establishes trust • Assures patient they were not at fault • Reassures patient against further harm • Shows provider is “suffering” too – levels the playing field

Full Disclosure
“Apologizing may be the most important thing that we do after an serious event, both to help the patient begin to heal and to heal ourselves”
Lucian Leape Adjunct Professor of Health Policy Harvard School of Public Health Co-Founder of the NPSF

Disclosure reduces Liability
• Children's hospital of Minneapolis has seen nearly a 50% drop in malpractice lawsuits since it began the full disclosure program.

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Perioperative Positioning Injuries and Their Prevention
Robert Morell, MD
Objective: At the conclusion of this course, the participant will be able to 1) identify the most common position related injuries; 2) appreciate predisposing factors and the etiology of position related injuries and 3) become familiar with the types of perioperative visual loss and risk factors, and the diagnosis of these injuries.

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Sunday, April 19

Sunday April 19, 2009
7:00 am-5:00 pm 8:00 am-11:00 am 11:00 am-12:00 pm Registration Breakfast, Annual Business Meeting, Delegate Assembly Break with Exhibitors Update on Pediatric Inductions Ann Bailey, MD Post-Operative Nausea and Vomiting Tricia A. Meyer, PharmD Coffee Break with Exhibitors Clinical Instructors’ Educational Workshop Shane Angus, AA-C Pediatric PACU Ann Bailey, MD Medication Safety in the Operating Room Tricia A. Meyer, PharmD Break with Exhibitors Jeopardy—No CME credit awarded Student Social and Job Fair in Exhibit Area

12:00 pm-1:00 pm 1:00 pm-2:00 pm
concurrent sessions

2:00 pm-2:30 pm

2:30 pm-4:30 pm 2:30 pm-3:30 pm 3:30 pm-4:30 pm 4:30 pm-5:00 pm 5:00 pm-6:00 pm 6:00 pm-8:00 pm

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Update on Pediatric Inductions
Ann Bailey, MD
Objective: At the conclusion of this course, the participant will understand the common methods of premedication and induction of anesthesia including having parents present in the operating room.

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Induction Techniques in Children: 2009 Ann Bailey M.D. FAAP When discussing pediatric induction techniques, one must consider premedication options, whether parents will participate in the actual induction event, and which pharmacologic agents will be used for the induction. While some feel that premedication is not necessary, others have demonstrated that decreasing the anxiety of the child may improve postoperative outcomes and may increase parental satisfaction. Premedication can involve many different drugs and routes of administration. Midazolam is the most commonly used pediatric premedication in the United States. It can be used intranasally in a dose 0.2 mg/kg with rapid bioavailability (5-10 min). A burning sensation in the nose and bitter taste on the posterior tongue make this less pleasant than oral midazolam. When using the commercial oral preparation (Roche), 0.5 mg/kg was found to be the minimally effective dose for a decrease in anxiolysis within 20 minutes. The IV preparation used orally may be better absorbed and therefore work more quickly. Most anesthesiologists use a maximum dose of 20 mg PO. Midazolam can be used rectally (0.3-1 mg/kg) or IM (0.1 mg/kg) but usually require specific indications. Ketamine is another drug with multiple routes of administration. It can be used nasally (3-5 mg/kg), rectally (5-10 mg/kg), IM (2-5 mg/kg), or PO (3-9 mg/kg). Its advantages include less respiratory depression, immobility and analgesia. The disadvantages include hallucinations and secretions. Its most popular use is perhaps the PO or IM injection in patients who are combative. Often it is mixed with midazolam to allow lower doses and fewer side effects (e.g., 3 mg/kg K + 0.25 mg/kg M PO; 3 mg/kg K + 0.05 mg/kg M IM). Alpha 2 agonists dexmedetomidine and clonidine have emerged as possible premedicants. Both have been used orally and nasally. They taste better than midazolam, but have a completely different effect on the child. While midazolam often produces a disinhibited child, the alpha-2 agonists render the child sleepy if no one arouses him/her. Unfortunately, onset of this type of sedation may take up to 60 minutes. Typical doses of both PO and nasal clonidine and dexmedetomidine are 1-4 mcg/kg. Other premedicants such as oral fentanyl and rectal brevital have been used for pediatric patients, but their use is limited by issues such as respiratory depression. Very few anesthesiologists use these techniques regularly. Parental presence at the induction of anesthesia (PPIA) has grown in popularity primarily in children’s hospitals. While parental satisfaction is improved when they are allowed to accompany their children to the OR, not all children are helped by this. Only those parents who are calm are able to help an anxious child. There is much data to support pharmacologic premedication as a superior anxiolytic. However, having a motivated and calm parent can helpful in some circumstances. Before embarking on a policy of PPIA in your hospital, write a policy to avoid the angry parents who insist on staying with their child, though it might be more detrimental than helpful. Define which children this will

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pertain to (usually greater than 9 months), how many parents may go back, situations where contraindications are present (RSI), and specify that the anesthesia provider has the final word on allowing parents. You must also engage your OR nurses in this policy, as they must accompany the parent from the OR while your induction proceeds. The actual induction of pediatric patients can be accomplished by IM, IV or inhalational methods. IM Ketamine is often reserved for those patients with cardiovascular compromise or combative/highly uncooperative patients without IV access. The typical induction dose is 5 mg/kg IM, but a smaller ― stun dose‖ of 2-3 mg/kg will often render the patient immobile and sedated in order to achieve IV access. IV propofol or pentothal can be used for inductions in children. Much as the inhalation agents have age-related MAC requirements, the IV agents have age-related ED-50 dose requirements. In the first 14 days of life, 2-3.5 mg/kg of pentothal is required with an increase of up to 6 mg/kg by 6 months of age. It declines to 4-5 mg/kg as the child gets older. Propofol should be 1-2 mg/kg in the first few weeks of life, increasing to 3 mg/kg by 6 months of age. Obviously the stability of the child dictates whether these doses are appropriate in the actual OR setting. Propofol will cause pain in the extremity which is often not muted with fentanyl or lidocaine. Inhalation inductions most often occur with sevoflurane, as halothane is rarely used anymore in this country. Desflurane and isoflurane are too pungent to allow an inhalation induction. While the classic teaching of incremental increases of sevoflurane remains popular, there is little scientific evidence to support this practice. If there is no contraindication to nitrous oxide, it should be used in a concentration of 70% with 30% oxygen prior to starting sevoflurane in a cooperative child. Once the child is sedated, sevoflurane should be added with an almost immediate jump to 8%. The child will have a quicker transition through stage 2 and less agitation. Because of the large alveolar ventilation to FRC ratio (5:1) in infants and neonates, induction will be very fast and may be accompanied by apnea. Bradycardia can occur, but is less common than with halothane. With rapid administration of 8% sevoflurane, seizure activity has been reported late in induction. The use of nitrous oxide may be protective against this activity. Hypocapnea associated with assisted ventilation, may provoke it. Should this occur, it is usually selflimiting with a reduction in sevoflurane concentration and allowing the CO2 to rise. REFERENCES FOR INDUCTION TECHNIQUES 1. Almenrader N, Larsson P, Passariello M, Haiberger R, Pietropaoli P, Lonnqvist P, Eksborg S. Absorption pharmacokinetics of clonidine nasal drops in children. Paediatr Anaesth 2009 (in press) 2. Almenrader N, Passariella M, Coccetti B, Haiberger R, Pietropaoli P. Steal induction after clonidine premedication: a comparison of oral and nasal route. Paediatr Anaesth 2007: 17: 977-82

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3. Almenrader N, Passariello M, Coccetti B, Haiberger R, Pietropaoli P. Steal-induction after clonidine premedication: a comparison of the oral and nasal route Pediatric Anesthesia 17 (3), 230–234 4. Baum V, Yemen T, Baum L. Immediate 8% sevoflurane induction in children: a comparison with incremental sevoflurane and incremental halothane. Anesth Analg 85; 313-6; 1997 5. Bergendahl H, Lonnqvist P, Eksborg S et al. Clonidine vs. Midazolam as premedication in children undergoing adeno-tonsillectomy: a prospective, randomized controlled clinical trial. Acta Anaesthesiol Scand 48; 1292-1300; 2004 6. Berry F. Midazolam as premedication: is the emperor naked or just half-dressed?. Pediatric Anesthesia 2007; 17:4, 400–401 7. Brosius K, Bannister C. Oral Premedication in Preadolescents and Adolescents. Anesth Analg 94; 31-6; 2002 8. Caldwell-Andrews A, Kain Z, Mayes L, et al. Motivation and Maternal Presence during induction of anesthesia. Anesthesiology 103; 478-483; 2005 9. Christiansen E, Chambers N. Induction of anesthesia in a combative child: management and issues. Pediatric Anesthesia 15; 421-25; 2005 10. Constant I, Dubois M, Piat V et al. Changes in EEG and autonomic CV activity during induction of anesthesia with sevoflurane compared with halothane in children. Anesthesiology 91; 1604-15; 1999 11. Constant I, Seeman R, Murat I. Sevoflurane and epileptiform EEG changes. Paediatr Anaesth 15; 266-74; 2005 12. Cote’ C. Preoperative preparation and premedication. Br J Anesth 83; 16-28; 1999 13. Cote C, Cohen I, Suresh S et al. A comparison of 3 doses of commercially prepared oral midazolam syrup in children. Anesth Analg 94; 37-43; 2002 14. Dubois M, Piat V, Constant I et al. Comparison of three techniques for induction of anesthesia with sevoflurane in children. Pediatr Anaesth 9; 19-23; 1999 15. Fazi L, Jantzen E, Rose J et al. A comparison of oral clonidine and oral midazolam as preanesthetic medications in the pediatric tonsillectomy patient. Anesth Analg 92; 56-61; 2001 16. Feld L, Negus J, White P. Oral midazolam preanesthetic medication in pediatric outpatients. Anesthesiology 73; 831-4; 1990 17. Finley G, Stewart S, Buffet-Jerrott S et al. High levels of impulsivity may contraindicate midazolam premedication in children. Canadian Journal of Anesthesia 53:73-78 2006 18. Kain Z, Caldwell-Andrews A, Maranets I et al. Preoperative Anxiety and Emergence Delirium and Postoperative Maladaptive Behaviors. Anesth Analg 99; 1648-54; 2004 19. Kain Z, Caldwell-Andrews A, Maranaets I et al. Predicting which child-parent pair will benefit from PPIA: a decision-making approach. Anesth Analg 102; 81-4; 2006 20. Kain ZN, Mayes LC, Wang SM, et al.: Parental presence during induction of anesthesia versus sedative premedication: Which intervention is more effective? Anesthesiology 1998; 89:1147–56 21. Kain ZN, Maclaren J, Wienber M, Juszti H, Anderson D, Mayes L. How many parents should we let into the operating room? Pediatr Anesth 2009, in press 22. Kain Z, Mayes L, Wan S, et al. Parental Presence and sedative premedicant for children undergoing surgery: a hierarchical study. Anesthesiology 92; 939-7; 2000

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23. Kain Z, Caldwell-Andrews A, Krivutza D et al. Trends in the Practice of PPIA and the use of preoperative sedative premdication in the US, 1995-2002: Results of a follow-up national survey. Anesth Analg 98; 1252-9; 2004 24. Karl H, Rosenberger J, Larach MG. Transmucosal administration of midazolam for pediatric patients. Comparison of the nasal and sublingual routes. Anesthesiology. 78(5):885-91 1993 25. Kogan A, Katz J, Efrat R, Eidelman L. Premedication with midazolam in young children: a comparison of four routes of administration. Pediatric Anesth 12; 685-89; 2002 26. Lerman J. Anxiolysis—by the parent or for the parent? Anesthesiology 92; 925; 2000 27. Lonnqvist P, Habre W. Midazolam as premedication: Is the emperor naked or just halfdressed? Pediatric Anesthesia 2005; 15 (4), 263–265. 28. McCann M, Kain Z. The Management of Preoperative Anxiety in Children: an Update. Anesth Analg 93; 98-105; 2001 (great review article!) 29. Palermo T, Tripi P, Burgess E. Parental presence during anesthesia induction for outpatient surgery of the infant. Pediatric Anesthesia 10; 487-91; 2000 30. Sarner J, Levine M, Davis P et al. Clinical Characteristics of Sevoflurane in Children: A Comparison with Halothane. Anesthesiology 82; 38-46; 1995 31. Weber F, Wulf H, Gruber M, Biallas R. S-Ketamine and s-norketamine plasma concentrations after nasal and iv administration in anesthetized children. Pediatric Anesthesia 14; 983-988; 2004 32. Scheepers L, Montgomery C. Kinahan A et al. Plasma concentration of flumazenil following intranasal administration in children. Can J Anaesth 47; 120-4 2000 33. Stella M, Bailey A. Intranasal clonidine as a premedicant: three cases with unique indications. Paediatr Anaesth 2008: 18; 71-3. 34. Yuen VM, Hui TW, Irwin MG, Yeun MK. A comparison of intranasal dexmedetomidine and oral midazolam for premedication in pediatric anesthesia: a double-blinded randomized controlled trial. Anesth Analg 2008; 106; 1715-21 35. Zub D, Berkenbosch J, Tobias JD. Preliminary experience with oral dexmedetomidine for procedural and anesthetic premedication. Paediatric Anesthesia 15; 2005

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Post-Operative Nausea and Vomiting
Tricia A. Meyer, PharmD
Objective: At the conclusion of this course, the participant will be able to discuss recently published guidelines for PONV.

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Medication Errors in the OR By Tricia A. Meyer PharmD, MS, FASHP One of the most notable developments in the science of "medication errors and safety" is the Institute for Medication Safety (IOM) reports titled "To Err is Human: Building a Safer Health System" and “Preventing Medication Errors: Quality Chasm Series.” The first IOM report is an in-depth review of errors in the health care setting. The second IOM report highlighted that on average, a hospitalized patients is subject to at least one medication error per day with at least 1.5 million preventable adverse drug reactions resulting each year. Additionally, this report focused on medication safety strategies, both new and established, with recommendations for actions to be implemented now and in the future. More specifically directed to the perioperative setting, another national report in 2006 was published by The United States Pharmacopeia (USP) Center for the Advancement of Patient Safety’s book titled “ MEDMARX Data Report: A Chartbook of Medication Error Findings from the Perioperative Setting from 1998-2005”. The publication provides an in-depth review of errors occurring in the perioperative area. This includes outpatient surgery, preoperative holding area, operating room and the postanesthesia care unit. The report conducted an examination of 11,239 perioperative errors reported voluntarily to the MEDMARX system. The analysis found that 3.3% of errors in the outpatient surgery area resulted in harm; 2.8% of errors in the preoperative holding area resulted in harm; 7.3% of errors in the operating room resulted in harm; 5.8% of errors in the postanesthesia area resulted in harm.

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An estimated 72 million patients underwent surgical and non surgical procedures in 1996. The operating room is the most medication-intensive area of the hospital. Anesthesia care providers decide what medication and dose that is needed, prepare the medication and administer to the patient. With the large number of high risk pharmacologic agents used in the majority of these cases and with the volume of procedures increasing, so does the opportunity for medication errors. Regulatory agencies and voluntary safety groups, such as the Institute for Healthcare Improvement, Institute for Safe Medication Practices and the Joint Commission, have focused on medication error reduction and adopted safety goals or error reduction techniques to address this problem. The literature also contains research studies and reviews on medication safety strategies in the O.R. These include standardization (drug preparation procedures, layout of work space, syringe sizes, IV drug concentrations), prefilled and labeled syringes, distinctive and colored labels, separate storage areas for hazardous medications, bar coding etc. Other recommendations include a perioperative multidisciplinary team to include anesthesia care providers, representatives from nursing and pharmacy to develop processes for improved perioperative medication safety.

1. Kohn LT, Corrigan JM, Donaldson MS. To Err is Human-Building a safer health system. Committee on the Quality of Healthcare in America; Institute of Medicine. Washington DC: National Academy Press; 1999 2. Institute of Medicine. Preventing medication errors: Quality chasm series. Washington DC, National Academies Press; 2007

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3. Hicks R.W. , Becker, S.C. and Cousins, D.D. (2006). MedMarx Data Report: A Chartbook of Medication Error Findings from the Perioperative Settings from 1998-2005. Rockville, MD: USP Center for the Advancement of Patient Safety 4. Jensen L.S., Merry A.F., Webster, C.S., Weller, J. and Larsson, L. Evidencebased strategies for preventing drug administration errors during anaesthesia. Anaesthesia. 2004; 59:493-504 5. AORN Guidance Statement-Safe Medication Practices in Perioperative Practice Settings. Association of Operating Room Nurses. AORN Journal; 2004;79: 67476 6. Robinson, Z. . Pursuing Safe Medication Use and the Promise of Technology. MedSurg Nursing. 2007;16:92-99

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Clinical Instructors’ Educational Workshop
Shane Angus, AA-C
Objective: At the conclusion of this course, the participant will have 1) enhanced knowledge of learning methods; 2) enhanced teaching skills for management of the learning environment in the operating room and classroom; 3) improved teaching efficiency and 4) learned to provide more constructive feedback.

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Pediatric PACU
Ann Bailey, MD
Objective: At the conclusion of this course, the participant will understand the common problems encountered by pediatric patients in the recovery room and methods to prevent and/or treat them.

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PACU Problems in Children Ann Bailey, M.D. FAAP The pediatric patient who is emerging from an anesthetic will likely experience at least one problem in the PACU. The most frequently encountered complications are emergence delirium, pain, PONV, and airway problems. We will discuss these issues in more detail and the methods to prevent or treat them. One of the most disturbing events for a parent to witness is emergence delirium (ED) sometimes called emergence agitation. It has been defined as “a disturbance in a child's awareness of and attention to his/her environment with disorientation and perceptual alterations including hypersensitivity to stimuli and hyperactive motor behavior in the immediate postanesthesia period.” Although originally reported in 1961, the incidence has gone up dramatically with the introduction of sevoflurane and desflurane. Both agents are associated with more ED than halothane or isoflurane. Younger age (<5 yrs), short surgery, preoperative anxiety, and an emotional temperament predispose to ED. What can be done to prevent ED? First and foremost, insuring that the child is not awakening in pain is important. Fentanyl has been found to decrease the incidence of ED, even when used in anesthetics for radiologic procedures when no surgery was performed. Secondly, the type of anesthetic is very important. Propofol is associated with very little ED when used as a maintenance agent or given in a bolus of 1 mg/kg at the end of the anesthetic. In addition to narcotics and propofol, alpha-2 agonists have been successfully used during the course of the anesthetic to prevent ED. Clonidine 1-2 mcg/kg or dexmedetomidine (0.5-1 mcg/kg) given IV near the end of the anesthetic may prevent ED. In spite of efforts to prevent ED, some children will still experience wild thrashing in the PACU. Narcotics can be used as a first choice to insure that pain is not the causative factor. Alternatively, clonidine or dexmedetomidine have been used to treat ED in the PACU. Additionally, boluses of propofol have proven effective in the PACU, although one must insure that the airway remains patent, as the child may return to a state of general anesthesia transiently. As mentioned above, analgesia should be provided if the child is uncomfortable in the PACU. This should be accomplished through a multi-modal approach. Mild to moderate pain can be treated with acetaminophen. Ideally this would be administered as 10-15 mg/kg PO preoperatively or 40 mg/kg rectally intraoperatively to allow time to reach a peak effect in the PACU. In some cases of musculoskeletal pain, NSAIDs are highly effective analgesics. Ibuprofen 10 mg/kg can be given PO, and ketorolac 0.5 mg/kg (max dose 30 mg) can be given IV. While there are some contraindications (bleeding, renal failure), these types of drugs are highly effective in most children. Narcotics can be given as both IV and PO formulations in the PACU. Most anesthesia providers feel comfortable using fentanyl in 0.5-1 mcg/kg boluses up to 2 mcg/kg in the PACU. Alternatively, if the child is being admitted to the hospital, morphine 0.05-0.1 mg/kg IV has a longer effect. If the child is going home, PO narcotics can be given to provide pain relief in the car and upon arrival to the home environment. Oxycodone elixir is very effective in a dose of 0.1 mg/kg. Many surgeons still order codeine for
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postoperative analgesia. Codeine is metabolized to morphine which is the active agent. Unfortunately, 10% of the population doesn’t have the enzyme necessary to convert it to an active form. More worrisome, some patients are ultra-rapid metabolizers and convert quickly with resultant respiratory depression; death has been reported as a result. Regional anesthesia is another modality to provide for postoperative analgesia. Major blocks such as caudals can be performed in the OR for common procedures such as hernia or hypospadius repairs. Equally important, local anesthesia in the area of the surgery placed by surgeons can be very effective at ameliorating the pain. PONV is another important complication in children. While thousands of studies have been reported in adults, less attention has been given to the children. In the most recent SAMBA guidelines for PONV prophylaxis, attention was directed to prophylaxis and management of the pediatric patient. Ondansetron and other 5 HT3 antagonists have clearly been demonstrated to be effective, as has dexamethasone. In combination, the effect is even greater. Other agents can be used be used, but have some issues. Promethazine (phenergan) is highly effective as a rescue drug, but is contraindicated in children less than 2 years of age. “Superhydration” with 30 ml/kg isotonic IV fluids was found to reduce the incidence of PONV in children. Conversely, forcing children to drink postoperatively before discharge may increase the incidence of vomiting. Finally, respiratory issues may complicate the recovery period. It is beyond the scope of this discussion to elaborate on the many different types of airway problems, especially as related to the abnormal airway. Croup remains a largely avoidable cause of delays in PACU discharge in children. It is largely preventable in children by using appropriate sized endotracheal tubes. Most textbooks will recommend that age/4 + 4 is the appropriate inner diameter in mm of an uncuffed ETT for most children. Cuffed endotracheal tubes are now being used by most pediatric anesthesiologists for all ages of children. Cuffed ETT’s are particularly advantageous for children with a risk of aspiration, procedures associated with low lung compliance (thoracoscopies and laparoscopies), and in cases where precise control of CO2 is necessary (neurosurgery). Newer tubes are being manufactured with very thin cuffs that do not change the outer diameter significantly. Although original articles recommended that the equation for cuffed ETT’s is age/4 + 3 in mm, most users are moving to a half-size smaller than an uncuffed ETT. Always when using a cuffed ETT, cuff pressures should be measured and the cuff should be inflated to just seal at 20-30 cm H2O. In summary, pediatric patients experience issues with emergence delirium, pain, PONV, and croup in the PACU. By anticipating the problems, the anesthetic can be tailored to prevent their occurrence. However, in spite of the best anesthesia, problems will still arise, and the anesthesia provider should be prepared to treat them appropriately.

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References for Pediatric PACU Problems
1. Vlajkovic GP, Sindjelic RP. Emergence Delirium in children: many questions, few answers. Anesth Analg. 2007 Jan;104(1):84-91 (great review article!) 2. Aono, J, Wasa U, Kikyo M, Takimoto E, Manabe M. Greater Incidence of Delirium during recovery from Sevoflurane Anesthesia in Preschool Boys. Anesthesiology 1997; 87; 1298-1300 3. Sikich N, Lerman J. Development and psychometric evaluation of the pediatric anesthesia emergence delirium scale. Anesthesiology 2004;100:1138–45 4. Davis P, Cohen I, McGowan F, Latta K: Recovery Characteristics of Desflurane versus halothane for maintenance of anesthesia in pediatric ambulatory patients. Anesthesiology 1994; 80: 298-302 5. Cravero J, Surgenor S, Whalen K. Emergence agitation in pediatric patients after sevoflurane anesthesia and no surgery; a comparison with halothane. Paediatr Anaesth 2000; 10; 419-24 6. Welborn L, Hannallah R, Norden J, Ruttimann U, Callan C. Comparison of Emergence and Recovery Characteristics of Sevoflurane, Desflurane, and Halothane in Pediatric Ambulatory Patients. Anesth Analg 1996; 83; 917-20 7. Tobias, et al. Additional experience with Dexmedetomidine in Pediatric patients. South Med J. 2003 Sep;96(9):871-5 8. Ibacache et al; Single-Dose Dexmedetomidine Reduces Agitation After Sevoflurane Anesthesia in Children Anesth Analg. 2004 Jan;98(1):60-3 9. Isik et al. Dexmedetomidine decreases emergence agitation in pediatric patients after sevoflurane anesthesia without surgery. Pediatric Anesthesia 2006 10. Malviya S, et al: Clonidine for the prevention of emergence agitation in young children: efficacy and recovery profile. Pediatric Anesthesia; 16; 554-559; 2006 11. Lankiinen U, Avela R, Tarkkila R. The prevention of emergence agitation with tropsietron or clonidine after sevoflurane anesthesia in small children undergoing adenoidectomy. Anesth Analg 102; 1383-1386; 2006 12. Aouad MT, Yazbeck-Karam VG, Nasr VG et al. A single dose of propofol at the end of surgery for the prevention of emergence agitation in children undergoing strabismus surgery during sevoflurane anesthesia Anesthesiology. 2007 Nov;107(5):733-8 13. Abu-Shahwan I. Effect of propofol on emergence behavior in children after sevoflurane general anesthesia Paediatr Anaesth. 2008 Jan;18(1):55-9. 14. Galinkin J, Fazi L, Cuy R, Chiaviacci R, Kurth D, Shah U, Jacobs I, Watcha M. Use of intranasal fentanyl in children undergoing myringotomy and tube placement during halothane and sevoflurane anesthesia. Anesthesiology 2000; 90; 1378 15. Birmingham P, Tobin M, Fisher D, Henthorn T, Hall S, Cote’ C. Initial and Subsequent Dosing of Rectal Acetaminophen in Children. Anesthesiology 2001; 94: 385-9 16. Birmingham P, Tobin J, Henthorn T, Fisher Dm Berelhamer M, Smith F, Fanta K, Cote’ C: 24 hour pharmacokinetics of rectal acetaminophen in children. Anesthesiology 1997: 87; 244-52 17. Houck C, Wilder RT, McDermott J, Sethna N, Berde C. Safety of intravenous ketorolac therapy in children and cost savings with a unit dosing system. J Pediatrics 1996; 129; 292-6 18. Rusy L, Houck C, Sullivan L, Ohlms L Jones D, McGill T, Berde C. A double-blind evaluation of ketorolac tromethamine versus acetaminophen in pediatric tonsillectomy: analgesia and bleeding. Anesth Anal 1995: 80; 226-9 19. Anderson BJ, Holdord N, Woollard G, Kanagasundarum S, Mahadevan M. Perioperative pharmacodynamics of acetaminophen analgesia in children. Anesthesiology 1999; 90; 411-21 20. Tobias J. Weak Analgesics and Nonsteriodal Anti-inflammatory agents in the management of children with acute pain. Ped Clin N Amer 2000; 47; 527-43

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21. Finkel J, Cohen, Hannallah R, Patel K, Kim M, Hummer K, Choi S, Pena M, Schreiber S, Zalzal G. The effect of intranasal fentanyl on the emergence characteristics after sevoflurane anesthesia in children undergoing surgery for BMT placement. Anesth Analg 92; 2001: 1164-8 22. Clark E, Plint A, Corrett R et al. A randomized trial of acetaminophen, ibuprofen, and codeine for acute pain relief in children with musculoskeletal trauma. Pediatrics 2007; 119; 460-7 23. Hiller A, Meretoja O, Korpela R, et al. The analgesic efficacy of acetaminophen, ketoprofen, or their comgination for pediatric surgical patients having soft tissue or orthopedic surgery. Anesth Analg 102; 13651371; 2006 24. Madan R, Bhatia A, Chakithandy S, et al.Prophylactic Dexamethasone for Postoperative Nausea and Vomiting in Pediatric Strabismus Surgery: A Dose Ranging and Safety Evaluation Study. Anesth Analg 2005;100:1622-1626 25. Hertzka R, Gauntlett I, Fisher D, Spellman M. Fentanyl induced ventilatory depression: effects of age. Anesthesiology 70: 213-8: 1989 26. Edler A, Mariano E, Golianu B, Kuan C, Pentcheva K. An analysis of factors influencing postanesthesia recovery after pediatric ambulatory tonsillectomy and adenoidectomy; Anesth Analg 104; 784-89; 2007 27. Patel R, Davis P, Orr R, Ferrari L, Rimar S, Hannallah R, Cohen I, Colingo K, Donlon J, Haberkern C, McGowan F, Prillaman B, Parasuraman T, Creed M. Single-dose ondansetron prevents postoperative vomiting in pediatric patients. Anesth Analg 1997; 85; 538-45 28. Khalil S, et al.A Double-Blind Comparison of Intravenous Ondansetron and Placebo for Preventing Postoperative Emesis in 1- to 24-Month-Old Pediatric Patients After Surgery Under General Anesthesia. Anesth Analg; 2005;101:356-361 29. Goodarzi M, et al. A prospective randomized blinded study on the effect of intravenous fluid therapy on PONV in children undergoing strabismus surgery. Pediatric Anaesth 2006; 16; 49-53 30. Sadhasivam S, Shende D, Madan R. Prophylactic Ondansetron in prevention of postoperative nausea and vomiting following pediatric strabismus surgery. Anesthesiology 2000; 92; 1035-42 31. Schreiner M, Nicholson S, Martin T, et al: Should children drink before discharge from day surgery? Anesthesiology 1992; 76; 528-533 32. Gan TJ, Meyer TA, Apfel CC, et al.SAMBA guidelines for management of PONV. Anesth Analg 2007; 105: 1615-28 33. Eberhart LH, Geldner G, Kranke P, et al. The development and validation of a risk score to predict the probability of postoperative vomiting in pediatric patients. Anesth Analg. 2004 Dec;99(6):1630-7 34. Schreiner M, Nicholson S. Pediatric ambulatory anesthesia: NPO before or after surgery? J Clin Anesth; 1995; 7; 589-596 35. Khine et al: Comparison of cuffed and uncuffed endotracheal tubes in young children during general anesthesia. Anesthesiology 1997; 86: 627-31 36. Duracher et al. Evaluation of cuffed tracheal tube size predicted using the Khine formula in children. Pediatric Anesthesia 18 (2) , 113–118; 2008 37. James I: Cuffed tubes in children. Pediatric Anaesth 2001; 3; 259 38. Fine G, Borland L. The future of the cuffed endotracheal tube. Pediatric Anesthesia 2004; 14; 38-42 39. Dullenkopf, A., Gerber, A. C. & Weiss, M. Fit and seal characteristics of a new paediatric tracheal tube with high volume–low pressure polyurethane cuff.Acta Anaesthesiologica Scandinavica 49 (2), 232-237

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Medication Safety in the Operating Room
Tricia A. Meyer, PharmD
Objective: At the conclusion of this course, the participant will be able to recommend at least two strategies for improvement of medication safety in the operating room.

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Medication Errors in the OR By Tricia A. Meyer PharmD, MS, FASHP One of the most notable developments in the science of "medication errors and safety" is the Institute for Medication Safety (IOM) reports titled "To Err is Human: Building a Safer Health System" and “Preventing Medication Errors: Quality Chasm Series.” The first IOM report is an in-depth review of errors in the health care setting. The second IOM report highlighted that on average, a hospitalized patients is subject to at least one medication error per day with at least 1.5 million preventable adverse drug reactions resulting each year. Additionally, this report focused on medication safety strategies, both new and established, with recommendations for actions to be implemented now and in the future. More specifically directed to the perioperative setting, another national report in 2006 was published by The United States Pharmacopeia (USP) Center for the Advancement of Patient Safety’s book titled “ MEDMARX Data Report: A Chartbook of Medication Error Findings from the Perioperative Setting from 1998-2005”. The publication provides an in-depth review of errors occurring in the perioperative area. This includes outpatient surgery, preoperative holding area, operating room and the postanesthesia care unit. The report conducted an examination of 11,239 perioperative errors reported voluntarily to the MEDMARX system. The analysis found that 3.3% of errors in the outpatient surgery area resulted in harm; 2.8% of errors in the preoperative holding area resulted in harm; 7.3% of errors in the operating room resulted in harm; 5.8% of errors in the postanesthesia area resulted in harm.

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An estimated 72 million patients underwent surgical and non surgical procedures in 1996. The operating room is the most medication-intensive area of the hospital. Anesthesia care providers decide what medication and dose that is needed, prepare the medication and administer to the patient. With the large number of high risk pharmacologic agents used in the majority of these cases and with the volume of procedures increasing, so does the opportunity for medication errors. Regulatory agencies and voluntary safety groups, such as the Institute for Healthcare Improvement, Institute for Safe Medication Practices and the Joint Commission, have focused on medication error reduction and adopted safety goals or error reduction techniques to address this problem. The literature also contains research studies and reviews on medication safety strategies in the O.R. These include standardization (drug preparation procedures, layout of work space, syringe sizes, IV drug concentrations), prefilled and labeled syringes, distinctive and colored labels, separate storage areas for hazardous medications, bar coding etc. Other recommendations include a perioperative multidisciplinary team to include anesthesia care providers, representatives from nursing and pharmacy to develop processes for improved perioperative medication safety.

1. Kohn LT, Corrigan JM, Donaldson MS. To Err is Human-Building a safer health system. Committee on the Quality of Healthcare in America; Institute of Medicine. Washington DC: National Academy Press; 1999 2. Institute of Medicine. Preventing medication errors: Quality chasm series. Washington DC, National Academies Press; 2007

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3. Hicks R.W. , Becker, S.C. and Cousins, D.D. (2006). MedMarx Data Report: A Chartbook of Medication Error Findings from the Perioperative Settings from 1998-2005. Rockville, MD: USP Center for the Advancement of Patient Safety 4. Jensen L.S., Merry A.F., Webster, C.S., Weller, J. and Larsson, L. Evidencebased strategies for preventing drug administration errors during anaesthesia. Anaesthesia. 2004; 59:493-504 5. AORN Guidance Statement-Safe Medication Practices in Perioperative Practice Settings. Association of Operating Room Nurses. AORN Journal; 2004;79: 67476 6. Robinson, Z. . Pursuing Safe Medication Use and the Promise of Technology. MedSurg Nursing. 2007;16:92-99

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Monday, April 20

Monday April 20, 2009
7:00 am-6:00 pm 7:30 am-8:00 am Registration Continental Breakfast Trauma Anesthesia Roy Soto, MD Can/Should Simulation Be Used for Certification Assessment of AA Students Michael S. Nichols, AA-C Coffee Break Alpha-2 Agonists for Sedation and General Anesthesia Roy Soto, MD Cardiac Output after the Pulmonary Artery Catheter Joel Zivot, MD AA Spokesperson Training/Mock Legislative Committee Hearing (Leadership) No CME credit awarded Ellen Allinger, AA-C, MMSc Lunch on Own Student Forum Student Spokesperson Training Shane Angus, AA-C

8:00 am-9:00 am 9:00 am-10:00 am 10:00 am-10:30 am

10:30 am-11:30 am
concurrent sessions

11:30 am-12:30 pm 11:30 am-12:30 pm 12:30 pm-2:00 pm 2:00 pm-4:00 pm

4:00 pm-5:00 pm

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Trauma Anesthesia
Roy Soto, MD
Objective: At the conclusion of this course, the participant will be able to 1) discuss leading causes of injury in the United States with associated morbidity and mortality; 2) understand the importance of initial evaluation and immediate resuscitation of the trauma patient; 3) discuss appropriate transfusion triggers for blood and blood components in the trauma patient and 4) discuss appropriate management of the patient with the unstable cervical spine.

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Anesthesia for Trauma Surgery Roy G. Soto, M.D. Introduction Depending on the practice you ultimately choose, trauma may become a daily part of your anesthetizing life. Patients presenting with traumatic injuries can represent a significant challenge to many aspects of your practice, with airway and IV challenges being the norm, and hemodynamic stability being a constant challenge. In this discussion we will discuss the epidemiology, assessment, and specific challenges associated with traumatic injury. Epidemiology Injuries are the leading cause of death in America for children and young adults, with 150,000 deaths and 450,000 new patients suffering permanent disability each year. 1/3 of all hospital admissions are for injury, and the estimated annual cost of trauma care exceeds $400 billion. Contrary to common belief, trauma is not a random occurrence, and these patients have an increased likelihood of drug abuse, intoxication, and hepatitis/HIV infection. Regional trauma care is organized on the premise that most patients die soon after injury, and care received in the “golden hour” after injury is most likely to reduce mortality. Level 1 and 2 trauma centers were developed in an attempt to get “the right patient to the right hospital at the right time.” Mechanisms of injury Data from the National Trauma Data Bank reveal the following trends: 1) The majority of reported traumas occur in young males 2) Case fatality rises with age at time of injury 3) Motor vehicle accidents are the main cause of injury in young and middle-aged patients, with falls becoming predominant in elderly patients 4) The vast majority of injuries are blunt 5) Penetrating injuries have the highest associated mortality 6) Burns result in the longest hospital stay 7) America leads the world in firearm related deaths in both adults and children, with an incidence 4x higher than any other industrialized country 8) Firearm deaths occur predominantly in African-American men Patient assessment It is very important to remember that traumatic injuries rarely occur in isolation, meaning that a dislocated shoulder following an MVA is probably not the patient’s only injury. As a result, a number of scoring systems have been developed to ensure uniformity in the approach to injury. Airway/Breathing/Circulation/Disability represent the “A, B, C, and D” approach to initial assessment, and Advanced Trauma Life Support, taught by the American College of Surgeons, is designed to assess a patient in a standardized fashion, ensuring a “tube or finger in every orifice”. The patient’s clothes are removed, IV access is obtained, and the entire body is visually examined for injury. The Injury Severity Scale correlates well with risk of coagulopathy, case fatality, and hospital stay, and takes into account severity of injury of separate body parts:

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ISS = A2 + B2 + C2 A, B, C = AIS score of three most injured of: Head Face Thorax Abdomen Extremities (incl. pelvis) *AIS=Abbreviated Injury Scale

The Glasgow Coma Scale (GCS) was developed to assess level of neurologic injury, and includes assessments of movement, speech, and eye opening:

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Regardless of assessment method, however, it is vital to remember that these scores do not predict ease of intubation/ventilation, or reflect volume, pulmonary, or cardiac status. In other words, a patient with a high GCS and low ISS may still require urgent intubation or may be suffering myocardial ischemia due to injury-related stress. Specific challenges Many hospitals routinely call anesthesia personnel to the emergency department for incoming trauma patients. As a result, anesthesia providers are frequently involved in resuscitation and airway management within minutes of patient arrival. Since initial trauma care occurs on a continuum from the emergency department to operating room, many of the following discussion points are pertinent to each specialty and each locale. As a result, anesthesia providers must be prepared to “work” in a potentially unfamiliar environment with a different (not necessarily better or worse) level of help and equipment than is typically available in a well-stocked trauma operating room. The trauma arrest Patient’s requiring CPR following trauma have an almost universally poor prognosis, with blunt trauma + arrest mortality approaching 100%, and penetrating trauma + arrest being just as bad, with the exception of young, otherwise healthy patients receiving hospital care within 10min of their injury. For any hope of survival, early intubation with appropriate oxygenation and ventilation is required, as is aggressive fluid management. The trauma airway Emergent management of the trauma airway can be the single most challenging aspect of anesthesia care, and proper preparation and multiple backup plans are equally important. Airway damage, cervical spine injury, intoxication, and coexisting injury can combine to create a situation requiring experience, expertise, and luck! Fiberoptic intubation may be impossible due to airway blood or patient belligerence. Rapid sequence induction may be contraindicated due to neck or head injury. LMA placement may be complicated by a full stomach. The patient may come with a Combitube in place, but then require positive pressure ventilation for increased ICP. My own “combative trauma airway” plan looks something like this:

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If the airway appears “easy” (and that’s certainly open to interpretation), then I proceed with an asleep intubation with inline stabilization (inline traction used to be used, but was associated with neck injury). If the airway is “difficult” (again, open to interpretation, hence the asterisk) I would proceed, again, with RSI with ENT backup (meaning that they’re standing next to me with a knife ready) or try to hedge my bets and give a dose of intravenous or intramuscular ketamine with the hopes that ventilation would be maintained, and I’d be able to proceed with awake techniques. If at all possible, and I find myself on the red side of the flowchart, I prefer to bring the patient to the operating room for the intubation. I can manage my equipment better there, I have help that is used to dealing with airway management, and I have a well lit, non-chaotic environment to work in. Finally, if intubating in the ER, and someone else wants to try the intubation first, the answer is always “no”! The first attempt is always the best. One of my favorite sayings? “Good judgement comes from experience, and experience comes from bad judgement” (that would be represented by the question-mark box). Good luck! Clearing the C-spine Typical scenario: A patient comes to the operating room from the CT scanner for urgent splenectomy. He’s been poked, prodded and scanned prior to arrival, but is still wearing a C-collar. Is it OK to take it off? Just how does one clear the C-spine definitively? The short answer is that all imaging studies must be negative, and the patient must be able to clearly tell you that nothing hurts. That said, patients frequently can’t do that. So for me to clear a C-spine, I need: 1) Cleared films (X-ray, CT, and/or MRI). Note that following an MVA the most likely injuries are to C1 > C5 > C6 > C7, and following a fall C5 > C6 > C7 2) The patient has to be awake, coherent, and cooperative

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3) The patient cannot be intoxicated (alcohol, drugs, or otherwise) 4) The patient cannot have a distracting injury that is causing more pain than he may have in his neck 5) The patient cannot have received a significant dose of opiates (just how much is significant is unclear, but if the patient is somnolent, I don’t trust that the opiates haven’t blunted subjective pain complaints) 6) The patient cannot have tenderness to neck palpation or tenderness to gentle neck flexion/extension If all of these criteria are not met (they rarely are), then I again proceed with a rapid sequence induction with inline stabilization (given a normal airway). The job of the person holding stabilization is to not only hold the head/neck in neutral position, but also to inform the intubator if the neck is moving due to vigorous laryngoscopy. Note that there will be another person holding cricoid pressure during this process, and I therefore always remove the anterior portion of the cervical collar during intubation. Head trauma Patients presenting with head trauma can pose a difficult challenge to anesthesia providers. Laryngoscopy, succinylcholine, and sedation/hypoventilation are associated with increases in intracranial pressure (ICP). Techniques to maintain cerebral perfusion pressure >60mmHg (MAP minus ICP) while also keeping ICP as low as possible include: Fluid restriction (difficult if coexisting injuries present) Diuresis with mannitol (0.5gm/kg) Steroids (dexamethasone 1mg/kg) Barbiturates or hypothermia in rare instances for reduction of cerebral metabolic rate 5) Hyperventilation to a PaCO2 of 26-30mmHg 6) Lidocaine and/or opiates to attenuate laryngeal/tracheal response to intubation 7) Slight head-up position 8) Avoidance of ketamine 9) Avoidance of hyperglycemia 10) Hypertonic saline (unproven benefit, although may be beneficial for volume resuscitation of other injuries in the brain-injured patient) As always, communication with the surgeon is important, as is having a high index of suspicion for coexisting injuries that may complicate management. As a rule, “conscious sedation” of brain injured patients is contraindicated as it may result in hypoventilation, hypercapnea, and acidosis. Similarly, spontaneous ventilation under general anesthesia (for instance with an LMA) is also associated with predictable hypercapnea and should be avoided. Bleeding All bleeding stops eventually…unfortunately it’ll stop either with or without your help! Trauma patients frequently need volume resuscitation, blood, coagulation factors, and more volume resuscitation while surgeons attempt to fix whatever was broken, ruptured, or eviscerated. ATLS requires trauma patients to have large-bore IV access, ideally via central catheters. Femoral venous lines are frequently placed, but beware of vena caval 1) 2) 3) 4)

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injuries and resuscitation through a groin line. It does no good for blood to be pumped by you into the patient’s abdomen and onto the floor! Consider a line above and below the suspected area of injury. Progressive hypothermia, coagulopathy, and hypovolemia/acidosis (the so-called “lethal triad”) result in progressive mortality. Resuscitation efforts must be geared towards avoiding all three, and aggressive volume replacement, room/fluid temperature control, and blood product/factor replacement must be addressed simultaneously.  Hypothermia: Trauma ORs should be kept warm, all fluids should be warmed (ideally starting in the ER), and irrigation should be near body temperature. Rapid fluid infusers do a good job of warming fluids quickly, and should be used whenever possible for massive tranfusion. Hypovolemia/acidosis: Commonly administered crystalloid solutions are acidic, with 0.9% normal saline having a pH of 5.0, and lactated ringers having a pH of 6.2. Large volumes of crystalloid resuscitation can result in metabolic acidosis from the fluids alone, let alone from the initial hypovolemia, so care in fluid choice should be given. Colloids have not been shown consistently to be better or worse than crystalloids, and many providers will mix and match in an attempt to avoid giving too much of any one thing. In the face of uncontrolled bleeding, evidence suggests that the goal should be a BPs of ~80mmHg, although existing head trauma and CPP should be kept in mind (see below).

Coagulopathy: Crystalloid/colloid resuscitation can result in dilutional coagulopathy, which can worsen coagulopathy from blood replacement or hypothermia. Rather than giving factors only if laboratory values are abnormal, most hospitals have adopted a massive transfusion protocol aimed at replacing factors at pre-set intervals. Recombinant Factor VIIa has been used by some in trauma resuscitation, and it appears that survival may be improved with its use. The high cost of the drug (>$5000/dose), however, limits its utility. Finally, calcium replacement must be considered during massive transfusion as calcium is a cofactor in both the intrinsic and extrinsic clotting pathways, and citrate in transfused blood can result in hypocalcemia. (see below for our hospital’s trauma blood/massive transfusion protocol)

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Trauma Blood, William Beaumont Hospital  O-neg x 2 units, then  O-pos if o Male o Obviously non-child bearing age  Continue with O-neg Massive Transfusion Protocol, William Beaumont Hospital • Thaw 4u FFP and 1u Cryo • Crossmatch 6u PRBC and 1u Plt • Deliver to OR • Cooler #1: 4u PRBC • Cooler #2: 2u PRBC + 3u FFP • Bucket: Cryo + Plt • Continue to replenish coolers/bucket until told to stop A final word about bleeding. Surgeons are very good at packing wounds to stop them from bleeding, and at times it is important to ask the surgeons to “stop working, pack the wound, and let me get caught up on blood loss here (please)”. Similarly, there are times when an injury should be packed and the patient sent to the ICU, with a plan to bring the patient back another day for a staged repair. As eloquently stated by one author: “The key underlying principle is that the completeness of the anatomic repair is temporarily sacrificed so as to address the patient's physiologic insult before the patient's fragile physiologic envelope is shattered.” Always remember, your surgeon is your ally in this bloody battle, and you must communicate back and forth throughout the trauma case.

References: 1. Sell SL, Avila MA, Yu G, Vergara L, Prough DS, Grady JJ, DeWitt DS. Hypertonic resuscitation improves neuronal and behavioral outcomes after traumatic brain injury plus hemorrhage. Anesthesiology. 2008; 108:873-81 2. Spinella PC, Perkins JG, McLaughlin DF, Niles SE, Grathwohl KW, Beekley AC, Salinas J, Mehta S, Wade CE, Holcomb JB. The effect of recombinant activated factor VII on mortality in combat-related casualties with severe trauma and massive transfusion. J Trauma. 2008; 64:286-93 3. Hirshberg A, Stein M, Adar R. Reoperation. Planned and unplanned. Surg Clin North Am. 1997; 77:897-907

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Can/Should Simulation Be Used for Certification Assessment of AA Students
Michael S. Nichols, AA-C
Objective: At the conclusion of this course, the participant will be able to 1) describe current AA certification testing mechanisms; 2) describe elements of validity and reliability in performance testing; 3) relate positive aspects and potential pitfalls of utilizing simulation-based assessment and 4) understand the theory behind potential changes in the AA certification process.

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Can or Should Simulation Be Used for Assessment of Anesthesiologist Assistant Competence for Clinical Practice
Michael S. Nichols, AA-C, MSA Assistant Program Director Anesthesiologist Assistant Program Assistant Professor Nova Southeastern University College of Allied Health & Nursing Immediate Past President American Academy of Anesthesiologist Assistants

Course Purpose: A basic explanation of the rationale behind various high-stakes testing modalities used to assess clinical competence. Additionally, the course will cover an explanation of the positive and negative aspects of utilizing simulation and/or oral board examinations as a component of the anesthesiologist assistant certification. Learning Objectives: (1) Define the need for assessment of clinical competence in anesthesia practice (2) Describe current AA certification testing and evaluation mechanisms (3) Describe elements of validity and reliability in performance testing, with a focus on simulation (4) Relate positive aspects and potential pitfalls of utilizing simulation-based assessment in high-stakes testing

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There is only one sort of licensing test that is significant, namely a test that ascertains the practical ability of the student confronting a concrete case to collect all relevant data and to suggest the positive procedure applicable to the conditions disclosed. A written examination may have some incidental value; it does not touch the heart of the matter. (Flexner, 1910)

Introduction
It is generally accepted that the public perceives that board certification, such as by the National Commission for the Certification of Anesthesiologist Assistants (NCCAA) or American Board of Anesthesiology (ABA) is the “gold standard” and, if a clinician possesses this credential, he or she has the knowledge and skills required to be competent. However, evidence is mixed as to whether successfully attaining these qualifications actually results in safe and competent practice (McIntosh, 2009). Trends in modern health care are patient-centered, incorporating as much customer service and patient safety as medical knowledge. This ‘new, old paradigm of medicine’ (Sween, 2009) includes a demand that the performance of clinicians be assessed formally. Additionally, pressure is now coming from a variety of sources, whether external regulation or internal quality control, to provide evidence that graduates from training programs have reached a satisfactory standard (Glavin & Gaba, 2008). However, there is little or no understanding of the difficulties involved in the design of valid tests of performance. Of the many problems facing an investigator who is setting out to measure performance, one of the greatest is devising a standardized procedure. The complexity of evaluation of medical competence has been well documented in the educational literature (Morgan & Cleave-Hogg, 2000), which is compounded by the lack of reliable and valid techniques with which to teach and evaluate the clinical skills of students and seasoned clinicians, having long been recognized as a deficiency of medical education (Murray, 2002). Simulation is one method that can be used to evaluate a clinician’s ability to integrate diagnostic hypotheses and provide treatment in situations that require rapid action. Assessment of clinical competence is moving away from testing what a clinician knows, towards assessing what a he or she does in clinical practice (Weller, 2003). Direct observation of performance in the workplace would be the most valid method for assessing clinical performance, but has obvious limitations. Even more difficult is assessment of performance in a crisis situation. In this presentation we will review some of these developments, discuss the limitations and pitfalls in the assessment of clinical reasoning, and offer suggestions for future assessment practice.

The Role of Assessment in Defining Clinical Competence
A competency is the ability to handle a complex professional task by integrating the relevant cognitive, psychomotor and affective skills. More specifically, one can define competence in medicine as “…the habitual and judicious use of communication, knowledge, technical skills, clinical reasoning, emotions, values, and reflection in daily practice for the benefit of the individuals and communities being served...” (Crossley J, 2002). Work on the assessment of competent clinical reasoning began in the 1960s and 1970s. At that time clinical reasoning was perceived as a generic quality-a personal attribute reflecting the ability to solve problems in the clinical domain. As such it was thought to be largely independent of factual knowledge and procedural skills; in other words, a good problem-solver would be effective in solving problems irrespective of the clinical circumstances. From this perspective clinical reasoning was akin to a psychological characteristic or personality trait. In that era, clinical reasoning was typically measured by asking students to respond to problems that could be presented in standardized format with objective scoring of answers. Ideally, the assessment of competence (what the student or physician is able to do) should provide insight into actual performance (what he or she does habitually when not observed), as well as the capacity to adapt to change, find and generate new knowledge, and improve overall performance (Epstein, 2007). It is also essential to be able to assess

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these skills explicitly to provide structured feedback about performance and to allow training effectiveness to be evaluated (Fletcher, 2003). To the detriment of the students, traditional medical education tends to persist an inclination to break down the competency trying to be assessed into smaller units, which are then assessed separately in the conviction that mastery of the parts will automatically lead to competent performance of the integrated whole (Crossley J, 2002). However, a vital component of the education of competent anesthesia providers is the integration of these competencies into clinical practice. Modern educational theory dictates that learning is facilitated when tasks are integrated. Educational programs that are restricted to the “stacking” of components or sub-skills of competencies are less effective in delivering competent professionals than methods in which different task components are represented and practiced in an integrated fashion, which creates conditions that are conducive to transfer. These theories were illustrated by noted psychologist George Miller in 1990, when he proposed a framework for assessing clinical competence. At the lowest level of the pyramid is knowledge (knows), followed by competence (knows how), performance (shows how), and action (does). In this framework, Miller distinguished between "action" and the lower levels. "Action" focuses on what occurs in practice rather than what happens in an artificial testing situation. Work based methods of assessment target this highest level of the pyramid and collect information about clinicians’ performance in their normal practice. In this pyramid, assessment moves from the “knows” stage via “knows how” (paper and computer simulations) and “shows how” (performance simulations) to the final “does” level of habitual performance in day-to-day practice. The competency movement is a plea for an integrated approach to competence, which respects the (holistic or tacit) nature of expertise. Van der Vleuten (2005) argues that the learning and assessing of professional judgment is the essence of what medical competence is about. This means that, rather than being a quality that augments with each rising level of Miller’s pyramid, authenticity is present at all levels of the pyramid and in all good assessment methods. A good illustration of this is the way test items of certifying examinations in the United States are currently being written. Compared with a few decades ago, today’s items are contextual, vignette-based or problemoriented and require reasoning skills rather than straightforward recall of facts.

Unique Considerations of Competence in Modern Anesthesia Practice
It can be said that there exist a common set of important personal traits that are shared amongst all aspects of medicine and patient care, but there are specific skills that can be acknowledged as specialty-based or contextspecific, especially in anesthesiology. Anesthesiology has experienced dramatic technological innovations, the introduction of increasingly potent, shorter-acting drugs, increasingly complex medical patients, and advances in surgical techniques; all of this has created new educational challenges while experiencing increasing pressure to be time-and-cost effective and practice safe medicine. Although anesthesiologists historically have given safety the highest priority, forces from inside and outside the specialty are directing more resources toward reducing the already low risk of anesthesia. Studies have identified deficiencies in human performance as an important component in the causation of critical incidents in anesthesia (Holzman, 1995). The dynamic, tightly-coupled, and critical nature of anesthesia practice can be most accurately described as a complex adaptive system; that is, the successful operation involves many different elements, each of which is subject to direct or indirect influence from a variety of sources, and all of which interact in ways that are constantly subject to change. The vocabulary, theories, and techniques of human factor analysis created in the wake of nuclear power, aviation, and space flight disasters can be applied to the performance of anesthesia providers. It is incumbent upon an educational system (i.e. anesthesiologist assistant educational programs) to reorganizes, changes its focus, or adds new systems to respond to the perceived needs of students, professionals, and the culture in which they function.

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Decision making in anesthesiology, as in relatively few medical specialties, is a special subset of decision making because it is an event-driven phenomenon. The environment in which the anesthesia provider works-complex technical machines, patients with variably disordered physiologic systems, and a constantly changing surgical milieu-has many interconnected, “tightly-coupled” parts. What happens in one part of the system directly affects other portions of the system. There is usually some degree of uncertainty about the data indicating the patient’s physiologic state; it may be ambiguous, incomplete, insensitive, or erroneous. Finally, there is the constant presence of risk. This combination of factors is characteristic of the practice of anesthesiology and is not the typical task environment of most medical professionals (Holzman, 1995). While the basis of expert reasoning is intimately connected to the fund of knowledge of the practitioner, it is not simply the knowledge but the way the knowledge is stored, retrieved, and used that distinguishes the expert from the novice. The expert clinician accumulates knowledge in the context of concrete medical problems a process that enhances the chance of effective retrieval. With experience, the need for a reasoning process diminishes as the mental processes become automated into patterns or "scripts" (Klein, 2007). The process becomes highly efficient and effective. Professional expertise thus develops as a transition from a conceptually high and rational knowledge base (acquired from educational experience) to a non-analytical ability to recognize and handle familiar clinical situations (acquired from extensive clinical experience) (van der Vleuten & Newble, How can we test clinical reasoning?, 1995). Students begin their training at a novice level, using abstract, rule-based formulas that are removed from actual practice. At higher levels, students apply these rules differentially to specific situations. During the program, trainees make judgments that reflect a holistic view of a situation and eventually take diagnostic shortcuts based on a deeper understanding of underlying principles. Experts are able to make rapid, context-based judgments in ambiguous reallife situations and have sufficient awareness of their own cognitive processes to articulate and explain how they recognize situations in which deliberation is essential. Clinical expertise implies the practical wisdom to manage ambiguous and unstructured problems, balance competing explanations, avoid premature closure, note exceptions to rules and principles, and — even when under stress — choose one of the several courses of action that are acceptable but imperfect (Klein, 2007). Testing either inductive thinking (the organization of data to generate possible interpretations) or deductive thinking (the analysis of data to discern among possibilities) in situations in which there is no consensus on a single correct answer presents formidable psychometric challenges (Epstein, 2007).

Current Assessment Techniques in Anesthesiologist Assistant Education
The assessment of clinical competence is one of the most difficult tasks facing medical education (Howley, 2004). Whether the purpose is to certify a level of achievement, provide feedback to students about their clinical skills, or provide faculty with information about curriculum effectiveness, the method of assessment has a powerful effect on how and what students learn. If the assessments are inappropriate or primarily focused on basic cognitive skills, misinformation will be given back to students, and poor decisions will be made. Ultimately, inferior assessment practices will result in dissatisfied patients and compromised health care. The field of medical education is becoming increasingly more complex. What once was considered a credible form of education and assessment now falls below our acceptable level of standards (Howley, 2004). Traditionally, clinical evaluation methods consisted primarily of faculty and/or preceptor observations, oral examinations, and multiple-choice tests; however, as evidence in assessment effectiveness and the demand for assurance of clinical competence grows, the anesthesiologist assistant community must adapt to meet the needs of the population we serve. Important Aspects of Assessment Techniques A sound assessment modality must include a clear statement of purpose, a detailed description of what is to be measured, a set of instructions for feasible administration and scoring, and guidelines for data interpretation (Howley, 2004). If intended to measure complex cognitive skills, it is reality based and taps into the high-level skills of application, analysis, synthesis, and evaluation. Additionally, besides such classical criteria as reliability and validity, any assessment model must include consideration of elements such as educational impact, the acceptability of the method to the stakeholders and the investment required in terms of resources, as well as other perfunctory components such as transparency, meaningfulness to the profession, cognitive complexity, directness and fairness.

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Finally, it must also includes sufficient evidence that the scores derived from the modality are reliable and valid indicators of students’ clinical competencies (Epstein, 2007). In the anesthesiologist assistant educational community, the most prominent and heavily weighted assessment methods of clinical competence include (a) faculty observations of clinical performance with rating scales, and (b) multiple choice examinations of clinical competence. Faculty and clinical preceptor observation of students’ clinical performance remains the primary evaluation method in AA education. Multiple Choice Exams An important aspect of both the anesthesiologist assistant educational programs and the certification process’ assessment program is the measurement of knowledge, and this can be done efficiently with methods such as the multiple choice question (MCE). Multiple-choice examinations are commonly used for assessment because they can provide a large number of examination items that encompass many content areas, can be administered in a relatively short period, and can be graded by computer. These factors make the administration of the examination to large numbers of AAs and AA students straightforward and standardized. Formats that ask the examinee to choose the best answer from a list of possible answers are most commonly used (Epstein, 2007). However, newer formats may better assess processes of diagnostic reasoning. The down-side of this strategy is that many multiple choice examinations have been shown to measure little more than the ability to reproduce isolated facts; and a growing awareness of the detrimental effect this may have on student learning, and on acquisition of clinical reasoning skills, has encouraged the development of alternative test formats (van der Vleuten & Newble, How can we test clinical reasoning?, 1995). Multiple-choice examinations may also create situations in which an examinee can answer a question by recognizing the correct option, but could not have answered it in the absence of options (Epstein, 2007). This effect, called ‘cueing’, is especially problematic when diagnostic reasoning is being assessed, because premature closure — arriving at a decision before the correct diagnosis has been considered — is a common reason for diagnostic errors in clinical practice (Epstein, 2007). Preceptor, Faculty & Student-Self Evaluations Though feedback, both summative and formative, from the preceptor to the AA student is critical to day-to-day correction of deficiencies or reinforcement of best practice is critical to the maturation of the student, the formalized clinical evaluation may be so subjective as not to be reliable. Although, the reliability of our clinical assessments has yet to be formally investigated, several studies have shown wide interfaculty ratings of same student performance, evident on daily clinical evaluations (Morgan & Cleave-Hogg, 2000). There is little `control' over the intra-operative teaching sessions and student feedback has indicated a wide variation in day-to-day experiences with clinical faculty in this setting. During observations of student performance on the high-fidelity simulator, we had anticipated a higher correlation between the clinical and simulator evaluations since the simulator environment replicates the operating room. However, it is evident that most students have not experienced many of the events that occur during the simulator session, nor have they witnessed a preceptor managing similar problems. Consequently, evaluation mechanisms for clinical experience are inherently different than those in the simulated environment. Student self-assessments are often included as a component of AA programs’ evaluation modalities, however, fundamental cognitive limitations in the ability of humans to know themselves as others see them restrict the usefulness of self-assessment (Epstein, 2007). Furthermore, rating oneself on prior clinical performance may not achieve another important goal of self-assessment: the ability to monitor oneself from moment to moment during clinical practice.

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Utility of Simulation as an Assessment Technique
There are several factors that place pressure on the health care simulation community to become involved increasingly in summative assessment. First, the development of the competency-based approach to training in the healthcare professions has moved the focus of assessment away from knowledge and simple practical skills (more suited to multiple choice examinations) to more complex clinical activities where non-technical skills such as information gathering, prioritization and effective team-working with other health care professionals are factors critical to successful management of a perioperative course (Glavin & Gaba, 2008). Second, the momentum of the patient safety movement (to which many from the health care simulation community have made significant contributions) is also focusing on the range of countermeasures to human error with expectations that clinicians may be expected to demonstrate their abilities to a recognized standard determined by the profession and the community it serves. To effectively determine if simulation offers a viable means of assessment of clinical competency, one must evaluate the utility of this method. Van der Vleuten (1995) describes five criteria for determining the usefulness of a particular method of assessment: (1) reliability (the degree to which the measurement is accurate and reproducible); (2) validity (whether the assessment measures what it claims to measure); (3) impact on future learning and practice; (4) acceptability to learners and faculty, and (5) costs (to the individual trainee, the institution, and society at large) (Epstein, 2007). Validity refers to whether an instrument actually does measure what it is supposed to. Newer developments concerning assessment methods in relation to validity have typically been associated with the desire to attain a more direct assessment of clinical competence by increasing the authenticity of the measurement (van der Vleuten & Schuwerth, 2005). The validity of an assessment has a number of components: (1) Content validity refers to how representative the test is of learning objectives or, stated another way, whether the test measures skills important and is valuable to learning the construct. Content validity is based on judgment, and would be high with simulator assessments so long as the simulation scenarios were designed such that it could be reasonably assumed that a minimally competent AA should be able to handle the situation. (2) Construct validity represents how well the test measures what it claims to be measuring, and can be measured by how well the test results meet expectations of performance. Construct validity can be evaluated by comparing the performance of groups of clinicians, where substantially better performance in one group would be expected. This has been confirmed in several studies assessing simulator performance where experienced anesthetists performed better than less experienced anesthetists, supporting the proposition that simulator performance has some validity as a measure of real-life performance (Weller, 2003). (3) Face validity refers to whether the instrument seems as though it is measuring the appropriate construct and relies heavily on how realistic the simulator, scenario, and environment are to the participants. Face validity of the simulator is high, in that it appears to assess what it sets out to assess (Weller, 2003). It is designed to be a highly realistic representation of an anesthetic crisis in an operating theatre. The predominant condition affecting the reliability of assessment is domain- or content-specificity, because competence is highly dependent on context or content (van der Vleuten & Schuwerth, 2005). This means that we will only be able to achieve reliable scores if we use a large sample across the content of the subject to be tested. The complex nature of the diagnostic and management skills required to implement therapy in an acute care setting can make the evaluation of a simulated performance complex. The multitude of cognitive, psychomotor, inferential and deductive skills required to treat the patient suggests that quantifying the results from a simulated performance via checklists (e.g. lists of appropriate medical and technical actions) or behavioral ratings of various patient management activities could be subject to several potentially confounding factors (Murray, 2002). Fortunately, initial studies have shown that anesthesiologists’ technical and behavioral performances in crisis settings can be scored reliably by faculty raters (Murray, 2002). Nevertheless, these investigations have generally been limited to quantifying sources of error attributable to the rater (i.e. inter-rater reliability studies) or the particular set of checklist items (internal consistency).

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Basically, the message is that no method is inherently unreliable and any method can be sufficiently reliable, provided sampling is appropriate across conditions of measurement (Crossley J, 2002). An important consequence of this shift in the perspective on reliability is that there is no need for us to banish from our assessment toolbox instruments that are rather more subjective or not perfectly standardized, provided that we use those instruments sensibly and expertly. Conversely, we should not be deluded into thinking that as long as we see to it that our assessment toolbox exclusively contains structured and standardized instruments, the reliability of our measurements will automatically be guaranteed. Although simulators have been judged to be highly realistic, able to improve the acquisition and retention of knowledge and produce reasonably consistent scores (Murray, 2002), additional psychometric studies are required. This reliability and validity testing is required before the patient simulator can be fully embraced as an evaluation tool. The advantage of high-fidelity simulation systems compared with the current method for testing and certification, including written and oral examinations, is that they allow the examinee to demonstrate clinical skills in a controlled clinical environment while still exhibiting cognitive and language skills (Issenberg, McGaghie, & Hart, 1999). While these simulation assessments are not perfect, they are no worse than our existing instruments and methods, and they certainly offer a unique window on performance that is not represented in our current assessment armamentarium. At present, simulation is perceived more as an educational tool than an instrument to be used for certification purposes. However, provided that barriers such as the high cost of construction and operation of a simulation center can be addressed, the ability to observe examinees demonstrating clinical skills in a controlled environment will definitely allow for a more legitimate and equitable assessment of competence, especially in high-stakes testing situations. The key element in the successful use of simulators is that they become integrated throughout the entire continuum of our anesthesiologist assistant education curriculum so that deliberate practice to acquire expertise over time is possible. By analogy, the number of years someone plays a sport or practices a profession bears limited relation to how well they perform. What does correlate with quality of performance is the amount of ongoing deliberate practice that includes “informative feedback and opportunities for repetition and correction of errors.” (Issenberg, McGaghie, & Hart, 1999)

Conclusions
Examinations define the curriculum, often in a way that is not intended by an academic staff or profession at large. The lesson is that, if we wish students to develop effective clinical reasoning skills, we must devise examinations that reflect this intent. It is the presenter’s view that the preceding discussion constitutes a strong plea for a shift of focus regarding assessment, that is, a shift away from individual assessment methods for separate parts of competencies towards assessment as a component that is inextricably woven together with all the other aspects of a training program. Clinical competence is an extremely complex construct and one that requires multiple, mixed, and higher order methods of assessment to support valid interpretations (Howley, 2004). Although our AA students are frequently tested, the methods of assessment are still primarily focused on low-level skills. If we expect excellence of our future AAs, we must begin to ensure competence in high-level skill areas. This begins with the use of simulationbased testing and other more authentic clinical performance assessments. The development of optimal performance assessments, at a local or national level, is complex—requiring time, commitment, resources, and substantial efforts. However, this is the price to pay if we are to ensure clinical competence, protect the quality of patient care, and subsequently “touch the heart of the matter.”

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References
Anderson, L., & Krathwohl, D. (2001). A Taxonomy for Learning, Teaching, and Assessing: A Revision of Bloom's Taxonomy of Educational Objectives. Longman: New York, NY. Crossley J, H. G. (2002). Assessing health professionals. Medical Education , 800-4. Epstein, R. (2007). Assessment in medical education. New England Journal of Medicine , 356:387-96. Fletcher, G. (2003). Anesthetists non-technical skills (ANTS): evaluation of a behavioral marker system. British Journal of Anesthesia , 90(5):580-8. Flexner, A. (1910). Medical Education in the United States and Canada. New York, NY: Carnegie Foundation for Higher Education. Gaba, D. (1992). Improving anesthesiologists' performance by simulating reality. Anesthesiology , 76:491-4. Glavin, R., & Gaba, D. (2008). Challenges and opportunities in simulation and assessment. Journal of Simulation in Healthcare , 3(2):69-71. Henrichs, B., & al, e. (2009). Performance of certified registered nurse anesthetists and anesthesiologists in a simulation-based skills assessment. Anesthesia & Analgesia , 108:255-62. Holzman, R. (1995). Anesthesia crisis resource management: real-life simulation training in operating room crises. Journal of Clinical Anesthesia , 7:675-87. Howley, L. (2004). Performance assessment in medical education: where we've been and where we're going. Evaluation & the Health Professions , 27(3):285-303. Issenberg, S., McGaghie, W., & Hart, I. (1999). Simulation technology for health care professionals skills training and assessment. Journal of the American Medical Association , 282(9):861-6. Klein, G. (2007). Sources of Power: Decision Making . Kyle, R., & Murray, W. (2008). Clinical Simulation: Operations, Engineering and Management. Burlington, MA: Elsevier. McIntosh, C. (2009). Lake Wobegon for anesthesia...where everyone is above average except those who aren't: variability in the management of simulated intraoperative critical incidents. Anesthesia & Analgesia , 6-9. Miller, G. (1990). The assessment of clinical skills/competence/performance. Academic Medicine , 65:S63-7. Morgan, P., & Cleave-Hogg, D. (2000). Evaluation of medical students' performance using the anesthesia simulator. Medical Education , 34:42-5. Murray, D. (2002). An acute skills evaluation for graduating medical students: a pilot study using clinical simulation. Medical Education , 36:833-41. Sween, S. (2009, February 9). Chairman, Physician Specialists in Anesthesia. (M. S. Nichols, Interviewer) Takien, A., McGuire, C., & McGaghie, W. (1999). Innovative Simulations for Assessing Professional Competence. Chicago, IL: University of Illinois at Chicago. van der Vleuten, C. P., & Newble, D. I. (1995). How can we test clinical reasoning? Lancet , 345:1032-4. van der Vleuten, C. P., & Schuwerth, L. W. (2005). Assessing professional competence: from methods to programmes. Medical Education , 39:309-17. Vreuls, D., & Obermeyer, R. (1985). Human system performance measurement in training simulators. Human Factors , (27):24150. Weller, J. (2003). Evaluation of high fidelity patient simulator in assessment of performance of anaesthetists. British Journal of Anaesthesia , 90(1):43-7.

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Alpha-2 Agonists for Sedation and General Anesthesia
Roy Soto, MD
Objective: At the conclusion of this course, the participant will be able to 1) evaluate methods for the systematic assessment of patient sedation and analgesia in acute care settings to optimize use of appropriate sedatives and analgesics; 2) analyze current research data to reevaluate use of sedatives and analgesics in specific patient populations and 3) summarize data comparing alpha-2 agonists to other sedatives in the perioperative setting.

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Perioperative Dexmedetomidine Roy G. Soto, M.D. Introduction For years clonidine has been the only alpha-2 agonist used in routine anesthetic practice, finding a niche in the world of regional anesthesia and pain management. Dexmedetomidine is an alpha-2 agonist with a significantly higher alpha-2 specificity than clonidine, and its unique pharmacokinetic and dynamic properties make it an ideal anesthetic adjunct for select patients. Sedation Although not as effective as propofol, dexmedetomidine is a reasonable sedative and is unique in that it produces a 'sleep-like' EEG pattern. What this means clinically is that even when someone is nicely sedated with dexmedetomidine, you can arouse them easily and they will wake up completely lucid. BIS studies have shown a rapid return of level of consciousness upon patient stimulation. In contrast, if a patient becomes oversedated and uncooperative during propofol sedation, there’s frequently no recourse but to wait it out. Analgesia Although not as effective as fentanyl, dexmedetomidine has a measurable opiate sparing effect. If used during general anesthesia, this results in a significant decrease in narcotics needed (plus the sedative effect allows you to use ~ 30% less volatile agent). Perfect for the morbidly obese...you need less other "stuff", so patients wake up more quickly. Ditto for the elderly. Less opiates and volatiles = (potentially) less postoperative confusion and emergence delay. Sympatholysis Although not as effective as lidocaine/esmolol/fentanyl, the sympatholytic effect of dexmedetomidine is still good...typically, patients gets ~ a 15% drop in MAP and HR, with a good sympatholytic effect that lasts as long as plasma levels are therapeutic. Again, nice for vasculopaths having minimally invasive procedures such as endovascular surgery. Note that an overaggressive loading bolus will result in vasoconstriction leading to hypertension due to high dose alpha-2 stimulation. The sympatholytic effect also has contributed to its increased use during cardiac surgery (although some authors suggest a direct cardioprotective effect of dexmedetomidine, akin to that of volatile anesthetics). Meta-analyses suggest that peri-CABG use of dexmedetomidine reduces morbidity and mortality, decreases ICU time, speeds extubation in the ICU, and reduces total hospital/ICU cost. Respiratory Properties No matter how much you give, you get absolutely no reduction in TV, RR, or minute ventilation. Again, beautiful choice for sedation in patients with sleep apnea, bad COPD, etc having procedural sedation. The Negatives Unlike propofol which yields a dramatic and immediate effect, dexmedetomidine takes a while to start working, mainly due to the requirement for a slow bolus. This makes the drug less useful

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for endoscopy and other rapid turnover procedures. I start my infusions as soon as the patient hits the room, so that plasma levels are therapeutic once the patient is prepped/draped and the surgeon is ready. Although having an agent that potentially can quicken wake-up, reduce use of other anesthetics, and enhance patient safety sounds great, many institutions have balked at the cost: $55/bottle (which should last about 3 hours) compared to less than $5/bottle for the new generic formulations of propofol. As mentioned previously, a unique aspect of dexmedetomidine is that patients wake up when you prod them, which can take some adjustment! This is how a typical first case goes with a new dexmedetomidine-user: your patient is perfectly sedated on the drug and they're snoring, and the surgeon asks "can I go ahead?" and you poke the patient and say "how're you doing?", the patient opens his eyes, smiles, and says "I'm fine, how're you?". Then you'll think he's not sedated enough, you'll give a bunch of fentanyl/versed/propofol and the next step involves an oral airway and jaw thrust! Leave the patient alone, make sure the surgeon uses enough local, and you'll be fine…please don’t send me hate mail until you’ve used it at least 5 times! Dosing 1. Drug is dosed in mcg/kg/hr, NOT per minute. This is common error #1 2. The bottle has 200mcg in 2cc. It says "100mcg/cc" on the bottle, and it's a small bottle, so people assume it's only 100mcg in there. This is common error #2 3. I mix the 200mcg into 50cc of diluent in a syringe pump yielding a concentration of 4mcg/cc (or 0.004mg/cc) 4. Dosing range is 0.2-0.8mcg/kg/hr...remember the decimal point! This is common error #3 5. Package insert says to load 1mcg/kg over 10min. This will occasionally cause hypertension or bradycardia. Most authors recommend a lower load, and I use 0.5mcg/kg over 20min. 6. Half-life is about 6-8min, so it'll go away very quickly if your syringe runs out, or you turn it off at the end of the case Appropriate Cases 1. Carotids, general or sedation 2. Obese patients, general or sedation: allows much less opiate and appreciably less volatile agent 3. Endovascular procedures under sedation (including the dreaded cath lab procedures): allows patients to tolerate lying on a hard bed forever 4. Frail patients having sedation procedures...the 100yo patient for toe debridement or AV fistula, for example 5. Awake fiberoptic intubation...in my opinion nothing’s better! 6. Smooth extubation...quells the "sympathetic storm of extubation” Summary Dexmedetomine is a unique drug that has definite advantages in a select subset of patients. It also has to be used appropriately, and requires some patience. If you're looking for a drug to zonk-out patients to tolerate leg amputation under sedation, this isn’t it. If you want an adjunct to general anesthesia that'll let you use the same amounts of volatile and opiate as always without hypotension this isn’t it either. For select patients, however, it fills a nice niche that no other drug does.

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References Hall JE, Uhrich TD, Barney JA, et al. Sedative, amnestic, and analgesic properties of smalldose dexmedetomidine infusions. Anesth Analg. 2000; 90:699-705 Feld JM, Hoffman WE, Stechert MM, et al. Fentanyl or dexmedetomidine combined with desflurane for bariatric surgery. J Clin Anesth. 2006; 18:24-8 Venn RM, Hell J, Grounds RM. Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care. Crit Care. 2000; 4:302-8 Dasta JF, Jacobi J, Sesti AM, McLaughlin TP. Addition of dexmedetomidine to standard sedation regimens after cardiac surgery: an outcomes analysis. Pharmacotherapy. 2006; 26:798-805 Wijeysundera DN, Naik JS, Beattie WS. Alpha-2 adrenergic agonists to prevent perioperative cardiovascular complications: a meta-analysis. Am J Med. 2003; 114:742-52. Biccard BM, Goga S, de Beurs J. Dexmedetomidine and cardiac protection for non-cardiac surgery: a meta-analysis of randomised controlled trials. Anaesthesia. 2008; 63:4-14 Kulkarni A, Price G, Saxena M, Skowronski G. Difficult extubation: calming the sympathetic storm. Anaesth Intensive Care. 2004; 32:413-6

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Cardiac Output after the Pulmonary Artery Catheter
Joel Zivot, MD
Objectives: At the conclusion of this course, the participant will be able to discuss the data that shows the limited value of PA catheters in changing clinical outcomes and explain new technologies that derive cardiac output by other measures.

Materials from this speaker were not available at time of publication.

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Tuesday, April 21

Tuesday April 21, 2009
7:00 am-12:00 n 7:30 am-8:00 am Registration Continental Breakfast Future Directions in Anesthetic Pharmacology Tong J. Gan, MD Intraoperative Fluid Management Tong J. Gan, MD Coffee Break and Committee Meet and Greet Perioperative Temperature Management Matt Zeleznik, MD Lipid Rescue for Local Anesthetic Toxicity Matt Zeleznik, MD 2nd Annual AAAA Golf Scramble

8:00 am-9:00 am 9:00 am-10:00 am 10:00 am-10:30 am

10:30 am-11:30 am 11:30 am-12:30 pm 2:00 pm

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Future Directions in Anesthetic Pharmacology
Tong J. Gan, MD
Objective: At the conclusion of this course, the participant will be able to 1) understand the pharmacology of novel drugs used in anesthesiology including antiemetics, sedatives, opioids, inhalational agents; 2) understand novel delivery systems including nasal, transdermal, buccal and liposomal route of delivery for anesthetic related drugs; and 3) understand data of drugs and new data of existing drugs.

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Intraoperative Fluid Management
Tong J. Gan, MD
Objective: At the conclusion of this course, the participant will be able to 1) discuss the physiology of fluid compartments; 2) discuss the various colloids and crystalloids for perioperative use; 3) discuss fluid administration strategies, goal directed versus restrictive; and 4) present data on fluid management and outcomes.

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Perioperative Temperature Management
Matt Zeleznik, MD
Objectives: At the conclusion of this course, the participant will be able to 1) define normal thermoregulation; 2) describe perterbations of normal thermoregulation under general and regional anesthesia; 3) identify complications of unintentional perioperative hypothermia and 4) learn strategies to avoid and treat perioperative hypothermia.

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“Some Like It Hot”
An Evidence Based Approach to Perioperative Temperature Management AAAA Annual Conference April 21, 2009 Matt Zeleznik, M.D.

Some Like it Hot
Please porridge hot, Please porridge cold, Please porridge in the pot, Nine days old; Some like it hot, Some like it cold, Some like it in the pot, Nine days old.

 Powerstation: Robert Palmer, John Taylor,

and Andy Taylor (from Duran Duran)

 Powerstation Performed “Some Like it Hot”

and “Bang a Gong” On SNL February 16, 1985.  “Some Like it Hot” rose to Number 6 on the Billboard Top 100

Some Like it Cold

Some Like it Cold
Wim Hof aka “The Iceman”

Coney Island Polar Bear Club

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Some Like it Cold

An Evidence Based Approach to Perioperative Temperature Management
 Normal human thermoregulation  Alterations in thermoregulation under

anesthesia  Perioperative Hypothermia
 Consequences  Treatment  Prevention

Normal Thermoregulation
 Afferent Input  Signals from cold receptors travel along A delta fibers  Signals from heat receptors travel along C fibers  Thermal information is then integrated within the spinal cord  The information then travels to the hypothalamus

Normal Thermoregulation
 Central Control  The hypothalamus is the main thermoregulatory control center in humans  Normal core temperature is 37o C  Varies 1oC with the circadian cycle and 0.5o with the menstrual cycle

Normal Thermoregulation
 Interthreshold Range:  The threshold for response to warmth (sweating, active vasodilation) normally exceeds the threshold for response to cold (vasoconstriction) by 0.2o C  This range is the interthreshold range  Temperature variations within this range do not trigger a response.

Normal Thermoregulation
 Core temperature is maintained within 0.2o

C of the target value

 Not as precise in the elderly

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Normal Thermoregulation
 Efferent Response
 Behavior - most effective  Hyperthermia
 Sweating and active cutaneous vasodilation are the most

GA - Thermoregulation
 Thermoregulation is inhibited by

important autonomic responses

 Hypothermia
 Vasoconstriction in arteriovenous shunts  Non-shivering thermogenesis - infants  Shivering - increases metabolic rate 2 - 3x normal

anesthetics in a dose dependent manner  Vasoconstriction is inhibited  Shivering is reduced  Overall, the interthreshold range is widened to 4o C

GA - Heat Balance
 Inadvertent hypothermia is by far the

GA - Heat Balance
 Normally there is a 2-4o C gradient from the

most common perioperative thermal disturbance.  Hypothermia occurs secondary to impaired thermoregulation and exposure to the cold environment.

core to periphery

 GA reduces the threshold for vasoconstriction

to a level below body temperature during the first hour.

 This decreases the core temperature 1-1.5o C  After that, the core temp decreases at a

slower rate due to body’s heat loss exceeding production.

GA - Heat Balance
 Redistribution of heat from the core to

GA - Heat Balance
 Heat loss continues for 3-5 hours until a

the periphery accounts for 80 % of heat loss in the first hour of anesthesia and 65% in the first 3 hours of anesthesia.

steady state is typically reached.

167

GA - Magnitude of Heat Loss Determinants
 Redistribution Phase  Initial body heat content  Body morphology - obese patients tend to redistribute less

GA - Magnitude of Heat Loss Determinants
 Linear Phase - Heat loss exceeding

production

 Radiation - Transfer of heat from one surface to

another via photons (60% of total). surface to another. important)

 Conduction - Direct transfer of heat from one  Convection - Heat loss to the air (second most  Evaporative - Important with large surgical

incisions and large prep areas.

Limb Tourniquets
 Slow the rate at which core

Regional Anesthesia Thermoregulation
 Normal activation of autonomic responses is

hypothermia develops  May cause precipitous hypothermia at release

prevented (primarily vasoconstriction).

 Central control is also impaired - the brain

incorrectly judges the temperature of blocked areas to be abnormally high.  Core temperatures that would normally trigger a response are wrongly tolerated.  Patients typically feel warm

Regional Anesthesia - Heat Balance
 Initial hypothermia is also due to heat

Perioperative Hypothermia
 Inadvertent hypothermia is the most

redistribution from core to periphery  From vasodilation of arteriovenous shunts in the legs  Subsequent heat loss occurs as heat loss exceeds production  Heat loss is continual

common perioperative thermal disturbance  Defined as core temperature less than 36o C

168

Perioperative Hypothermia
 Common  Bad for Patients  Treatable  Preventable

Benefits of Hypothermia
 Myocardial Protection in CPB  Protection against cerebral ischemia  Slows the triggering of MH  May reduce mortality in ARDS

Consequences of Hypothermia

Myocardial Ischemia

Myocardial Ischemia
Postoperative Shivering ⇓ Increased oxygen consumption by 400% ⇓ Hypoxemia ⇓ Myocardial ischemia in susceptible patients (elderly)

Myocardial Ischemia
 Oxygen consumption rarely increases

near 400%

 Elderly patients rarely shiver because

advanced age impairs thermoregulatory mechanisms  Shivering is not an important cause of postoperative hypoxemia  Hypoxemia inhibits shivering

169

Myocardial Ischemia
 300 patients undergoing vascular,

Myocardial Ischemia
Intraoperative Cardiac Outcomes
Hypothermic (n=158) Electrocardiographic event Myocardial Ischemia Ventricular Tachycardia 15 (10) 8 (6) 7 (5) Normothermic (n=142) 13 (9) 7 (6) 6 (5) P 0.76 0.99 0.95

general, or thoracic surgery.  Randomized to normothermia or hypothermia (1.3o C difference at end of case).  There was no significant difference between groups other than temperature.
Frank SM et al. JAMA 1997

Frank SM et al. JAMA 1997

Myocardial Ischemia
Postoperative Cardiac Outcomes
Hypothermic (n=158) Electrocardiographic Event Myocardial Ischemia Ventricular Tachycardia Morbid Cardiac Event Unstable Angina/ischemia Cardiac Arrest Myocardial Infarction Electrocardiographic or Morbid Cardiac Event 23 (16) 12 (9) 11 (8) 10 (6) 7 (4) 2 (1) 1 (1) 33 (21) Normothermic (n=142) 9 (7) 6 (5) 3 (2) 2 (1) 2 (1) 0 (0) 0 (0) 11 (8) P 0.02 0.17 0.04 0.02 0.02 0.02 0.02 0.001

Myocardial Ischemia
 Increased plasma norepinephrine levels  Patients are more hypertensive  Anesthetics seem to be protective

against cold mediated myocardial stress

Frank SM, et al. JAMA 1997

Frank SM, et al. JAMA 1997

Coagulopathy Coagulopathy
 Three Mechanisms  Impaired platelet function  Clotting factor enzyme dysfunction  Fibrinolytic Activity

170

EBL in THA
Gender (M/F)

EBL in THA
Normothermic 11/19 63 (10) 79 (13) 170 (11) 85 (31) 97 (13) 65 (12) 38 (4) 0.5 (0.2) 36.8 (0.3) 36.6 (0.4) 36.9 (0.3)
Age (yr) Weight (kg) Height (cm) Duration (min) MAP (mmHg) HR (bpm) EtCO2 (mmHg) Isoflurane (%)

Hypothermic 12/18 63 (10) 75 (13) 168 (9) 87 (24) 99 (17) 64 (10) 36 (4) 0.5 (o.1) 36.9 (0.7) 35.0 (0.5) 35.9 (0.6)

 60 Patients undergoing primary THA  General Anesthesia (STP, Vec, Fent,

N2O, Iso)  Preoperative acute normovolemic hemodilution and cell saver were used  Randomized to normothermia vs mild hypothermia
Schmied H et al. Lancet 1996

Temp - pre-op (0C) Temp - final intra-op (0C) Temp - 2 h post-op (0C)

Schmied H et al. Lancet 1996

EBL in THA
Normothermic Hgb Pre-op Hgb Post-op EBL at End EBL at 3h EBL at 12h EBL POD #1 Patients transfused 12.7 (1.3) 10.9 (1.1) 690 (230) 1310 (330) 1500 (310) 1670 (320) 1/30 Hypothermic 12.2 (1.2) 10.8 (1.4) 920 (400) 1700 (510) 1970 (560) 2150 (550) 7/30 p NS NS 0.008 <0.001 <0.001 <0.001 0.05

EBL in THA
 Conclusion  Mild hypothermia increases blood loss in primary THA  Hypothermic patients were more likely to require blood transfusions

Schmied H et al. Lancet 1996

Schmied H et al. Lancet 1996

Reduced EBL in THA
 150 Patients undergoing THA  Regional anesthesia with CSE  Cell saver was used  Randomized to normothermia (36.5o C)

Reduced EBL in THA
Aggressively Warmed Final Core Temp 36.5±0.3 Conventially Warmed 36.1±0.3 P <0.001

Intraoperative EBL

488 (368-721)

618 (480-864)

0.002

vs. mild hypothermia (36.00 C)

Total EBL

1531 (1055-1746)

1678 (1366-1965)

0.031

Total Units Transfused

62

86

0.061

Winkler M et al. Anesth Analg 2000

Winkler M et al. Anesth Analg 2000

171

Reduced EBL in THA
 Conclusion  Aggressive warming versus conventional warming reduces blood loss in patients undergoing primary THA with regional anesthesia

Wound Infection

Winkler M et al. Anesth Analg 2000

Wound Infection
 The overall incidence of surgical wound

Wound Infection
 Primary defense against surgical pathogens is

infection is between 1% and 3%  It is roughly 10% after colon surgery  Surgical wound infections increase hospital stay by about 1 week on average  In one series of cardiac patients each deep sternal wound infection increased the duration of stay by 16 days.

oxidative killing by neutrophils pressure of oxygen

 This process is dependent on the partial  Hypothermia reduces neutrophil oxidative

killing by decreasing tissue oxygen availability and by impairing the production of reactive oxygen intermediates.

Wound Infection
 Hypothermia triggers thermoregulatory

Wound Infection
 200 patients undergoing elective colorectal

vasoconstriction  This decreases subcutaneous oxygen tensions  The incidence of wound infection correlates directly with subcutaneous oxygen tension  Hypothermia directly impairs immune function
 Decreased T cell mediated antibody production  Decreased non-specific oxidative bacterial killing

by neutrophils

surgery randomized to either normothermia or hypothermia  Pre-op standard bowel prep and antibiotics  STP, Fent, Vec, Iso, Nitrous  Patient characteristics were similar between the two groups  Hypothermia group was 34.7± 0.6oC  Normothermia group was 36.6±0.5o C  Overall wound infection incidence was 12 %
Kurz A et al. NEJM 1996

172

Wound Infection
Normothermia (n=104) Infection #(%) Days to first solid Days to suture removal Length of stay 6 (6) 5.6±2.5 9.8±2.9 12.1±4.4 Hypothermia (n=96) 18 (19) 6.5±2.0 10.9±1.9 14.7±6.5 P .009 .006 .002 .001

Wound Infection
 Conclusion  Intraoperative core temperatures 2o C below normal triple the incidence of wound infection  Hospitalization was prolonged by 20 %

Kurz A et al. NEJM 1996

Kurz A et al. NEJM 1996

Wound Infection
 421 Patients having “clean surgery” -

Wound Infection
All warmed patients (n=278) Wound infection Hematoma Seroma Given post-op antibiotics 13 (5%) 6 (2%) 11 (4%) 18 (7%) Non-warmed patients (n=138) 19 (14%) 9 (7%) 8 (6%) 22 (16%) P

breast, hernia, varicose vein

 Randomized to one of 3 groups:

.001 .26 0.41 .002

standard therapy vs. systemic prewarming vs. local prewarming

Melling AC et al. Lancet 2001

Melling AC et al. Lancet 2001

Wound Infection
 Conclusion  Warming patients before clean surgery helps prevent postoperative wound infection  There were no side effects to prewarming

PACU Recovery

Melling AC et al. Lancet 2001

173

PACU Recovery
 150 Patients having elective abdominal
Aldrete Score > 13 Score > 13 & T core > 36o C Score > 12 Score > 14

PACU Recovery
Normothermic 53 ± 36 66 ± 46 45 ± 26 88 ± 63 Hypothermic 94 ± 65 159 ± 57 61 ± 47 132 ± 74 P <.001 <.001 <.001 <.001

surgery  STP, fentanyl, vec, isoflurane, nitrous  Groups randomized to normothermia (36.5oC) or hypothermia (34.5oC)  Patient characteristics were similar between the two groups

Lenhardt R et al. Anesthesiology 1997

Lenhardt R et al. Anesthesiology 1997

PACU Recovery
 Maintaining core normothermia

decreases the duration of PACU recovery

Postoperative Discomfort

Lenhardt R et al. Anesthesiology 1997

Postoperative Discomfort
 74 ASA I, II, and III patients undergoing

elective colon surgery

 STP, fentanyl, vec, isoflurane, nitrous  Randomized to hypothermic group or

Treatment of Perioperative Hypothermia

normothermic group

 Characteristics were similar between groups  VAS scores were significantly lower in the

hypothermia groups for 3 hours postoperatively

Kurz et al. J Clin Anes 1995

174

Cutaneous Warming
 Passive Insulation - blankets, surgical

Cutaneous Warming
 Active Cutaneous Heating  Circulating Water  Forced Air  Resistive Heating  Radiant Warmers  Hot Water Containers

drapes, gowns

 Single layer reduces heat loss by about

30%. Three layers by about 50%. benefit

 Adding additional blankets is of little  No difference between warm and

unwarmed blankets

Circulating Water
 Limited Efficacy  Relatively small fraction of the total surface area of the body  Most heat loss (90%) is from the anterior surface of the body  Restriction of flow in dependent areas of the body  May be associated with pressure heat necrosis

Forced Air
 Warm via radiant shielding and

convection

 Far more effective than passive

insulation and circulating water

Resistive Heating
 Electric blankets - efficacy is similar to

Radiant Warmers
 Use special incandescent bulbs to

forced air  Maybe more dangerous

generate infrared radiation trauma patients

 More helpful in pediatric surgery and

175

Hot water containers
 Warmed irrigation solutions placed in

Fluid Warming
 One unit of refrigerated blood or 1 L of

the groin or axilla  Not efficacious - limited warming area  Dangerous - heat will accumulated locally and may cause tissue damage  ASA closed claims study reveals that hot water bottles were by far the leading cause of perioperative thermal injury

crystalloid solution at room temperature decreases mean body temp by 0.25o C.  Fluid warmers minimize these losses  Fluid warming does not warm patients to any significant extent

Airway Heating & Humidification
 Less than 10% of metabolic heat

production is lost via the respiratory tract  Humidification can reduce these losses  No benefit to actively warming the gasses

Prevention of Perioperative Hypothermia

Prewarming
 Reduces hypothermia by 2 mechanisms  Decreasing the normal core-to-peripheral temperature gradient  Provoking vasodilation which decreases the effect of anesthesia induced vasodilation

Preinduction Warming
 6 Healthy volunteers at UCSF  Received either prewarming for 2 hours

or no warming

 Propofol and nitrous for 1 hour  Temperature decreased 1.1±0.3o C in

warming group and 1.9±0.3o C in control group

Hynson JM et al. Anesthesiology 1993

176

Preinduction Warming
 Conclusion  Redistribution hypothermia can be minimized by preinduction warming of peripheral tissues

Preop Skin Surface Warming
 16 patients undergoing elective THA

randomized to pre-warming for 90 minutes or no warming.  No differences in patient characteristics

Hynson et al. Anesthesiology 1993

Just B et al. Anesthesiology 1993

Preop Skin Surface Warming
Core Temp Unwarmed (n=8) Basal End of prewarming Admission to OR 60 min of anesthesia End of surgery 36.5±0.1 ---36.5±0.1 35.8±0.1 35.2±0.2 Core Temp Warmed (n=8) 36.5±0.1 37.0±0.1 36.9±0.1 36.5±0.1 36.3±0.1

Preop Skin Surface Warming
 Conclusion  Preanesthetic skin surface warming reduces postinduction hypothermia  Postoperative shivering is reduced by prewarming

Just B et al. Anesthesiology 1993

Just B et al. Anesthesiology 1993

Prewarming for OPCAB
 40 patients undergoing OPCAB

Prewarming for OPCAB
Baseline T 30 min T 60 min T 90 min

randomized into prewarming vs. no prewarming  Midazolam, Sufentanil, Roc, Iso  No difference between the 2 groups  Active warming duration was 49.7±9.9 min
Kim J Y et al. Eu J CT Surg 2006

Core Temp Control

36.7±0.2

36.0±0.5

35.5±0.6

35.2±0.6

Core Temp Prewarming

36.7±0.2

36.3±0.4

35.8±0.4

35.6±0.5

Kim J Y et al. Eu J CT Surg 2006

177

Prewarming for OPCAB
 Prewarming reduced the incidence and

Preop Plus Intraop Warming
 30 ASA I and II women undergoing

degree of redistribution hypothermia in patients undergoing OPCAB  It does not delay the induction of anesthesia

elective abdominal surgery

 Randomized to no warming, intraop

warming, or prewarming (60 minutes) + intraop warming  No physical differences among groups  No patients in the prewarming group were hypothermic (T < 36o C)
Vanni SMD et al. J Clin Anes 2003

Kim J Y et al. Eu J CT Surg 2006

Duration of Prewarming
 7 male volunteers warmed for 2 hours  Half started sweating during the second hour

of warming  None of the volunteers felt uncomfortable during the first hour of warming  Thirty minutes of forced-air warming increased the peripheral heat tissue content by more than the amount normally redistributed during the first hour of anesthesia

All patients should be prewarmed

Sessler DI et al. Anesthesiology 1995

Still Not Convinced?
 SCIP (Surgical Care Improvement

Conclusions
 Human thermoregulation is precisely

Project) Measure ID # SCIP-Inf-7  “Colorectal surgery patients with immediate postoperative normothermia” (core temperature greater than or equal to 96.8o F)

controlled

 GA and regional anesthesia upset this

homeostasis

 Intraoperative hypothermia is mostly

due to redistribution of core heat to the periphery

178

Conclusions
 Hypothermia is bad for patients  Myocardial damage  Coagulopathy  Wound infection  Delayed wound healing  Increased PACU time  Thermal discomfort

Conclusions
 Intraoperative hypothermia can be

treated effectively with forced air warming  Intraoperative hypothermia can be prevented (or substantially reduced) by preoperative warming

References
    

References
 Mauermann JW, et al. The anesthesiologist’s role in the prevention of

Frank SM, et al. Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events. JAMA 277:1127-1134, 1997 Hynson JM, et al. The effects of preinduction warming on temperature and blood pressure during propofol/nitrous oxide anesthesia. Anesthesiology 79:219228, 1993. Hynson JM, et al. Intraoperative warming therapies: a comparison of three devices. J Clin Anesth 4:194-199, 1992. Just B, et al. Prevention of intraoperative hypothermia by preoperative skin surface warming. Anesthesiology 79:214-218, 1993. Kim JY, et al. The effect of skin surface warming during anesthesia preparation on preventing redistribution hypothermia in the early operative period of offpump coronary artery bypass surgery. Eu J Cardio Thor Surg 29:343-347, 2006. Kurz A, et al. Perioperative normothermia to reduce the incidence of surgical wound infection and shorten hospitalization. NEJM 334:1209-1215,1996.

surgical site wound infections. Anesthesiology 105:413-421, 2006. wound infection after clean surgery: a randomised controlled trial. Lancet 358:876-880, 2001. Anesthesiology 82:674-681, 1995. Anesthesiology 95:531-543, 2001. 1997.

 Melling AC, et al. Effects of preoperative warming on the incidence of

 Sessler DI, et al. Optimal duration and temperature of prewarming.  Sessler DI. Complications and treatment of mild hypothermia.  Sessler DI. Mild perioperative hypothermia. NEJM 336:1730-1737,  Sessler DI. Perioperative heat balance. Anesthesiology 92:578, 2000.  Sessler DI, et al. Nonpharmacological prevention of surgical wound

 Kurz A, et al. Postoperative hemodynamic and thermoregulatory

consequences of intraoperative core hypothermia. J Clin Anes 7:359366, 1995.  Lenhardt R, et al. Mild intraoperative hypothermia prolongs postanesthetic recovery. Anesthesiology 87:1318-1323, 1997.

infections. Healthcare Epidemiology 35:1397-1404, 2002.

 Schmied H, et al. Mild hypothermia increases blood loss and

transfusion requirements during total hip arthroplasty. Lancet 347:289292, 1996.

References
 Taguchi A, et al. Effects of a circulating water garment and forced air

warming on body heat content and core temperature. Anesthesiology 100:1058-1064, 2004.  Vanni SM, et al. Preoperative combined with intraoperative skin surface warming avoids hypothermia caused by general anesthesia and surgery. J Clin Anes 15:119-125, 2003.  Winkler M, et al. Aggressive warming reduces blood loss during hip arthroplasty. Anesth Analg 91:978-84, 2000.  Wong PF, et al. Randomized clinical trial of perioperative systemic warming in major elective abdominal surgery. Br J Surg 94:421-426, 2007.

179

Lipid Rescue for Local Anesthetic Toxicity
Matt Zeleznik, MD
Objective: At the conclusion of this course, the participant will be able to 1) discuss the normal mechanism of action and pharmacobiology of local anesthetics; 2) describe complications of local anesthetic toxicity; 3) identify the prevention and treatment of local anesthetic toxicity; and 4) describe in detail lipid rescue protocols for local anesthetic toxicity.

180

Lipid Rescue for Local Anesthetic Toxicity
AAAA Annual Conference April 21, 2009 Matt Zeleznik, M.D.

No Disclosures

What to Expect
 Local Anesthetic (LA) Structure and Activity  LA Toxicity in General  Historical Context of LA Toxicity  Development of Therapy for LA Toxicity
 Early Studies  Animal Models  Physiologic Models

Regional Anesthesia
 The use of regional anesthesia is

increasing

 Case Reports  Current Practice/Recommendations

 Benefits of regional anesthesia  Potential for reduced mortality  Reduction in major and minor morbidities  Enhanced tissue oxygenation  “Pain as the fifth vital sign”

Regional Anesthesia Complications
 Nerve injury  Wrong-sided block or surgery  LA toxicity

Local Anesthetics - Structure

181

Local Anesthetics - Activity
 Primary site of action is the intracellular

Local Anesthetics - Activity
 All LAs are weak bases formulated to

side of the sodium channel where LAs block sodium influx  Reversibly decrease the rate of depolarization of excitable membranes  Inhibit the propagation of action potentials

the hydrochloride salt to make them water soluble  They exist in equilibrium in the protonated and unprotonated form  Only the unprotonated form diffuses across the lipid membrane to the site of action

LA Systemic Toxicity
 Neurologic Toxicity
 CNS excitation - tinnitus, circumoral numbness,

LA Systemic Toxicity
 Intra-arterial injection  Interscalene, cervical plexus, stellate ganglion  Intravenous injection  Epidural  Peripheral Injection  Peripheral nerve blocks  Plastic surgery procedures

metallic taste in mouth

 Motor twitching followed by grand mal seizure

 Cardiac Toxicity
 Hypotension  Dysrhythmias  Cardiovascular collapse

Intra-arterial Injection
 Usually occurs with peripheral blocks in

Intravascular Injection
 Most commonly occurs in epidural or

the neck  Rapid onset of symptoms  Small quantities of LA  Seizures are typically short-lived

caudal anesthesia in pregnancy

 Epidural veins are engorged, especially  Seizures are more prolonged than with

intra-arterial injection

182

Peripheral Injection
 Onset of symptoms may be 20 to 30

Systemic Toxicity - Pre 1980
Author Blundell, 1955 Bonica, 1957 Moore, 1978 Kenepp, 1981 Epidural (n) 790 3,637 6,729 4,003 STR (n) 87 116 13 40 Rate (n/10,000) 110 320 20 100

minutes  Concentration of local anesthetic in the circulation may remain elevated longer than for intravascular injection  Blood levels depend on site of injection, total mass of drug, presence of vasoconstrictors

Systemic Toxicity
 Editorial by Albright in 1979  Called for research to elucidate the

Systemic Toxicity
 Incremental injection  Dose limitation  Use of markers of intravascular injection

reason for Bupivacaine’s proclivity for cardiac toxicity

(test dose)  Limitation of dosage to “maximum recommended doses”

Maximum Recommended Doses of Local Anesthetics
Chloroprocaine Chloroprocaine with epi Procaine Bupivacaine Bupivacaine with epi Levobupivacaine Lidocaine Lidocaine with epi Mepivacaine Mepivacaine with epi Ropivacaine Ropivacaine with epi 800 mg 1,000 mg 500 mg 175 mg 225 mg 150 mg 300 mg 500 mg 400 mg 550 mg 225 mg (300 mg for brachial plexus) 225 mg (300 mg for brachial plexus)

Systemic Toxicity - Post 1980
Author Blundell, 1955 Bonica, 1957 Moore, 1978 Kenepp, 1981 Tanaka, 1993 Brown, 1995 Auroy, 1997 Epidural (n) 790 3,637 6,729 4,003 17,439 16,870 30,413 STR (n) 87 116 13 40 20 2 4 Rate (n/10,000) 110 320 20 100 11 1.2 1.3

183

Systemic Toxicity - PNB
Author Brown, 1995 Auroy, 1997 PNB (n) 7,532 21,278 STR (n) 15 16 Rate (n/10,000) 20 7.5

Systemic Toxicity
 Overall risk of significant LA toxicity:  4 per 10,000 epidurals (0.04%)  7.5 to 20 per 10,000 peripheral nerve blocks (0.075% - 0.2%)

Bupivacaine Toxicity
 First synthesized in 1963  The most commonly used long-acting
1979

Bupivacaine Toxicity
 Case report by Albright in Anesthesiology in
 Reports on six anecdotal cases of sudden cardiac

aminoamide LA

collapse after Bupivacaine or Etidocaine nerve blockade  Thought initially that cardiac collapse was secondary to hypoxia  Concluded that simultaneous seizures and cardiovascular collapse may occur with Bupivacaine

Early Research
 Molecular mechanisms of Bupivacaine toxicity
 Electrophysiologic actions of LAs  Sodium and calcium channel research  LA-mediated changes in mitochondrial

Lipid Treatment
 1998 - chance observation that

bioenergetics

 Intracellular calcium processing

 Early treatments of Bupivacaine toxicity
 Pretreatment with Midazolam  Potassium channel openers (Lemakalim)  Bretylium and Lidocaine  Amrinone

intravenous lipid increased the dose of Bupivacaine to produce asystole in rats  Designed an experiment to test if lipid pretreatment shifts the dose-response curve for lethal intravenous infusion of Bupivacaine

184

Intralipid
 Approved for human use in 1962  Emulsion in water of soybean oil, mostly

Lipid Infusion and DoseResponse
 24 rats anesthetized (6 in each group)  Group 1 - saline pretreatment  Group 2 - 10% Intralipid pretreatment  Group 3 - 20% Intralipid pretreatment  Group 4 - 30% Intralipid pretreatment  Infusion of Bupivacaine 0.75% at 10

triglycerides, made isotonic with glycerin  Egg yolk phospholipid is the emulsifying agent

mg/min to an end point of 10s of asystole

Lipid Infusion and DoseResponse
Group 1 (placebo) Median Lethal Dose (mg/kg) Mean concentration at asystole (mcg/mL) p 17.8 (13.2-20.3) 93.3 Group 2 (10% Intralipid) 27.6 (22.2-31.7) Group 3 (20% Intralipid) 49.8 (41.3-57.8) Group 4 (30% Intralipid) 82.0 (71.3-101)

Lipid Treatment and DoseResponse
 Lipid:Aqueous ratio of Bupivacaine is

11.9 ± 1.77

 If equal plasma and lipid are mixed 75.3

115

177

212

± 1.32% of Bupivacaine is in the lipid phase

<0.001

<0.001

<0.001

<0.001

Lipid Treatment and DoseResponse
 Conclusions  Lipid pretreatment shifts the lethal dose response curve to the right for Bupivacaine toxicity in rats  Lipid may act as a “sink” for Bupivacaine reducing the aqueous plasma concentration  Lipid appears to have a high capacity or retaining Bupivacaine

Lipid Infusion Rescue in Dogs
 12 Dogs (6 in each group)  Cardiac arrest from Bupivacaine toxicity  Group 1 - Treated with Intralipid  Group 2 - Treated with saline  No differences in baseline

characteristics among animals

185

Lipid Infusion Rescue in Dogs
Group No. Treatment MAP (mmHg) 91±12 HR (bpm) 122±17 PaO2 (mmHg) 236±69 PaCO2 (mmHg) 36±2 pH

Mechanism of Lipid Reversal
 The “lipid sink” hypothesis  Metabolic benefits of lipid therapy?  Study to determine whether lipid

Saline

6

Baseline

7.38±0.04

Saline

6

Recovery

10±3

0

Lipid

6

Baseline

96±14

128±21

228±63

35±2

7.39±0.02

reduces the Bupivacaine content in cardiac tissue

Lipid

6

Recovery

93±12

126±18

212±56

36±2

7.35±0.04

Mechanism of Lipid Reversal
 Isolated rat heart study  Radiolabeled Bupivacaine  Conclusions:
 Lipid accelerates recovery from Bupivacaine

Mechanism of Lipid Reversal
 Isolated rat heart study  Bupivacaine infusion leads to a decrease in  Lipid infusion increased contractility and

heart rate, contractility, and systolic pressure

induced asystole  Lipid reduces Bupivacaine myocardial tissue content  Lipid increases cardiac Bupivacaine washout

 Supports the “lipid sink” hypothesis

systolic blood pressure in Bupivacaine treated hearts  Lipid infusion may to have direct inotropic effect in Bupivacaine depressed isolated rat hearts

Mechanism of Lipid Reversal
 In vitro study that examined binding of

Lipid vs. Epinephrine
 15 rats (three groups of 5)
 Group 1 - saline  Group 2 - Epinephrine  Group 3 - Intralipid 30%

Intralipid with Bupivacaine, Ropivacaine, and Levobupivacaine  Concluded that there is rapid binding of these LAs to Intralipid  Further supports the “lipid sink” hypothesis

 Baseline characteristics were the same among

animals

 All lipid treated rats were resuscitated, with

less pulmonary edema, acidemia, and dysrhythmia compared to epinephrine

186

Lipid vs. Vasopressin + Epinephrine
 10 Pigs randomized to receive either

Lipid vs. Vasopressin + Epinephrine
 Vasopressor group - all five pigs

Intralipid 20% or Vasopressin + Epinephrine after Bupivacaine-induced cardiac arrest  Tried to simulate real arrest conditions  No differences in baseline characteristics among animals

survived  Lipid group - none of the pigs had ROSC (SBP > 80 mmHg > 5 min)  Vasopressor group had higher coronary perfusion pressure, higher pH, and better survival

Lipid vs. Vasopressor
18 rats (6 in each group)
 Group 1 - Intralipid 30%  Group 2 - Vasopressin  Group 3 - Vasopressin + Epinephrine  No differences in baseline characteristics among

Lipid vs. Vasopressor
 Differences in study protocol probably

account for the different results
 Pigs had hypoxic arrest

animals  All lipid-treated rats were resuscitated with better hemodynamics, less pulmonary edema, and less acidosis compared to the vasopressor-treated groups

 Pigs had lower dose of Bupivacaine  End-point definition was different between

the two studies

 Clinically, patients receive a

combination of therapies

Lipid Rescue Video
 Rat model of lipid rescue  Courtesy of Guy

Case Report 1
 58-yr-old 82 kg man for shoulder

arthroscopy

 s/p CABG 15 yrs. prior  Interscalene nerve block with Bupivacaine

Weinberg, M.D and YouTube

0.5% 20mL + Mepivacaine 20 mL 0.5%

 Seizure 30 seconds after injection  Asystolic cardiac arrest 90 seconds later

187

Case Report 1
 Standard ACLS protocol
Intubation Continuous chest compressions Epinephrine 3 mg, Atropine 2 mg, Amiodarone

Case Report 1
 Chest compressions were continued and one

shock of 360 J was given on the ECG

 Within seconds a single sinus beat appeared  Epinephrine 1 mg and Atropine 1 mg  Within 15 seconds NSR at 90 bpm was

300mg, Vasopressin 40 units Defibrillation x multiple attempts VT, asystole, VF

 Intralipid 20% 100 mL given

restored

 He was extubated 2.5 hrs later  Total recovery

Case Report 2
 75-yr-old ASA III female for ORIF femur

Case Report 2
 Sedated and intubated  Intralipid 20% 100 mL was given within

fracture

 L4 lumbar plexus block  Levobupivacaine 0.5% 20 mL  Unresponsiveness, seizure, wide

4 minutes

 Rapid normalization of ECG with stable

hemodynamics anesthesia

complex ECG tracing

 Uneventful surgery under general  Uneventful recovery

Case Report 3
 60-yr-old 83 kg man for left upper AVF

Case Report 3
 ACLS was started  Chest compressions  Atropine 1 mg, Epinephrine 1 mg, Vasopressin 40 units, Bicarbonate, Magnesium  Defibrillation x 11 attempts with brief returns to perfusing heart rhythms

revision  Supraclavicular block with Mepivacaine 1.5% 30mL + Bupivacaine 0.5% 10 mL  Five minutes later he developed apnea and unresponsiveness

188

Case Report 3
 Liposyn III 20% was started 10 minutes

Case Report 4
 91-yr-old 57 kg ASA III man for olecranon

after ACLS was initiated  CPR and defibrillation (x 15 attempts)  Gradually he became hemodynamically stable (~30 min) and was transferred to the ICU  Discharged 3 days later

bursitis surgery

 Infraclavicular brachial plexus block with

Mepivacaine 1% 30 mL + Prilocaine 1% 10 mL  20 minutes after infraclavicular block and 5 minutes after axillary block he became agitated then unresponsive  He developed ventricular bigeminy

Case Report 4
 Intralipid 20% 100 mL was given  An Intralipid infusion was started as

Case Report 5
 83-yr-old 75kg ASA III man for TKA  Combined single shot sciatic block and

well at 14 mL/min  He regained consciousness 5 minutes later  Surgery was performed and the patient had an uneventful recovery

continuous femoral nerve catheter planned  Sciatic block with Bupivacaine 0.5% 26 mL  Abrupt loss of consciousness, seizure, and asystole

Case Report 5
 Midazolam given for seizure  CPR begun and intubation performed  Intralipid 20% 250 mL bolus given  Epinephrine 1 mg, Atropine 1 mg  Intralipid infusion 0.2mL/kg/min started  Patient was in normal rhythm within 5

Case Report 5
 Two of the responders had been trained

minutes

 Uneventful course afterward

with this scenario 8 weeks prior to this clinical event  Their problem recognition and therapy was strongly influenced by their participation in a crisis resource management training simulator

189

Current Practice
 LA choice  Bupivacaine 55%  Ropivacaine 43%  Monitoring  69% pulse oximetry, NIBP, ECG  15% pulse oximetry and NIBP  16% pulse oximetry only

Current Practice
 Resuscitation for Bupivacaine toxicity  74% WOULD NOT USE LIPID!  26% of centers would consider lipid therapy
Located Located Located Located

in in in in

OR pharmacy 39% hospital pharmacy 35% code cart 22% drug dispensing machine 4%

 Only 41% of respondents have a plan for

mechanical cardiopulmonary support

Recommendations
 Have lipid rescue available at block

Recommendations
 No standard therapy for lipid emulsion exists  Current recommendations by Weinberg for LA

locations

 Inform ancillary staff of lipid protocol  Have a plan for cardiopulmonary bypass

cardiac arrest not responsive to standard therapy

(if available) should the need arise

 Chest compressions  Intralipid 20%  1.5 mL/kg as an initial bolus, then  0.25 mL/kg for 30-60 minutes  Bolus may be repeated and infusion rate may be

increased

Recommendations
 www.lipidrescue.com ™
 Protocol for lipid rescue  Blog  Links to recent papers  Registry proposal  Sample rescue kit
 

References
Albright GA. Cardiac arrest following regional anesthesia with Etidocaine or Bupivacaine. Anes 1979;51:285-7 Corcoran W, et al. Local anesthetic-induced cardiac toxicity: a survey of contemporary practice strategies among academic anesthesiology departments. Anes Analg 2006;103:1322-26 Foxall G, et al. Levobupivacaine-induced seizures and cardiovascular collapse treated with Intralipid. Anaesthesia 2007;62:516-8 Gregorio GD, et al. Lipid emulsion is superior to Vasopressin in a rodent model of resuscitation from toxin-induced cardiac arrest. Crit Care Med 2009;37 Greensmith JE, et al. Complications of regional anesthesia. Curr Opin Anes 2006;19:531-7 Groban L and Butterworth J. Lipid reversal of Bupivacaine toxicity:has the silver bullet been identified? Reg Anes Pain Med 2003;28:167-9 Litz RJ, et al. Reversal of central nervous system and cardiac toxicity after local anesthetic intoxication by lipid emulsion injection. Anes Analg 200;106:1575-7

    

190

References
    

References
 

Mayr VD, et al. A comparison of the combination of Epinephrine and Vasopressin with lipid emulsion in a porcine model of asphyxial cardiac arrest after intravenous injection of Bupivacaine. Anes Analg 2008;106:1566-71 Mazoit JX, et al. Binding of long-lasting local anesthetics to lipid emulsions. Anes 2009;110:380-6 Mulroy MF. Systemic toxicity and cardiotoxicity from local anesthetics: incidence and preventive measures. Reg Anesth Pain Med 2002;27:556-61 Rosenberg PH, et al. Maximum recommended dose of local anesthetics: a multifactorial concept. Reg Anesth Pain Med 2004;29:564-75 Rosenblatt MA, et al. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed Bupivacaine-related cardiac arrest. Anes 2006;105:217-8 Santos AC, et al. Systemic toxicity of Levobupivacaine, Bupivacaine, and Ropivacaine during continuous intravenous infusion to nonpregnant and pregnant ewes. Anes 2001;95:1256-64 Smith HM, et al. Simulation education in anesthesia training: a case report of successful resuscitation of Bupivacaine-induced cardiac arrest linked to recent simulation training. Anes Analg 208;106:1581-4

   

Stehr, SN, et al. The effects of lipid infusion on myocardial function and bioenergetics in L-Bupivacaine toxicity in the isolated rat heart. Anes Analg 2007;104:186-92 Warren JA, et al. Intravenous lipid infusion in the successful resuscitation of local anesthetic-induced cardiovascular collapse after supraclavicular brachial plexus block. Anesth Analg 2008;106:1578-80 Weinberg GL, et al. Pretreatment or resuscitation with a lipid infusion shifts the dose-response to Bupivacaine-induced asystole in rats. Anes 1998;88:1071-5 Weinberg GL, et al. Lipid emulsion infusion rescues dogs from Bupivacaineinduced cardiac toxicity. Reg Anesth Pain Med 2003;28:198-202 Weinberg GL. Lipid infusion resuscitation for local anesthetic toxicity. Anes 2006;105:217-8 Weinberg GL, et al. Lipid infusion accelerates removal of Bupivacaine and recovery from Bupivacaine toxicity in the isolated rat heart. Reg Anesth Pain Med 2006;31:296-303 Weinberg GL. Resuscitation with lipid versus Epinephrine in a rat model of Bupivacaine overdose. Anes 2008;108:907-13

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Wednesday, April 22

Wednesday April 22, 2009
7:00 am-12:00 n 7:30 am-8:00 am 8:00 am-9:00 am Registration Continental Breakfast Myocardial Ischemia and Postoperative Monitoring John Ellis, MD CAAHEP/ARC-AA Update Claire Chandler, AA-C Coffee Break Preoperative Cardiac Evaluation John Ellis, MD

9:00 am-10:00 am 10:00 am-10:30 am

10:30 am-11:30 am

192

Myocardial Ischemia and Postoperative Monitoring
John Ellis, MD
Objective: At the conclusion of this course, the participant will be able to 1) understand the pathophysiology of endothelial and vascular dysfunction in cardiovascular surgical patients; 2) describe the negative consequences of chronic and acute hypertension in surgical patients; and 3) manage perioperative hypertension with new pharmacologic options, including the third generation dihydropyridine calcium channel blocker, clevidipine.

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330 Page 1

Myocardial Ischemia and Postoperative Monitoring
John E. Ellis MD Chicago, Illinois

Introduction Tremendous morbidity remains associated with coronary artery disease (CAD) in surgical patients. Perioperative myocardial infarction (PMI) may be lethal or compromise a patient's functional status after surgery. Patients who suffer PMI may on average incur an additional $10,000 - $20,000 in additional hospital costs. Attempts to improve perioperative outcome of patients at risk for having CAD have focused on 3 approaches: (i) preoperative identification of high-risk patients who might benefit from myocardial revascularization, (ii) improved detection of perioperative myocardial ischemia to allow for prompt therapeutic intervention, and (iii) the prophylactic use of anesthetic and antiischemic techniques to decrease the prevalence and severity of postoperative myocardial ischemia. This lecture will address the last two approaches after reviewing the pathophysiology, demographics, and prognosis of postoperative myocardial ischemia and infarction in patients undergoing noncardiac surgery. Many of studies referenced have been undertaken in vascular surgery patients. Myocardial Ischemia Vs. Myocardial Infarction: Myocardial ischemia is the surrogate that is more often addressed in the research reviewed in this lecture. To demonstrate reductions in the rate of infarction (typically reported at ~ 5% in vascular surgical series) with a therapy requires thousands of patients and millions of dollars to show statistical differences. We now have multi-center trials in the anesthesia literature, the use of meta-analysis to combine the results of trials by different investigators of similar interventions, and the analysis of large databases and registries to evaluate therapies. Some of these suggest that examining only surrogate markers may be misleading. Predictors And Prognosis: Demographic predictors (prior probability). Risk factors may include known CAD, congestive heart failure, peripheral vascular disease, advanced age, severely limited exercise tolerance, chronic renal insufficiency, uncontrolled hypertension and left ventricular hypertrophy, impaired glucose tolerance and/or diabetes, and the use of digoxin. Evidence of decompensated heart disease, such as arrhythmias or CHF, appears particularly associated with adverse outcomes. Multifactorial indices, such as the RCRI, have been proposed to risk-stratify patients. Lee et al determined preoperative predictors of adverse cardiac events after noncardiac surgery in a large cohort; these predictors include previous MI, CHF, cerebrovascular disease, major surgery, and diabetes treated with insulin. Resting echocardiographic indicators (systolic dysfunction) may also have additive predictive value (above and beyond clinical risk factors) for predicting perioperative myocardial infarction in high-risk patients. The most recent AHA/ACC guidelines have deemphasized the role of preoperative stress testing, after the CARP study showed no benefit to preop stress testing and coronary revascularization before vascular surgery. Dynamic postoperative predictors. Factors that may increase the likelihood of postoperative myocardial ischemia that we can control include tachycardia, anemia, hypothermia, shivering, hypoxemia, endotracheal suctioning, and less-than-optimal analgesia. For patients undergoing noncardiac surgery, perioperative MI may be associated with higher postoperative heart rates and higher pain thresholds, but not necessarily angina (most are silent). Other factors, such as postoperative hypercoagulability, and REM sleep rebound are more speculative culprits. Prognosis. Postoperative myocardial ischemia confers increased risk to surgical patients. The longer the ischemic episode(s) and the greater the ST segment change, the worse the prognosis. Modern preop preparation, surgery, and anesthesia may be associated with less myocardial ischemia than in the past. We believe that patients with documented severe postoperative myocardial ischemia should be referred to a cardiologist, since they are at high risk for adverse long-term cardiac outcomes. PMI is still associated with 20-30% in-hospital mortality, and is a marker for poor prognosis after discharge in those who survive. Detection of Myocardial Ischemia and Infarction: Patients undergoing vascular surgery are most likely to manifest myocardial ischemia in the immediate postoperative period, usually on the day of surgery or the next. The "silent" nature of postoperative ischemia suggests that frequent ECG monitoring may be useful. Unfortunately, approximately 1/4 of vascular surgery patients will have baseline ECG abnormalities (LBBB, paced rhythm, digoxin effect, LVH with strain) that preclude the detection of myocardial ischemia. Other techniques of ischemia detection, such as the presence of v-waves in the PCWP tracing or decrements in regional wall motion detected with TEE, are less useful after surgery

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330 Page 2 because they are discontinuous, expensive, and relatively invasive. Troponin levels appear more specific in detecting perioperative myocardial infarction than CK-MB isoenzymes; troponin elevations are associated with lower survival after vascular surgery. Routine troponin surveillance appears to be cost effective for AAA surgery. Proposed Mechanisms Of Postoperative Myocardial Ischemia: Stable ischemic syndromes presumably occur with increased oxygen demand on the myocardium in a setting of fixed coronary plaques. Unstable syndromes are thought to be the result of plaque rupture with local thrombus and vasoreactivity that produce intermittent critical decreases in coronary oxygen supply. Patients with elevated coronary calcium on CT scan have greater rates of perioperative MI after vascular surgery. Endothelial function is impaired in CAD, hypertension, hypercholesterolemia, diabetes, and tobacco abuse, resulting in exaggerated vasoconstriction. Poor endothelial function is also associated with poor outcome after vascular surgery. Treatment to “heal” the endothelium (often with statin drugs) improves perioperative outcome, though effective therapy may have to begin weeks before surgery. Also, in patients with left ventricular hypertrophy (LVH), diminished coronary vasodilator reserve results in poor subendocardial perfusion. Early postoperative ischemia is usually associated with ST segment depression rather than ST elevation. ST segment depression usually precedes postoperative cardiac complications. Most perioperative MIs are of the non-Q wave variety. The postoperative period is characterized by adrenergic stress, which can induce myocardial ischemia in patients with CAD; cause coronary vasoconstriction, and facilitate platelet aggregation. Tachycardia limits diastolic time and coronary perfusion, and it can paradoxically reduce coronary artery diameter. Hypertension and tachycardia in the PACU have been shown in a large study to be associated with increased mortality and unplanned ICU admission (although association does not necessarily mean causation.) Surgery can induce a hypercoagulable response due to increased platelet number and function, diminished fibrinolysis, decreases in protein C and antithrombin III, and increases in procoagulants (including fibrinogen, factor VIII coagulant, and von Willebrand factor). These postoperative changes may contribute to an increased likelihood of coronary thrombosis in the postoperative period, but their relative importance in predicting postoperative coronary events remains speculative. TEG may identify high-risk patients. Cardiologists and internists are increasingly undertaking aggressive long-term pharmacologic risk reduction in patients with CAD. These strategies include cholesterol reduction with statins (which stabilize coronary plaques and reduce inflammation), antihypertensive therapy with ACE inhibitors and/or ARBs, and “tighter” glucose control in diabetics. These patients may be more prone to perioperative hypotension, bradycardia, and hypoglycemia. Prophylaxis And Treatment Of Postoperative Myocardial Ischemia: Beta Blockers. Beta adrenergic blocking drugs, through their ability to suppress perioperative tachycardia, appear most efficacious in preventing perioperative myocardial ischemia. They are well tolerated by most surgical patients and may reduce long-term cardiac events. Beta adrenergic blocking drugs have been approved for treatment of hypertension, supraventricular tachycardias, ventricular arrhythmias, angina, and myocardial infarction. They are a cornerstone of chronic post-MI therapy, as they reduce subsequent reinfarction. Antihypertensive effects of beta blockers are useful during adrenergic activation during events such as endotracheal intubation, extubation, ECT, and sternotomy. They also blunt tachycardia at these times, and this is likely the predominant mechanism of their antiischemic effects. Several trials which document the ability of beta blockers to improve perioperative cardiac outcomes have been published, though several very recent trials have questioned this conclusion. Recent work suggests that beta blockade is most efficacious in patients with many clinical risk factors and/or positive stress tests. The outcome benefit from perioperative blockade may persist for up to two years after vascular surgery in high-risk patients. Beta1 selective drugs are less likely to cause bronchospasm, even in patients with reactive airway disease. Still, asthma and COPD are relatively contraindications to beta blockade. There is a very small subset of patients with severe coronary artery disease (floridly positive stress tests in multi-vessel distributions) who appear not to benefit from beta blockade; such patients may be considered candidates for myocardial revascularization. Recent trials (MAVS, DIPOM) have questioned the perioperative protective effects of beta blockade. A recent (n=430 very high risk patients) Dutch RCT (DECREASES-V) suggests that HR control to 60 bpm with titrated beta blockade is better than stress testing +/- coronary revascularization. The larger POISE trial (n= 8351), however, suggests that while fixed-dosed beta blockade with metoprolol lowers rates of myocardial infarction and atrial fibrillation, these improvements come at the cost of increased stroke and death. The POISE trial may result in the scaling-back of CQI and P4P initiatives aimed at increasing the use of periop beta blockade.

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330 Page 3 Other anti-anginal drugs appear less promising. Two studies, one in noncardiac surgery, and one in fast-track CABG surgery, have found that prophylactic intravenous nitroglycerin failed to reduce the prevalence of perioperative myocardial ischemia or infarction. This may have been due to compensatory increases in heart rate. The short-acting calcium antagonist nifedipine may increase mortality after acute MI and should probably not be used as a first line drug for acute control of hypertension in patients with CAD. High Dose Narcotics / Prolonged Anesthesia. High-dose sufentanil anesthesia may reduce the stress response and improve overall outcome after abdominal aortic surgery. The McSPI group showed that postoperative infusion of sufentanil 1 mcg/kg/hr reduced myocardial ischemia following CABG. This approach, however, mandates overnight ventilation, which may not be a cost-effective therapy. The value of propofol, remifentanil, dexmedetomidine, or infusions of other short-acting intravenous agents in maintaining postoperative cardiovascular homeostasis remains unclear. A small trial has suggested that a propofol-based general anesthetic for carotid endarterectomy is associated with less myocardial ischemia than is an isoflurane-based technique; overall ourcomes were unchanged. Epidural Analgesia. Epidural anesthetics reduce cardiac preload and afterload, postoperative adrenergic and coagulation responses, and produce coronary vasodilatation (thoracic epidurals only). These effects suggest that they may reduce perioperative myocardial ischemia. However, evidence of benefits in cardiac outcome has been limited in individual trials. Concerns about respiratory depression, neuroaxis hematomas, and the expense of surveillance have limited the use of peridural narcotics in greater numbers of patients. Epidural anesthesia may improve other organ system outcomes, but its ability to reduce myocardial infarction remains speculative. Providing aggressive postoperative analgesia may be labor-intensive, and the cost-effectiveness remains unclear at this time. Two recent meta-analyses suggest that regional anesthesia may indeed be associated with a one-third reduction in perioperative myocardial infarction, especially if spinals or thoracic epidurals are used. Volatile Anesthetics. Volatile anesthetics reduce myocardial infarct size. The preconditioning effects of volatile anesthetics suggest that they should be incorporated into general anesthetic techniques for patients with known or suspected coronary artery disease. Non-steroidal anti-inflammatory drugs (NSAIDs) might be particularly useful in surgical patients with coronary artery disease due to their analgesic and antiplatelet effects. Ketorolac may reduce the stress response to surgery without increasing bleeding times or producing renal insufficiency. A randomized trial has demonstrated that the addition of ketorolac to morphine PCA can reduce the prevalence of myocardial ischemia following total joint arthroplasty. Whether this is due to improved analgesia or anti-platelet effects is not clear at this time. However, concerns about increased postoperative hemorrhage make the use of these therapies in surgical patients controversial. A decision analysis has suggested that the benefits of aspirin in vascular surgery patients exceed the risks. COX-2 inhibitors are effective analgesics in the perioperative period. However, their chronic use does not protect the heart as much as do NSAIDs with direct platelet actions, and they may impair preconditioning. COX2 drugs use appears contraindicated in cardiac surgery, and possibly in vascular surgery, due their prothrombotic and vasoconstrictor effects. Dual antiplatelet therapy (DAT). Patients who have drug-eluting coronary stents are at increased risk of acute stent thrombosis in the setting of surgery. This may occur because surgery produces a hypercoagulable state, and because surgeons may wish to stop DAT (aspirin and clopidogrel) before surgery to reduce blood loss. However, stent thrombosis has a high associated mortality. Elective surgery should probably be postponed until a year of DAT follow DES placement. When possible, consideration should be given to continuing DAT through the time of surgery. Some work suggests that such patients should have surgery in locations with the availability of invasive cardiologists and a cardiac catheterization lab should stent thrombosis occur. Alpha2 Agonists. Alpha2 adrenergic receptors at prejunctional sites mediate a reduction in norepinephrine release from presynaptic terminals, thereby decreasing noradrenergic central nervous system transmission and producing sedation, anxiolysis, and analgesia. Clonidine premedication reduces hypertension, tachycardia, and norepinephrine levels in patients undergoing aortic reconstruction. Clonidine also suppresses the normal postoperative increase in fibrinogen levels and antagonizes epinephrine-induced platelet aggregation. Our work has shown that clonidine can reduce intraoperative myocardial ischemia. The more specific alpha2 agonists dexmedetomidine and mivazerol may also reduce postoperative myocardial ischemia. Statins. These drugs reduce cholesterol and reduce reinfarction in patients with coronary disease. They can reduce coronary calcium, which may be a predictor of perioperative cardiac events in vascular surgery patients. Several large observation studies and randomized trials have correlated statin use with reduced rates of perioperative death and postoperative cardiac events.

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330 Page 4 Hyperglycemia. Hyperglycemia appears to impair preconditioning mechanisms. It has been shown to be associated with worse outcomes in surgical ICU patients, CABG patients, and after acute myocardial infarction in nonsurgical patients. Impaired glucose tolerance and insulin sensitivity is common in patients with known or suspected coronary disease and is associated with endothelial dysfunction. Many such patients have not been classified as diabetic before surgery, yet manifest perioperative hyperglycemia. Recent perioperative studies have differed on whether “tight control” improves coronary and other outcomes. However, some payers have begun to target tight control of perioperative glucose levels in CQI and P4P initiatives. Anemia / Hypothermia. Anemia is associated with an increased prevalence of postoperative myocardial ischemia. Whether more aggressive transfusion lowers this risk is unclear. In high-risk patients and in those who demonstrate myocardial ischemia, we used to routinely transfuse PRBCs to augment hematocrit to 30%. This simple strategy is complicated by studies showing that transfusion (especially of old blood) also increases cardiac risks. The elusive goal of a blood substitute might allow safer augmentation of oxygen carrying capacity, but to date, the NO scavenging properties of hemoglobin-based preparations may actually be associated with higher rates of perioperative MI than autologous blood. Hypothermia is also associated with postoperative myocardial ischemia; aggressive warming and heat conservation are warranted during and after surgery in high-risk patients. Managing Acute MI. A cardiologist should see patients with suspected MI as soon as possible. Acute care for myocardial infarction may include prompt reperfusion (thrombolysis and DES placement requiring DAT are generally contraindicated after surgery), therapy with statins, aspirin and beta blockers in those who can tolerate them, the avoidance of calcium entry blockers, and the use of ACE inhibitors or ARBs in those with poor LV function. It is not known if these recommendations are necessarily transferable to the perioperative setting. In patients with evolving myocardial infarction, intraaortic balloon pumping (IABP) can improve coronary blood flow while decreasing workload. Anecdotal reports exist of IABP placement as prophylaxis against postoperative coronary events for NCS, but definitive studies are lacking. IABP use may be particularly risky in patients with peripheral vascular disease. The Future: Improvements in our management of these patients appear to be reducing perioperative cardiac morbidity to the point where other organ system dysfunction may be responsible for the majority of in-hospital deaths. If this is true, then we are truly making remarkable strides. At present, there are rapid changes in the understanding of the pathogenesis of coronary artery disease. This may lead to more widespread primary and secondary prevention (cholesterol reduction, reduction of inflammation) and more aggressive and better revascularization (PTCA/stents). These factors might reduce perioperative cardiac complications. Indeed, in the CARP trial, there were no differences in survival of vascular surgery patients with CAD, whether they were randomized to receive coronary revascularization or not before vascular surgery. In both groups, the majority of patients received beta blockers, aspirin, and statins before surgery. Additionally, given improved medical and revascularization therapy, patients previously considered “too sick” for surgery will present to our ORs (for outpatient procedures, no less!) Future improvements in preventing cardiac deterioration after noncardiac surgery may also involve modulation of the adrenergic response (alpha2 agonists, intensive analgesia) and the coagulation system. The key will be to identify cost-effective strategies that improve outcome and to identify patients most likely to benefit. References:
ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg. 106:685-712. 2008 Bennett-Guerrero E, Veldman TH, Doctor A, et al. Evolution of adverse changes in stored RBCs. Proc Natl Acad Sci U S A. Oct 23;104(43):17063-8. 2007 Boersma E, Poldermans D, Bax JJ, et al. Predictors of cardiac events after major vascular surgery: Role of clinical characteristics, dobutamine echocardiography, and beta-blocker therapy. JAMA 285:1865-73, 2001 (defines which patients most likely to benefit from beta blockade) Brady AR, Gibbs JS, Greenhalgh RM, et al. (POBBLE trial investigators). Perioperative beta-blockade (POBBLE) for patients undergoing infrarenal vascular surgery: results of a randomized double-blind controlled trial. J Vasc Surg. 41:602-9. 2005 (Beta blockers do not reduce cardiac risk, but do shorten hospital stay)

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de Souza DG, Baum VC, Ballert NM. Late thrombosis of a drug-eluting stent presenting in the perioperative period. Anesthesiology 106:1057-9. 2007 (illustrative case report and discussion of dangers of stopping antiplatelet therapy) Durazzo AE, Machado FS, Ikeoka DT, et al. Reduction in cardiovascular events after vascular surgery with atorvastatin: a randomized trial. J Vasc Surg 39:967-75, 2004 (statins started roughly a month before vascular surgery and continued until 2 weeks after surgery reduced cardiac events) Ellis JE, Drijvers G, Pedlow S, et al. Premedication with oral and transdermal clonidine provides safe and efficacious postoperative sympatholysis. Anesth Analg 79:1133-40, 1994 (clonidine premedication reduces heart rate and intaoperative myocardial ischemia) Feringa HH, Schouten O, Karagiannis SE, et al. Intensity of statin therapy in relation to myocardial ischemia, troponin T release, and clinical cardiac outcome in patients undergoing major vascular surgery. J Am Coll Cardiol. 50:1649-56, 2007 (the lower the LDL, the less likely periop CV complications) Fleisher LA, Poldermans D. Perioperative beta blockade: where do we go from here? Lancet. 371(9627):1813-4. 2008 (letter to the editor discussing POISE trial). Frank SM, Fleisher LA, Breslow MJ, et al. Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events. JAMA. 277:1127-34,1997 (warming reduces cardiac complications) Grines CL, Bonow RO, Casey DE Jr, et al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association, with representation from the American College of Physicians. Circulation. 115:813-8. 2007 Juul AB, Wetterslev J, Gluud C, et al. ( DIPOM Trial Group) Effect of perioperative beta blockade in patients with diabetes undergoing major non-cardiac surgery: randomised placebo controlled, blinded multicentre trial. BMJ. 2006 Jun 24;332(7556):1482. (Beta blockers not protective) Kim LJ, Martinez EA, Faraday N, et al. Cardiac troponin I predicts short-term mortality in vascular surgery patients. Circulation 106:2366-71, 2002 (troponin leak dramatically increases perioperative and 6 month MI risk, with a dose-response relationship) Koch CG, Li L, Sessler DI, et al. Duration of red-cell storage and complications after cardiac surgery. N Engl J Med. 358:122939, 2008 (blood > 2 weeks old associated with more death, sepsis, and renal and respiratory failure) Landesberg G.The pathophysiology of perioperative myocardial infarction: Facts and perspectives. J Cardiothorac Vasc Anesth 17:90-100 2003 (review of pathophysiology, plaque rupture, increased demand, and prolonged stress) Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation 100:1043-9, 1999 (Six independent predictors of complications were identified: high-risk type of surgery, history of ischemic heart disease, history of CHF, history of cerebrovascular disease, preoperative treatment with insulin, and preoperative serum creatinine >2.0 mg/dL.) Le Manach Y, Perel A, Coriat P, et al. Early and delayed myocardial infarction after abdominal aortic surgery. Anesthesiology.102:885-91. 2005 (Intense postoperative cTnI surveillance revealed two types of PMI according to time of appearance and rate of increase in cTnI. The identification of early and delayed PMI may be suggestive of different pathophysiologic mechanisms) Lindenauer PK, Pekow P, Wang K, Gutierrez B, Benjamin EM. Lipid-lowering therapy and in-hospital mortality following major noncardiac surgery. JAMA. 291:2092-9, 2004 (Large retrospective study suggesting that statins are associated with an odds ratio for death of 0.62 in elderly patients undergoing major noncardiac surgery, and that the number needed to treat to prevent one death was 30 among those with a revised cardiac risk index score >4) Mangano DT, Layug EL, Wallace A, Tateo I. Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. Multicenter Study of Perioperative Ischemia Research Group. N Engl J Med.335:1713-20, 1996 (perioperative beta blockade with atenolol has survival benefits that last for 2 years) Mantha S, Foss J, Ellis JE, Roizen MF. Intense cardiac troponin surveillance for long-term benefits is cost-effective in patients undergoing open abdominal aortic surgery: a decision analysis model. Anesth Analg. 105:1346-56, 2007 (cost-effectiveness analysis suggesting routine troponin surveillance after open AAA surgery)

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McCrath DJ, Cerboni E, Frumento RJ, et al. Thromboelastography maximum amplitude predicts postoperative thrombotic complications including myocardial infarction. Anesth Analg. 100:1576-83, 2005 (hypercoagulable states may contribute to periop MI). McFalls EO, Ward HB, Moritz TE, Goldman S, Krupski WC, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med. 351:2795-804, 2004. (Aggressive medical therapy appears as efficacious as coronary revascularization) Norris EJ, Beattie C, Perler BA, et al. Double-masked randomized trial comparing alternate combinations of intraoperative anesthesia and postoperative analgesia in abdominal aortic surgery. Anesthesiology 95:1054-67, 2001 (well-designed trial suggesting that anesthetic technique does not affect cardiac outcome after abdominal aortic surgery if heart rate is well controlled in the ICU) Nussmeier NA, Whelton AA, Brown MT, et al. Complications of the COX-2 inhibitors parecoxib and valdecoxib after cardiac surgery. N Engl J Med. 352:1081-91. 2005 (myocardial infarction, cardiac arrest, stroke, and pulmonary embolism were more frequent among the patients given COX-2s than among those given placebo) POISE Study Group, Devereaux PJ, Yang H, et al. Effects of extended-release metoprolol succinate in patients undergoing noncardiac surgery (POISE trial): a randomised controlled trial. Lancet 371(9627):1839-47. 2008 (fixed-dose long-acting metorprolol reduces myocardial ischemia, but increases stroke) Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in highrisk patients undergoing vascular surgery. Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group. N Engl J Med. 341:1789-94, 1999 (perioperatve beta blockade reduces perioperative mortality and infarction in high risk vascular surgery) Poldermans D, Schouten O, Vidakovic R, et al (DECREASE Study Group). A clinical randomized trial to evaluate the safety of a noninvasive approach in high-risk patients undergoing major vascular surgery: the DECREASE-V Pilot Study. J Am Coll Cardiol. 49:1763-9, 2007 (aggressive beta-blockade superior to stress testing approach) Rodgers A, Walker N, Schug S, McKee A, Kehlet H, van Zundert A, Sage D, Futter M, Saville G, Clark T, MacMahon S. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials. BMJ. 321:1493-7, 2000. (regional anesthesia, especially spinals and thoracic epidurals, may be associated with reduced perioperative death and myocardial infarction) Tanaka K, Ludwig LM, Kersten JR, Pagel PS, Warltier DC. Mechanisms of cardioprotection by volatile anesthetics. Anesthesiology 100:707-21. 2004 (Excellent review) van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive insulin therapy in the critically ill patients. N Engl J Med. 345:1359-67, 2001. (Tight glucose control between 80 and 110 mg/dL reduces mortality in surgical ICU patients) Zaugg M, Tagliente T, Lucchinetti E, Jacobs E, Krol M, Bodian C, Reich DL, Silverstein JH. Beneficial effects from betaadrenergic blockade in elderly patients undergoing noncardiac surgery. Anesthesiology 91:1674-86, 1999 (beta blockade not only reduces troponin release, but hastens emergence and improves analgesia after general anesthesia) Zaugg M, Bestmann L, Wacker J, et al. Adrenergic receptor genotype but not perioperative bisoprolol therapy may determine cardiovascular outcome in at-risk patients undergoing surgery with spinal block. Anesthesiology. 107:33-44, 2007 (adding beta blockade to SAB might not be beneficial; genomics of beta receptors influence outcome).

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CAAHEP/ARC-AA Update
Claire Chandler, AA-C
Objective: At the conclusion of this course, the participant will be able to identify the didactic and clinical standards required for accreditation of AA educational programs. Students and instructors will have a better idea of what to expect within their respective educational programs as these new standards are implemented.

Materials from this speaker were not available at time of publication.

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Preoperative Cardiac Evaluation
John Ellis, MD
Objective: At the conclusion of this course, the participant will be able to 1) describe the epidemiology of the aging of Western societies; 2) contrast age-related deterioration of different organs and their functions with age; and 3) describe the epidemiology of cognitive decline after surgery.

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Postoperative Myocardial Ischemia and Infarction
John E. Ellis MD

johnellis1700@gmail.com Happy to share slides

http://circ.ahajournals.org/cgi/content/abstract/CIRCULATIONAHA.107.185699v1

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http://circ.ahajournals.org/cgi/content/abstract/CIRCULATIONAHA.107.185699v1

Personal recommendations • Less invasive surgery = less workup? • Limited preoperative cardiac evaluation
–Symptomatic patients –Very high risk? –Patient with a coronary stent

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Personal recommendations

• Routine pharmacologic prophylaxis
–Beta blockade –Statins –Aspirin +/- clopidogrel

Personal recommendations

• Aggressive prophylactic perioperative care
–Normothermia –Euglycemia –Correct anemia?

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Personal recommendations

• Aggressive prophylactic perioperative care
–Excellent analgesia –Troponin surveillance –Cardiologist followup

Acute Thrombosis

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Postoperative Myocardial Ischemia
50% 40% 30% 20% 10% 0% Holter Ischemia
Mangano DT. NEJM, 1990

Preop Intraop Postop

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Coronary Artery Disease Stenosis vs. Plaque Rupture?

Mechanisms of perioperative MI
• Supply/demand mismatch
– Subendocardial MI – ST changes, Troponin rise

• Plaque rupture • Plaque hemorrhage • Thrombosis
– Transmural MI – Q wave, ↑ Troponin rise
Anesthesiology. 2005 May;102(5):885-91

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Predominant mechanism?

Increased Demand?

Decreased Supply?

21 patients Postop MI or cardiac death Poorly collateralized total occlusions ~2/3 “Non-obstructive” lesions ~1/3

Ellis S, et al. (Cleveland) Am J Cardiol 1996

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Predominant mechanism?

Increased Demand? 2/3 of PMIs?

Decreased Supply? 1/3 of PMIs? Plaque rupture?

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Surgery is a hypercoagulable state

Hypercoagulability associated with thrombotic events

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Anesth Analg 2005;100:1576 –83)

Anesth Analg 2005;100:1576 –83)

All MIs occurred in hypercoagulable patients

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• Platelets are known to play a significant role in coronary thrombosis in nonoperative settings • Polymorphisms in the genes encoding platelet glycoprotein (GP) IIIa and GPIbα are associated with myocardial ischemic morbidity in nonsurgical settings

Points TAA = 6 DM = 4 AAA = 4

Met145 = 3
angina = 2 s/p MI = 2

Pro33 = 2

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Platelets on damaged endothelium

• A 69-yr-old male patient was scheduled to undergo hand-assisted laparoscopic nephroureterectomy for ureteral tumor. • s/p CAD with 2 two paclitaxel DES placed 29 months ago. • Dual antiplatelet therapy (DAT) with clopidogrel and aspirin for the 1st year.

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• After 1st year, clopidogrel was stopped • Patient continued to take aspirin. Preoperative assessment showed him to be angina free, with good effort tolerance and no CHF. • At the request of the surgeon, aspirin was stopped 10 days preoperatively.

• In PACU:
– ST changes – Vtach (pulseless) – Cardioversion x 4 – Mg++, amiodorone – BP 70/40 – Off to the cath lab….

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Algorithm for preop management of antiplatelet therapy

Chassot, P.-G. et al. Br. J. Anaesth. 2007 99:316-328; doi:10.1093/bja/aem209

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• The “CARP” study

No difference in outcome!

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Do your patients get such good medical Rx?

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J Am Coll Surg 2007;204:1199

• 2 outcomes:
–Transmural (Q wave) MI –Cardiac arrest

• N ~ 180,000!
–Prospective data collection!

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J Am Coll Surg 2007;204:1199

J Am Coll Surg 2007;204:1199

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J Am Coll Surg 2007;204:1199

None of this relies on stress tests or coronary history!

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Biomarkers to predict risk and outcome

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When does POMI occur?

39% of PMIs silent! ~ 2:1 non-Q vs Q

Badner et al. Anesth 1998

Two patterns of injury / troponins

Anesthesiology: 102(5) 2005pp 885-891

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(Circulation. 2002;106:2366-2371.)

Anesth Analg 2007;105:000 –000

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Anesth Analg 2007;105:000 –000

B type Natriuretic Peptide (BNP)
• Natriuretic peptides help regulate salt and water balance • Levels increase as heart failure symptoms worsen. • BNP levels are used to help diagnose CHF.

225

860 pg/ml

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Anemia

227

Blood is bad
• Anemia is bad • Blood loss is bad • Blood transfusion is bad
–Old blood particularly bad

• I’m still confused!

Tight glucose control?

228

Which comes first? Is hyperglycemia itself bad? Or does it just predict sicker patients?

229

Beta blockade 2008 • Earlier trials show protection • More recent trials questionable • POISE (n>8000)
–Less MI, but more CVA

J Am Coll Cardiol 2006;48:964 –9)

230

J Am Coll Cardiol 2006;48:964 –9)

J Am Coll Cardiol 2006;48:964 –9)

231

Aggressive beta blockade at least as good as stress test algorithm

POISE – the definitive trial??
• The dose of metoprolol:
– 100 mg preop – 100 mg in the 6hr postoperative period – 200 mg 12 hours later – 200 mg daily thereafter out to 30 days – Doses were not titrated – Drug stopped for BPs < 100 mm Hg.
AHA 2007

232

POISE – the definitive trial??

AHA 2007

vs.

POISE – the definitive trial??

AHA 2007

vs.

233

POISE – the definitive trial??

AHA 2007

vs.

POISE – the definitive trial??

AHA 2007

234

Lancet editorial re: POISE
• Poldermans and Fleisher suggest that patients in the POISE trial were overdosed with metoprolol, receiving functionally twice the dose of patients in the DECREASE-V trial.
Lancet. 2008 May 31;371(9627):1813-4.

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Mars and Venus?
• ~1000 vascular surgery patients evaluated retrospectively • After risk-stratification, the high-risk women who received β-blockade had a statistically worse outcome (36.8% v 5.9%, p = 0.02) because of an increased incidence of CHF. • By logistic regression, β-blockade improved outcomes in men but not women
Journal of Cardiothoracic and Vascular Anesthesia 2008 Vol 22 P 354-360

Marty London opines
• "What I think will happen is that it will become a class 2b indication—possibly effective but based on limited data," • "Like it or not, this is a bombshell in the whole area. What it means is that hospitals that have jumped on the betablocker bandwagon fairly aggressively, in large respect to try to boost their performance measures, will have to reconsider."http://www.medscape.com/viewarticle/574526?src=top10

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Marty London opines
• Nevertheless, there will always be patients in whom it is necessary to use beta blockers, London concludes. • "I do a lot of high-risk surgery anesthesia, and I know if I can't control that stress period with an anesthetic drug, I will get a beta blocker out and use that sparingly and carefully. Most of the time, I don't see any big drops in BP or heart rate."
http://www.medscape.com/viewarticle/574526?src=top10

• 3 polymorphisms were independent predictors of PMI
– proinflammatory cytokine interleukin 6 – intercellular adhesion molecule-1 (ICAM1) – E-selectin

(Circulation. 2006;114[suppl I]:I-275–I-281.)

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Statins 2008
• Two randomized trials show benefit • Many retrospective studies show benefit • Many benefits besides lipid lowering
– Reduced inflammations – NOS

• Risks of rhabdomyolysis very low

238

JACC 2007; 50:1649

JACC 2007; 50:1649

239

Le Manach Y et al. Anesth Analg 2007;104:1326

Le Manach Y et al. Anesth Analg 2007;104:1326

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DECREASE 3
• • • • Randomized clinical trial ~500 patients for vascular surgery All on beta blockers European Society Cardiologists 2008

DECREASE 3 – ECG / troponin

241

DECREASE 3 MI/cardiac death

Postoperative analgesia

Epidural working

Epidural stopped

242

• Retrospective cohort study of 259 037 patients, >40 yo, who underwent elective intermediate-to-high risk non-cardiac surgical procedures between 1994, and 2004, in Ontario, Canada • Epidural in ~ 20-25% of cases

Lancet Vol 372, Issue 9638, 16 August 2008 Pages 562-569

• Reduced 30 d mortality
– 1·7% vs 2·0%; relative risk 0·89, 95% CI 0·81–0·98, p=0·02

• Epidurals reduced 30 d mortality
– 1·7% vs 2·0% – relative risk 0·89 – 95% CI 0·81–0·98, p=0·02

• Number needed to treat = 447!
Lancet Vol 372, Issue 9638, 16 August 2008 Pages 562-569

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Journal of Cardiothoracic and Vascular Anesthesia , Volume 21 , Issue 4 , Pages 502 - 511

244

“Breakfast of Champions!”

The future?
Personalized (genetic) testing and therapy Stem cells to repair injured myocardium?

245

Slides available (PDF)
johnellis1700@gmail.com

246

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Product Descriptions

Abbott...........................................................................................................................................................18
Ultane (sevoflurane) Nimbex (cisatracurium besylate)

ApolloMD.......................................................................................................................................................1
ApolloMD is a physician-owned and operated multispecialty group with nearly 30 years experience. ApolloMD provides Emergency Medicine, Anesthesia and Radiology Services to hospitals, teaching facilities and top-tier health systems throughout the country. With our core group of over 700 Medical Directors, Board Certified Physicians and Mid-Level Practitioners, ApolloMD joins forces with hospitals every day, treating more than 2,000,000 patients per year while managing patient volume, streamlining throughput time, and deepening customer satisfaction. ApolloMD’s core group of Board Certified Anesthesiologists and Anesthetists serve hospitals, surgery centers and ambulatory care centers, delivering quality anesthesia services while improving efficiency, core measures of quality and increasing patient satisfaction scores. The ApolloMD Mission: To provide quality physician services to healthcare facilities by recruiting and retaining accomplished and dedicated physicians. To provide systematic leadership, inspiring dedication and a commitment to ‘give each patient our best. David T. Heil, CPC Physician Recruiter & Liaison, Anesthesia Services ApolloMD 5665 New Northside Dr., Suite 320 Atlanta, GA 30328 770-595-0707 Cell 770-874-6888 Office 770-874-6889 Fax dheil@apollomd.com 

Associated Anesthesiologists, Inc.......................................................................................................22
Associated Anesthesiologists, Inc., is a 29 physician, 31 CRNA, 6 PA, and 2 AA, single specialty group that provides a broad range of anesthesiology services to the patients of Tulsa and the surrounding communities. www.cityoftulsa.org AAI has been in existence since 1961 and has continually serviced Saint Francis Hospital www.saintfrancis.com since it opened as a hospital in 1961. Since that opening, we now provide out-patient anesthesiology services at the Natalie Ambulatory Surgery Center, an 8 OR facility on the Saint Francis Campus and the Oklahoma Surgical Hospital, a 15 OR multi-specialy, physician owned hospital in Tulsa. www.orthooklahoma.com Recently, AAI began providing services at the Saint Francis sister hospital, Saint Francis South, in south Tulsa. www.saintfrancis.com/south Saint Francis South is a relaxed, 4 OR community hospital. AAI is looking for well trained Anesthesiologist Assistants to join our group. We provide stable, predictable work hours, are honorable in the way we treat our staff. Our compensation package includes an attractive salary, pension, health care, medical education expenses as well as disability and other benefits. Our group has received 4 and 5 star 360 evaluations for the past three years since the evaluations began. The group provides adult and pediatric cardiac, as well as just about every other kind of anesthesiology services available with the exception of burn, liver and cardiac transplantation anesthesiology services. If you would like to discuss joining our group, please contact John Barnes, M.D. , rennieb@msn.com 

Children’s Medical Center at Dallas.......................................................................................................3 Elsevier USA...................................................................................................................................................9
Stephanie McKenzie, MBA, SPHR stephanie.mckenzie@emoryhealthcare.org 404-778-5409

Emory Healthcare......................................................................................................................................19

Greater Houston Anesthesiology, P.A..................................................................................................6 Lippincott, Williams & Wilkins...............................................................................................................14
Representatives from the Missouri Society of Anesthesiologists will be present to discuss opportunities for AAs in Missouri as well as to showcase our new AA School at UMKC. Come and meet representatives from the first AA school west of the Mississippi and the first publically-funded AA school. Among employers represented: Full time AA positions with Professional Anesthetic Care, Inc. We provide all anesthesia services at Liberty Hospital, a 285 bed acute med-surg hospital located 15 minutes from the central business district of Kansas City, Missouri, and 25 minutes from the world-famous Plaza shopping district. All surgical subspecial248

Missouri Society of Anesthesiologists.................................................................................................7

ties with the exception of transplant and heart. Liberty hospital is a clinical training site for the new M.S. in Anesthesia at U. of Mo. Kansas City and opportunities are available to participate in this exciting new program. Salary and benefits commensurate with training and experience. Please contact: Robert Adams 816461-1323, email: radams@midland-med.com. AA positions full time with call or part time. Western Anesthesiology Associates, Inc. at St. John’s Mercy Medical Center, St. Louis, MO. Offer a great variety of cases at Level I Trauma Center. No OB. Excellent salary and benefit package. For inquiry contact Sue Chrismer at schrismer@waai.net  or 636-386-9224 ext. 193. Full-time AA positions are available at Cardinal Glennon Children’s Hospital, St. Louis University Hospital or combination. Both hospitals are Level 1 Trauma Centers and provide an excellent diversity of anesthetic challenges. For information please contact James DeBoard, MD, Interim Chair, St. Louis University Department of Anesthesiology and Critical Care, 314-577-8750 or deboarjw@slu.edu. A full package of university-based benefits is offered.

Nationwide Anesthesia Services.....................................................................................................................................................20 Northside Anesthesiology Consultants.......................................................................................................................................23
Nova Southeastern University (NSU) has become the leader in AA education and has recognized the need for graduating highly educated AAs. To meet this demand, NSU opened the first AA in Ft. Lauderdale in June 2006, and will be opening the newest AA program in Tampa, Florida in June, 2009. Located on a beautiful 300-acre campus in Fort Lauderdale, NSU has more than 26,000 students and is the largest independent institution of higher education in Florida. Nova Southeastern University is the largest independent institution of higher education in the Southeast, and it is the 6th largest independent institution nationally. NSU awards associate’s, bachelor’s, master’s, educational specialist, doctoral, and first-professional degrees in a wide range of fields. The university is comprised of undergraduate, graduate and professional schools of osteopathic medicine, pharmacy, optometry, allied health and nursing, medical sciences, dental medicine, law, marine biology and oceanography, business and entrepreneurship, computer and information sciences, humanities, conflict resolution, family therapy, interdisciplinary studies, education, psychology and counseling, and family programs.

Nova Southeastern University.........................................................................................................................................................17

Oklahoma Society of Anesthesiologists......................................................................................................................................11
Wanted - Anesthesiologist Assistants in Oklahoma! In 2008, Oklahoma became the 18th state to license Anesthesiologist Assistants. Many of our member groups practice in the anesthesia care team model and AAs are a great asset to that team. Student rotations began earlier this year in Oklahoma City at Mercy, a tertiary care center providing approximately 15,000 anesthetics per year. Cases include general surgery, urology, plastics, gynecology, pediatrics, ophthalmology, orthopedics, ENT, interventional radiology, spine surgery, neurosurgery including craniotomies for both tumor and aneurysm and obstetrics. An additional rotation site will be available at Integris Baptist later this year. The first two AAs will begin their practice in Tulsa, Oklahoma in May. As always, the demand for quality anesthesia providers far exceeds the supply. With the introduction of AAs into Oklahoma, the demand for those providers has skyrocketed. The leadership of Oklahoma is exploring the development of an AA training program in the state. With the guidance and support of individual AAs throughout the country, this goal may be realized within a few short years. We say – Welcome to Oklahoma! PharMEDium is the national leading outsourced pharmacy provider, rigorously ensuring the accuracy and sterility of all your customized IV and epidural preparations.  PharMEDium is a nationwide network of state licensed and federally registered pharmacy outsourced, compounding centers, providing trusted solutions to more than 1,800 hospitals throughout the United States.  Managed by licensed pharmacists and staffed by certified technicians, we are compliant with all appropriate state laws and FDA Regulations, including USP Chapter <797> and DEA requirements.

PharMEDium Services, LLC................................................................................................................................................................. 4

ProMed Assistance Group.................................................................................................................................................................24
ProMed Assistance Group is a Medical Search Firm specializing in anesthesia. We have been in the business of placement of anesthesia personnel for 18 years and working with Anesthesiologist Assistants for approximately 10 years. ProMed Assistance Group placed the first AA-C in Vermont and was the introductory agent to the facility in Vermont. The facility became the driving force for licensure of AA-C’s in the state. Thus we were instrumental in getting the first AA-C licensed in Vermont (licensure #AAA-0000001). We believe in and continue to work toward the “Anesthesia Team Concept”. Having an “Anesthesia Team Concept” thought process throughout the placement procedure, whether permanent or locum, we look for strong clinicians with skills and personalities that compliment the anesthesia profession. ProMed Assistance Group is geared to operate effectively at assisting you in finding locum and/or permanent positions that will interest you. We have the experience and the knowledge to work with the hospital/group and the AA-C for the betterment of the whole. We are strong advocates of the win/win/win philosophy. ProMed Assistance Group is aware that when each Anesthesia Team Member is in place, that the patient population wins, and isn’t that ultimately what it is all about? Sheridan Healthcare Inc. is the nation’s leading Anesthesia provider. Established in 1953, Sheridan holds exclusive contracts at 80+ clinical sites in more than a dozen states. Our continued growth creates multiple career opportunities for motivated Anesthesia providers. Interested in learning more about joining the Sheridan family? Contact: (800) 816-6791. careers@sheridanhealthcare.com www.sheridanhealthcare.com
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Sheridan Healthcare............................................................................................................................................................................21

Space City Anesthesia.........................................................................................................................................................................16
Space City Anesthesia PLLC provides the exclusive anesthesia services at St. John Hospital, St. John Ambulatory Surgery Center and Patients Medical Center Hospital. Our practice is in the NASA/Clear Lake area southeast of Houston Texas. Our practice employs 10 physicians, 5 CRNAs and one Anesthesiologist Assistant. We are seeking 2-3 more full time AAs to provide for expanded services at Patients Medical Center which is a newly built physician owned hospital. With the growth of the new hospital we anticipate a greater need for our services. PMC is one of the very few hospitals in Texas that permits AA practice and has been supportive of our efforts to introduce AAs here. We have teaching affiliations with South University, Case Western and NOVA who have all had students rotate with us. PMC is an acute care hospital with a wide range of cases with the exception of open heart and obstetrics. Our employment package is competitive with the greater Houston market. Our size allows us to remain friendly and respectful of all of members talents and contributions to the practice. New this year—representatives from Ozark Anesthesia Associates of Springfield, Missouri will be present. Please send all correspondence to: Space City Anesthesia PLLC Steve Coggins MD 714 FM 1960 West, Suite 206 , Houston TX 77090 281-397-6527, ljohnson@dbmed.net  In association with Sheridan Healthcare Inc. Sheridan Healthcare Inc. is the nation’s leading Anesthesia provider. Established in 1953, Sheridan holds exclusive contracts at 80+ clinical sites in more than a dozen states. Our continued growth creates multiple career opportunities for motivated Anesthesia providers. Interested in learning more about joining the Sheridan family? Contact: (800) 816-6791 careers@sheridanhealthcare.com www.sheridanhealthcare.com

TIVA HealthCare....................................................................................................................................................................................21

Exhibitor Floor Plan
Main Level Salon A–D Exhibitor Hours Saturday, April 18, 2009 7:00 am –2:00 pm
7:30 am – 8:00 am Continental Breakfast with Exhibitors 10:00 am – 10:30 am Coffee Break with Exhibitors 1:00 – 2:00 pm Lunch on the Exhibit Floor 6:00 pm – 8:00 pm Welcome Reception Sunday, April 19, 2009 10:00 am – 8:00 pm 11:00 am – 12:00 pm Break with Exhibitors 2:00 pm – 2:30 pm Coffee Break with Exhibitors 4:30 pm – 5:00 pm Break with Exhibitors 6:00 pm – 8:00 pm Student Social and Job Fair

Oklahoma Society Anest.

250

American Academy of Anesthesiologist Assistants

33rd Annual Conference
Supporters & Exhibitors
AAAA would like to thank our Supporters and Exhibitors:

PLATINUM EXHIBIT LEVEL
Nova Southeastern University
2009 Conference Student Social and Registration Bags

ProMed Assistance Group
2009 Saturday LUNCH for AAAA on the Exhibit Floor COMMERCIAL SUPPORTER
This program was supported by an educational grant from Baxter Healthcare

“Future Directions in Anesthetic Pharmacology” BRONZE EXHIBIT LEVEL
Associated Anesthesiologists, Inc. PharMEDium Services, LLC EXHIBITORS
Abbott ApolloMD

Missouri Society of Anesthesiologists Nationwide Anesthesia Services Northside Anesthesiology Oklahoma Society of Anesthesiologists Sheridan Healthcare Space City Anesthesia TIVA Healthcare

Associated Anesthesiologists, Inc. Children’s Medical Center at Dallas Emory Healthcare Greater Houston Anesthesiology Lippincott, Williams & Wilkins

251

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