AnesthesiaExam Podcast

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

This is a premium episode, which requires a MyLibsyn subscription to access it. Click here to sign up or login.

ACLS Free update as of February 2017 0

Feb 7, 2017

Dr. Rosenblum, reviews the latest guidelines (as of 2017 for ACLS)

Discussed in this podcast are new revelations bout lidocaine, vasopressin, etc.

References

ACLS.net

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For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

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Breast Pain Free Version 0

Jan 31, 2017

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For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

https://en.wikipedia.org/wiki/Breast_pain

BeLieu RM. Mastodynia. Obstetrics and Gynecology Clinics of North America [1994,21(3):461-477]

Raj, PP. Radiographic imaging for regional anesthesia and Pain Management. 2005. p302-311

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Breast Pain and Intrathecal Pump - Pain Unit 0

Jan 31, 2017

Pain Unit

Breast Pain and Intrathecal Pump

References

https://en.wikipedia.org/wiki/Breast_pain

BeLieu RM. Mastodynia. Obstetrics and Gynecology Clinics of North America [1994,21(3):461-477]

Raj, PP. Radiographic imaging for regional anesthesia and Pain Management. 2005. p302-311

AnesthesiaExam Podcast- Subscription Premium Episodes Now Available

For Board Review and Practice Management Updates TEXT the word

ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

This is a premium episode, which requires a MyLibsyn subscription to access it. Click here to sign up or login.

Tarsal Tunnel syndrome- free version 0

Jan 24, 2017

A review of tarsal tunnel syndrome

Free version does not contain patellofemoral syndrome

Reference

https://en.wikipedia.org/wiki/Tarsal_tunnel_syndrome

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ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

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Patellofemoral syndrome and tarsal tunnel syndrome 0

Jan 24, 2017

Patellofemoral pain syndrome and tarsal tunnel syndrome

an in depth review

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For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

This is a premium episode, which requires a MyLibsyn subscription to access it. Click here to sign up or login.

Medical Marijuana - Finally! 0

Nov 8, 2016

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ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Paianful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

This is a premium episode, which requires a MyLibsyn subscription to access it. Click here to sign up or login.

Knobology and Lower Extremity Nerve Blocks 0

Aug 17, 2016

Lower Extremity nerve block review for the Anesthesia Boards

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For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Paianful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

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Tietze Syndrome 0

Jul 5, 2016

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For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Paianful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

Frontera: Essentials of Physical Medicine and Rehabilitation, 2nd ed.

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Cervical Spondylotic Myelopathy 0

Jun 23, 2016

Dr. Rosenblum discusses the evaluation and management of Cervical Spondylotic Myelopathy

Be sure to Check out our partner Boston Biolife

The next Hands on Boston Biolife Workshops is on July 16-17, and features:

-Stem Cell Therapies

-Biologics

Focusing on Regenerative Applications in Pain Medicine

Hands-On Overview:

Each participant will attend a variety of diverse educational workstations.
Each station will be structured to a particular technology and offer a comprehensive review of the principles and their applications.
In addition to the clinical workstations the attendee will participate in other informative, small group sessions that relate to practice management and professional development surrounding regenerative medicine.

CME Presentation Topics:

Clinical Applications & Research Landscape of Stem Cell Therapy
Cellular Anatomy of Regenerative Medicine
Fundamentals of Implementing Regenerative Medicine in your Pain Practice
Musculoskeletal (MSK) Regenerative Medicine Research & Historical Perspective
Adipose Derived Regenerative Medicine
Computerized Radiographic Measurement Analysis (CRMA)
Biochemistry of Alpha2 Macroglobulin (A2M)
Comprehensive Approach to Regeneration of Injured Skeletal Muscles via Delivery of Growth Factors & Progenitor Cells
3D Targeting Analytics for BMAC Harvesting

Day 1 Agenda*

7:00 - 8:00 am Registration/Breakfast
8:00 - 1:00 pm CME Lecture Series
2:30 - 6:30 pm CME Break-out Stations

Day 2 Agenda*

7:00 - 8:00 am Registration/Breakfast
8:00 - 11:45 am CME Lecture Series
11:45 - 4:45 pm CME Break-out Stations

*Lunch & breaks are included on both days - Times / agenda subject to change
For all travel plans: Please plan on course completion at 4:45 on Day 2

Hands-On Stations:

(Completed Over 2-Days) You will participate in 4 workstations on day 1 AND 4 workstations on day 2 (all workstations will remain the same on both days). There will be time during and after for questions and answers.

Platelet Rich Plasma (PRP)
• Anatomy • Composition • Processing
Bone Marrow Acquisition Techniques with Cadaver
• Anatomy • Composition • Harvesting Techniques
Stem Cell Basics
• Biochemical Composition, Amniotic Fluid • Stem Cells
• Growth Factors & Cytokines
Lipo Aspiration Techniques with Cadaver
• Clinical Techniques • Acquisition & Processing • Equipment
Flouroscopic Interventional Biologics for Pain Management with Cadaver
• Joints • Discs • Fibrin & Other Biologics
Bone Marrow Aspiration Imaging Technologies
• Imaging • Targeting • Bone Marrow Acquisitions
Live Patient MSK Joint Imaging & Anatomy Using Ultrasonography
• Shoulders, Knees, Elbows, Ankles
Laboratory Fundamentals for Regenerative Medicine
• Protocol Development • Sample Preparation • GMP

CME

18 CME Credits Offered for this course (complies with ACCME standards)

For more information Call: 978 569-8080

AnesthesiaExam Podcast- Subscription Premium Episodes Now Available

For Board Review and Practice Management Updates TEXT the word

ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Paianful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

Frontera: Essentials of Physical Medicine and Rehabilitation, 2nd ed.

Download this Episode

Pain Series- Greater Trochanteric Bursitis for the Anesthesia Boards 0

May 31, 2016

AnesthesiaExam Podcast- Subscription Premium Episodes Now Available

For Board Review and Practice Management Updates TEXT the word

ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Paianful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

Frontera: Essentials of Physical Medicine and Rehabilitation, 2nd ed.

Download this Episode

Total Hip Arthroplasty- Free Version 0

May 24, 2016

AnesthesiaExam Podcast- Subscription Premium Episodes Now Available

For Board Review and Practice Management Updates TEXT the word

ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Paianful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

Frontera: Essentials of Physical Medicine and Rehabilitation, 2nd ed.

Does Regional anaesthesia improve outcome after total hip arthroplasty? A systematic review

Br. J.anaesth. (2009)103 (3) 335-345

Download this Episode

Neuromuscular Blocking Agents- Free Version 0

May 17, 2016

A Brief Review of Neuromuscular Blocking Agents

For the Premium Version, Subscribe here

AnesthesiaExam Podcast

For Board Review and Practice Management Updates TEXT the word

ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

Neuromuscular Blocking Agents- Premium Version 0

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

Skeletal Muscle relaxants

Classification

Peripherally acting (Neuromuscular blockers)
1. Pre synaptic neuromuscular blocker
  - Inhibit Ach synthesis: triethylacholine – hemicholinium
  - Inhibit Ach release: Mg, aminoglycosides, botulinum toxin
2. Post synaptic neuromuscular blocker
  - Competitive (non depolarizing blockers):
    - d- tubocurarine
    - Gallamine
    - Atracurium
    - Pancuronium
    - Vecuronium
  - Depolarizing blockers: succinylcholine (suxamethonium)
Centrally acting skeletal muscle relaxants
1. Baclofen – Diazepam
Direct acting skeletal muscle relaxants
1. Dantrolene

Mechanism of action

Non depolarizing relaxant drugs
- All neuromuscular blocking agents used in USA except succinylcholine are classifies as non depolarizing agents
- When small doses of nondepolarizing muscle relaxants are administered, they act predominantly at nicotinic receptor site by competing with acetylcholine
- The least potent relaxant (eg. Rocuronium) have the fastest onset and the shortest duration of action
- In large doses, nondepolarizing drugs enter the pore of ion channel to produce a more intense motor blockade. This action further weakens neuromuscular transmission and diminishes the ability of the cholinesterase inhibitor (eg. Neostigmine, edrophonium, pyridostigmine) to antagonize the effect of non depolarizing muscle relaxants.
- They also block prejunctional sodium channels. As a result of this action, muscle relaxants interfere with the metabolization of acetylcholine at the nerve ending.
- Both halothane and succinylcholine increase the intensity and duration of action of pancuronium. (1)

Depolarizing relaxant drugs
1. Phase I block (depolarizing)
  - Succinylcholine is the only available depolarizing neuromuscular blocking drug. (2)
  - It produces a longer effect at the myoneural junction
  - It reacts with the nicotinic receptor to open the channel and cause depolarization of the motor end plate, and this in turn spreads to the adjacent membranes, causing contractions of muscle motor units.
  - Because succinylcholine is not metabolized at the synapse, the depolarized membranes remain depolarized and unresponsive to subsequent impulses
  - This is called Phase I (depolarizing) block, not reversed by cholinesterase inhibitors
2. Phase II block (desensitizing)
  - With prolonged exposure to succinylcholine, initial end plate depolarization decreases and the membrane become repolarized
  - Despite this repolarization, the membrane cannot be easily depolarized again because it is desensitized
  - The channel block is more important than agonist action at the receptor in phase II of succinylcholine’s neuromuscular blocking action
  - Later in phase II, the characteristics of the blockade are nearly identical to those of a non depolarizing block (ie, a nonsustained twitch response to a titanic stimulus) with possible reversal by acetylcholinesterase inhibitors

Succinylcholine produce reversible contracture of intrafusal fibers of the muscle spindle and leads to acceleration of the afferent discharge. (3)
Another study by Martin Jeevendra and Duriex Marcel E found that: (4)

1. Succinylcholine caused initial activation of the muscle AchR followed by desensitization

2. At clinically relevant concentrations, succinylcholine has no stimulatory or inhibitory interactions with α3β2 (presynaptic) or α3β4 (ganglionic) AchRs

3. High doses of succinylcholine caused inhibition of both α3β2 and α3β4 receptor.

Pharmacokinetics of neuromuscular blocking drugs

Succinylcholine has the fastest onset of action among all the muscle relaxants. (5)
The elimination of succinylcholine appears to follow first order kinetics with linear relationship between intensity of the effect and logarithm of the dose. The rate of recovery is independent of dose for each age group. The rate of recovery is faster in children than in infants; the rate of recovery is faster in infants than in adults. The elimination rate constant for infabts was similar to that of children, but is dissimilar from those of adults. (6)

Drug	Elimination	Clearance (mL/kg/min)	Approximate duration of action (minutes)	Approximate potency relative to Tubocurarine
Atracurium	Spontaneous	6.6	20-35	1.5
Cisatracurium	Mostly spontaneous	5-6	25-44	1.5
Doxacurium	Kidney	2.7	> 35	6
Metocurine	Kidney (40%)	1.2	> 35	4
Mivacurium	Plasma ChE (Butyrylcholinesterase)	70-95	10-20	4
Tubocurarine	Kidney (40%)	2.3-2.4	> 50	1
Pancuronium	Kidney (80%)	1.7-1.8	> 35	6
Pipecuronium	Kidney (60%) and liver	2.5-3.0	> 35	6
Rocuronium	Liver (75-90%) and kidney	2.9	20-35	0.8
Vecuronium	Liver (75-90%) and kidney	3-5.3	20-35	6
Succinylcholine	Plasma ChE (100%) (Butyrylcholinesterase)	>100	< 8	0.4

Soutce: Bertram G. Katzung, Susan B. Masters and Anthony J. Trevor. Basic amd Clinical Pharmacology. 11th Edition. Chapter 27. Skeletal Muscle Rexants. Page 451-465.

Pharmacology of Neuromuscular blocking drugs

Drug		ED95a (mg/kg)	Intubating dose (mg/kg)	Onset timeb (s)	Clinical durationc(min)
Succinylcholine		0.3	1.0d	60	10
Benzylisoquinolone	Tubocurarine	0.5	0.5-0.6	220	80+
	Atracurium	0.23	0.5	110	43
	Mivacurium	0.08	0.15-0.2	170	16
	Doxacurium	0.025	0.05	250	83
	Cisatracurium	0.05	0.1	150	45
Aminosteroids	Pancuronium	0.07	0.1	220	75
	Vecuronium	0.05	0.1	180	33
	Pipecuronium	0.045	0.08	300	95
	Rocuronium	0.3	0.6	75	33
	Rapacuronium	1.2	1.5	<75	15

a: The dose that depresses the twitch height by 95%

b: time to 95% depression of first twitch of train-of-four

c: time to 25% recovery of first twitch of train-of-four

d: This is about three times the ED95

Source: Jonnas Appiah-Ankam, Jennifer M Hunter. Pharmacology of neuromuscular blocking drugs. Contin Educ Anaesth Crit Care Pain. 2004;4(1):2-7.

Side effects of succinylcholine: (2)

Cardiovascular effects: bradycardia. It can cause arrhythmias when administered with halothane anesthesia
Muscle pain: experienced the day after surgery and is worse in ambulatory patients. It is more common in the young and healthy with a large muscle mass. The pain is thought to be a result of the initial fasciculations and occurs in unusual sites, such as the diaphragm, intercostal muscles and between the scapulae.
Hyperkalemia: Administration of succinylcholine 1.0 mg kg−1 produces a small increase (∼0.5 mmol litre−1) in serum potassium concentration in patients undergoing halothane anaesthesia.
Malignant hyperthermia: Succinylcholine is a recognized trigger factor for malignant hyperthermia and may also precipitate muscle contracture in patients with myotonic dystrophies.
Hypersensitivity: Succinylcholine accounts for about 50% of hypersensitivity reactions to NMBDs. The incidence is estimated to be 1 in 4000 administrations.
Increased intraocular pressure: The average increase in intra-ocular pressure after succinylcholine 1.0 mg kg−1 is 4–8 mm Hg. The increase occurs promptly after intravenous injection, peaking at 1–2 min and lasting as long as the neuromuscular block.
Increased intragastric pressure:
This complication is likely to occur in patients with delayed gastric emptying (those with diabetes), traumatic injury, esophageal dysfunction and morbid obesity.
Prolonged paralysis: Reduced plasma cholinesterase activity, a result of inherited or acquired factors, may alter the duration of action of succinylcholine, leading to prolonged paralysis.

Effects of muscle relaxants:

Vecuronium, pipecuronium, doxacurium, cisatracurium and rocuronium all have minimal cardiovascular effects
Pancuronium, atracurium and mivacurium produce cardiovascular effects that are mediated by either autonomic or histamine receptors
Tubocurarine and to lesser extent metocurine, mivacuronium and atracurium can produce hypotension as a result of histamine release
With larger doses, ganglionic blockade may occur with tubocurarine and metocurine
Pancuronium causes a moderate increase in heart rate and a smaller increase in cardiac output, with little or no change in systemic vascular resistance
Pancuronium induced tachycardia is primarily due to vagolytic action, release of norepinephrine from adrenergic nerve endings and blockade of neuronal uptake of norepinephrine may be secondary mechanisms

Drug	Effect on autonomic ganglia	Effect on cardiac muscarinic receptors	Tendency to cause histamine release
Atracurium	None	None	Slight
Cisatracurium	None	None	None
Doxacurium	None	None	None
Metocurine	Weak block	None	Slight
Mivacurium	None	None	Moderate
Tubocurarine	Weak block	None	Moderate
Pancuronium	None	Moderate block	None
Pipecuronium	None	None	None
Rocuronium	None	Slight	None
Vecuronium	None	None	None
Gallamine	None	Strong block	None
Succinylcholine	Stimulation	Stimulation	Slight

Source: Bertram G. Katzung, Susan B. Masters and Anthony J. Trevor. Basic amd Clinical Pharmacology. 11th Edition. Chapter 27. Skeletal Muscle Rexants. Page 451-465.

Interactions with other drugs

Anesthetics
- Inhaled anesthetic potentiate the neuromuscular blockade produced by non depolarizing muscle relaxants in dose dependent fashion
- Inhaled anesthetic augment the effect of muscle relaxants in the following order:

Isoflurane (most); sevoflurane, desflurane, enflurane and halothane; nitrous oxide (least)

Rare interaction of succinylcholine with volatile anesthetics results in malignant hyperthermia
Isobolographic and fractional analysis of the suxamethonium-mivacurium and suxamethonium-atracurium combinations demonstrated antagonistic interactions. (7)
The recovery from the effects of one nondepolarizing muscle relaxant given after partial recovery from another, more resembles the recovery from the muscle relaxant given first. (8)

Antibiotics
- Neuromuscular blockade is enhanced by antibiotics (eg. aminoglycosides)
- For patients treated with gentamycin and tobramycin, atracurium offers advantage over vecuronium when prolonged block is not desired. (9)
- Many antibiotics have shown to cause a depression of evoked release of acetylcholine similar to that caused by administering magnesium. The mechanism of this prejunctional effect appears to be blockade of specific P-type calcium channels in the motor nerve terminal

Antiarrhythmic drugs and local anesthetics
- The antiarrhythmics lidocaine, procainamide, propanolol and diphenylhydantoin increase the intensity and duration of d-Tubocurarine neuromuscular blockade. (10)
- Higher concentrations of bupivacaine have been associated with cardiac arrhythmias independent of the muscle relaxant used.
- In small doses, local anesthetics can depress posttetanic potentiation via a prejunctional neural effect.
- In large doses, local anesthetics can block neuromuscular transmission
- With higher doses, local anesthetics block acetylcholine- induced muscle contractions as a result of blockade of the nicotinic receptor ion channels
- Neuromuscular blocking agents potentiate the action of local anesthetics by acting on different sites of the neuromuscular junction. The block caused by combination of local anesthetic and neuromuscular blocking agent can be reversed by 4-aminopyridine. (11)

Other neuromuscular blocking drugs
- The end plate depolarizing effect of succinylcholine can be antagonized by administering a small dose of non depolarizing blocker
- To prevent the fasciculation associated with succinylcholine administration, a small non paralyzing dose of a nondepolarizing drug can be given before succinylcholine (eg. d-tubourarine, 2 mg IV, or pancuronium, 0.5 mg iv)
Lithium: Lithium enhances the myoneural blocking effects of suxamethonium, pancuronium and vecuronium. (12)

Reversal of nondepolarizing neuromuscular blockade

The cholinesterase inhibitors effectively antagonize the neuromuscular blockade caused by nondepolarizing drugs
Neostigmine and pyridostigmine antagonize the nondepolarizing neuromuscular blockade by increasing the availability of acetylcholine at the motor end plate, mainly by inhibition of acetylcholinesterase
Edrophonium antagonized the neuromuscular blockade purely by inhibiting acetylcholinesterase activity. Edrophonium has a more rapid onset of action but may be less effective than neostigmine in reversing the effects of nondepolarizing blockers in the presence of a profound degree of neuromuscular blockade.
A novel cyclodextrin reversal drug, sugammadex, has been submitted for FDA approval. It can rapidly inactivate steroidal neuromuscularblocking drugs by forming an inactive complex, which is excreted in the urine.

References:

Katz Ronald L. Modification of the action of pancuronium by succinylcholine and halothane. Anesthesiology December 1971;35(6).
Jonnas Appiah-Ankam, Jennifer M Hunter. Pharmacology of neuromuscular blocking drugs. Contin Educ Anaesth Crit Care Pain. 2004;4(1):2-7.
Cedric M Smith, Earl Eldred. Mode of action of succinylcholine on sensory endings of mammalian muscle spindles. JPET February 1961;131(2):237-242.
Martyn Jeevendra, Durieux Marcel E. Succinylcholine: New insights into mechanism of action of old drug. Anesthesiology April 2006;104(4):633-634.
Sluga M, Ummenhofer W, Studer W, Seigemund M, Marsch SC. Rocuronium versus succinylcholine for rapid sequence induction of anesthesia and endotracheal intubation: A prospective, randomized trial in emergent cases. Anesth Analg 2005;101:1356-61.
Cook DR, Wingard LB, Taylor FH. Pharmacokinetics of succinylcholine in infants, children and adults. Clinical Pharmacology and Therapeutics. 1976;20(4):493-498.
KS Kim, DJ Na, SU Chon. Interactions between suxamethonium and mivacurium or atracurium. British Journal of Anesthesia. 1996;77:612-616.
Harrop-Griffiths AW, Hood JR. Interactions between non depolarizing muscle relaxants. Anesthesiology 1997;86(1):263.
JY Dupuis, R Martin, JP Tetrault. Atracurium and vecuronium interaction with gentamycin and tobramycin. Can J Anaesth. 1989;36(4):407-11.
Katzung BG, Walter M, Harrah Marvin D. The interactions of d-Tubocurarine with Antiarrhythmic drugs. Anesthesiology October 1970;33(4).
Matsuo S, Rao DBS, Chaudry I, Foldes FF. Interaction of muscle relaxant and local anesthetics at the neuromuscular junction. Anesthesia & Analgesia. September/October 1978;57(5).
Saarnivaara L, Ertama P. Interactions between lithium/rubidium and six muscle relaxants. A study on the rat phrenic nerve-hemidiaphragm preperation. Des Anaesthesist. 1992;41(12):760-764.

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May 12, 2016

A Brief Review of Neuromuscular Blocking Agents

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DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

Skeletal Muscle relaxants

Classification

Peripherally acting (Neuromuscular blockers)
1. Pre synaptic neuromuscular blocker
  - Inhibit Ach synthesis: triethylacholine – hemicholinium
  - Inhibit Ach release: Mg, aminoglycosides, botulinum toxin
2. Post synaptic neuromuscular blocker
  - Competitive (non depolarizing blockers):
    - d- tubocurarine
    - Gallamine
    - Atracurium
    - Pancuronium
    - Vecuronium
  - Depolarizing blockers: succinylcholine (suxamethonium)
Centrally acting skeletal muscle relaxants
1. Baclofen – Diazepam
Direct acting skeletal muscle relaxants
1. Dantrolene

Mechanism of action

Non depolarizing relaxant drugs
- All neuromuscular blocking agents used in USA except succinylcholine are classifies as non depolarizing agents
- When small doses of nondepolarizing muscle relaxants are administered, they act predominantly at nicotinic receptor site by competing with acetylcholine
- The least potent relaxant (eg. Rocuronium) have the fastest onset and the shortest duration of action
- In large doses, nondepolarizing drugs enter the pore of ion channel to produce a more intense motor blockade. This action further weakens neuromuscular transmission and diminishes the ability of the cholinesterase inhibitor (eg. Neostigmine, edrophonium, pyridostigmine) to antagonize the effect of non depolarizing muscle relaxants.
- They also block prejunctional sodium channels. As a result of this action, muscle relaxants interfere with the metabolization of acetylcholine at the nerve ending.
- Both halothane and succinylcholine increase the intensity and duration of action of pancuronium. (1)

Depolarizing relaxant drugs
1. Phase I block (depolarizing)
  - Succinylcholine is the only available depolarizing neuromuscular blocking drug. (2)
  - It produces a longer effect at the myoneural junction
  - It reacts with the nicotinic receptor to open the channel and cause depolarization of the motor end plate, and this in turn spreads to the adjacent membranes, causing contractions of muscle motor units.
  - Because succinylcholine is not metabolized at the synapse, the depolarized membranes remain depolarized and unresponsive to subsequent impulses
  - This is called Phase I (depolarizing) block, not reversed by cholinesterase inhibitors
2. Phase II block (desensitizing)
  - With prolonged exposure to succinylcholine, initial end plate depolarization decreases and the membrane become repolarized
  - Despite this repolarization, the membrane cannot be easily depolarized again because it is desensitized
  - The channel block is more important than agonist action at the receptor in phase II of succinylcholine’s neuromuscular blocking action
  - Later in phase II, the characteristics of the blockade are nearly identical to those of a non depolarizing block (ie, a nonsustained twitch response to a titanic stimulus) with possible reversal by acetylcholinesterase inhibitors

Succinylcholine produce reversible contracture of intrafusal fibers of the muscle spindle and leads to acceleration of the afferent discharge. (3)
Another study by Martin Jeevendra and Duriex Marcel E found that: (4)

1. Succinylcholine caused initial activation of the muscle AchR followed by desensitization

2. At clinically relevant concentrations, succinylcholine has no stimulatory or inhibitory interactions with α3β2 (presynaptic) or α3β4 (ganglionic) AchRs

3. High doses of succinylcholine caused inhibition of both α3β2 and α3β4 receptor.

Pharmacokinetics of neuromuscular blocking drugs

Succinylcholine has the fastest onset of action among all the muscle relaxants. (5)
The elimination of succinylcholine appears to follow first order kinetics with linear relationship between intensity of the effect and logarithm of the dose. The rate of recovery is independent of dose for each age group. The rate of recovery is faster in children than in infants; the rate of recovery is faster in infants than in adults. The elimination rate constant for infabts was similar to that of children, but is dissimilar from those of adults. (6)

Drug	Elimination	Clearance (mL/kg/min)	Approximate duration of action (minutes)	Approximate potency relative to Tubocurarine
Atracurium	Spontaneous	6.6	20-35	1.5
Cisatracurium	Mostly spontaneous	5-6	25-44	1.5
Doxacurium	Kidney	2.7	> 35	6
Metocurine	Kidney (40%)	1.2	> 35	4
Mivacurium	Plasma ChE (Butyrylcholinesterase)	70-95	10-20	4
Tubocurarine	Kidney (40%)	2.3-2.4	> 50	1
Pancuronium	Kidney (80%)	1.7-1.8	> 35	6
Pipecuronium	Kidney (60%) and liver	2.5-3.0	> 35	6
Rocuronium	Liver (75-90%) and kidney	2.9	20-35	0.8
Vecuronium	Liver (75-90%) and kidney	3-5.3	20-35	6
Succinylcholine	Plasma ChE (100%) (Butyrylcholinesterase)	>100	< 8	0.4

Soutce: Bertram G. Katzung, Susan B. Masters and Anthony J. Trevor. Basic amd Clinical Pharmacology. 11th Edition. Chapter 27. Skeletal Muscle Rexants. Page 451-465.

Pharmacology of Neuromuscular blocking drugs

Drug		ED95a (mg/kg)	Intubating dose (mg/kg)	Onset timeb (s)	Clinical durationc(min)
Succinylcholine		0.3	1.0d	60	10
Benzylisoquinolone	Tubocurarine	0.5	0.5-0.6	220	80+
	Atracurium	0.23	0.5	110	43
	Mivacurium	0.08	0.15-0.2	170	16
	Doxacurium	0.025	0.05	250	83
	Cisatracurium	0.05	0.1	150	45
Aminosteroids	Pancuronium	0.07	0.1	220	75
	Vecuronium	0.05	0.1	180	33
	Pipecuronium	0.045	0.08	300	95
	Rocuronium	0.3	0.6	75	33
	Rapacuronium	1.2	1.5	<75	15

a: The dose that depresses the twitch height by 95%

b: time to 95% depression of first twitch of train-of-four

c: time to 25% recovery of first twitch of train-of-four

d: This is about three times the ED95

Source: Jonnas Appiah-Ankam, Jennifer M Hunter. Pharmacology of neuromuscular blocking drugs. Contin Educ Anaesth Crit Care Pain. 2004;4(1):2-7.

Side effects of succinylcholine: (2)

Cardiovascular effects: bradycardia. It can cause arrhythmias when administered with halothane anesthesia
Muscle pain: experienced the day after surgery and is worse in ambulatory patients. It is more common in the young and healthy with a large muscle mass. The pain is thought to be a result of the initial fasciculations and occurs in unusual sites, such as the diaphragm, intercostal muscles and between the scapulae.
Hyperkalemia: Administration of succinylcholine 1.0 mg kg−1 produces a small increase (∼0.5 mmol litre−1) in serum potassium concentration in patients undergoing halothane anaesthesia.
Malignant hyperthermia: Succinylcholine is a recognized trigger factor for malignant hyperthermia and may also precipitate muscle contracture in patients with myotonic dystrophies.
Hypersensitivity: Succinylcholine accounts for about 50% of hypersensitivity reactions to NMBDs. The incidence is estimated to be 1 in 4000 administrations.
Increased intraocular pressure: The average increase in intra-ocular pressure after succinylcholine 1.0 mg kg−1 is 4–8 mm Hg. The increase occurs promptly after intravenous injection, peaking at 1–2 min and lasting as long as the neuromuscular block.
Increased intragastric pressure:
This complication is likely to occur in patients with delayed gastric emptying (those with diabetes), traumatic injury, esophageal dysfunction and morbid obesity.
Prolonged paralysis: Reduced plasma cholinesterase activity, a result of inherited or acquired factors, may alter the duration of action of succinylcholine, leading to prolonged paralysis.

Effects of muscle relaxants:

Vecuronium, pipecuronium, doxacurium, cisatracurium and rocuronium all have minimal cardiovascular effects
Pancuronium, atracurium and mivacurium produce cardiovascular effects that are mediated by either autonomic or histamine receptors
Tubocurarine and to lesser extent metocurine, mivacuronium and atracurium can produce hypotension as a result of histamine release
With larger doses, ganglionic blockade may occur with tubocurarine and metocurine
Pancuronium causes a moderate increase in heart rate and a smaller increase in cardiac output, with little or no change in systemic vascular resistance
Pancuronium induced tachycardia is primarily due to vagolytic action, release of norepinephrine from adrenergic nerve endings and blockade of neuronal uptake of norepinephrine may be secondary mechanisms

Drug	Effect on autonomic ganglia	Effect on cardiac muscarinic receptors	Tendency to cause histamine release
Atracurium	None	None	Slight
Cisatracurium	None	None	None
Doxacurium	None	None	None
Metocurine	Weak block	None	Slight
Mivacurium	None	None	Moderate
Tubocurarine	Weak block	None	Moderate
Pancuronium	None	Moderate block	None
Pipecuronium	None	None	None
Rocuronium	None	Slight	None
Vecuronium	None	None	None
Gallamine	None	Strong block	None
Succinylcholine	Stimulation	Stimulation	Slight

Source: Bertram G. Katzung, Susan B. Masters and Anthony J. Trevor. Basic amd Clinical Pharmacology. 11th Edition. Chapter 27. Skeletal Muscle Rexants. Page 451-465.

Interactions with other drugs

Anesthetics
- Inhaled anesthetic potentiate the neuromuscular blockade produced by non depolarizing muscle relaxants in dose dependent fashion
- Inhaled anesthetic augment the effect of muscle relaxants in the following order:

Isoflurane (most); sevoflurane, desflurane, enflurane and halothane; nitrous oxide (least)

Rare interaction of succinylcholine with volatile anesthetics results in malignant hyperthermia
Isobolographic and fractional analysis of the suxamethonium-mivacurium and suxamethonium-atracurium combinations demonstrated antagonistic interactions. (7)
The recovery from the effects of one nondepolarizing muscle relaxant given after partial recovery from another, more resembles the recovery from the muscle relaxant given first. (8)

Antibiotics
- Neuromuscular blockade is enhanced by antibiotics (eg. aminoglycosides)
- For patients treated with gentamycin and tobramycin, atracurium offers advantage over vecuronium when prolonged block is not desired. (9)
- Many antibiotics have shown to cause a depression of evoked release of acetylcholine similar to that caused by administering magnesium. The mechanism of this prejunctional effect appears to be blockade of specific P-type calcium channels in the motor nerve terminal

Antiarrhythmic drugs and local anesthetics
- The antiarrhythmics lidocaine, procainamide, propanolol and diphenylhydantoin increase the intensity and duration of d-Tubocurarine neuromuscular blockade. (10)
- Higher concentrations of bupivacaine have been associated with cardiac arrhythmias independent of the muscle relaxant used.
- In small doses, local anesthetics can depress posttetanic potentiation via a prejunctional neural effect.
- In large doses, local anesthetics can block neuromuscular transmission
- With higher doses, local anesthetics block acetylcholine- induced muscle contractions as a result of blockade of the nicotinic receptor ion channels
- Neuromuscular blocking agents potentiate the action of local anesthetics by acting on different sites of the neuromuscular junction. The block caused by combination of local anesthetic and neuromuscular blocking agent can be reversed by 4-aminopyridine. (11)

Other neuromuscular blocking drugs
- The end plate depolarizing effect of succinylcholine can be antagonized by administering a small dose of non depolarizing blocker
- To prevent the fasciculation associated with succinylcholine administration, a small non paralyzing dose of a nondepolarizing drug can be given before succinylcholine (eg. d-tubourarine, 2 mg IV, or pancuronium, 0.5 mg iv)
Lithium: Lithium enhances the myoneural blocking effects of suxamethonium, pancuronium and vecuronium. (12)

Reversal of nondepolarizing neuromuscular blockade

The cholinesterase inhibitors effectively antagonize the neuromuscular blockade caused by nondepolarizing drugs
Neostigmine and pyridostigmine antagonize the nondepolarizing neuromuscular blockade by increasing the availability of acetylcholine at the motor end plate, mainly by inhibition of acetylcholinesterase
Edrophonium antagonized the neuromuscular blockade purely by inhibiting acetylcholinesterase activity. Edrophonium has a more rapid onset of action but may be less effective than neostigmine in reversing the effects of nondepolarizing blockers in the presence of a profound degree of neuromuscular blockade.
A novel cyclodextrin reversal drug, sugammadex, has been submitted for FDA approval. It can rapidly inactivate steroidal neuromuscularblocking drugs by forming an inactive complex, which is excreted in the urine.

References:

Katz Ronald L. Modification of the action of pancuronium by succinylcholine and halothane. Anesthesiology December 1971;35(6).
Jonnas Appiah-Ankam, Jennifer M Hunter. Pharmacology of neuromuscular blocking drugs. Contin Educ Anaesth Crit Care Pain. 2004;4(1):2-7.
Cedric M Smith, Earl Eldred. Mode of action of succinylcholine on sensory endings of mammalian muscle spindles. JPET February 1961;131(2):237-242.
Martyn Jeevendra, Durieux Marcel E. Succinylcholine: New insights into mechanism of action of old drug. Anesthesiology April 2006;104(4):633-634.
Sluga M, Ummenhofer W, Studer W, Seigemund M, Marsch SC. Rocuronium versus succinylcholine for rapid sequence induction of anesthesia and endotracheal intubation: A prospective, randomized trial in emergent cases. Anesth Analg 2005;101:1356-61.
Cook DR, Wingard LB, Taylor FH. Pharmacokinetics of succinylcholine in infants, children and adults. Clinical Pharmacology and Therapeutics. 1976;20(4):493-498.
KS Kim, DJ Na, SU Chon. Interactions between suxamethonium and mivacurium or atracurium. British Journal of Anesthesia. 1996;77:612-616.
Harrop-Griffiths AW, Hood JR. Interactions between non depolarizing muscle relaxants. Anesthesiology 1997;86(1):263.
JY Dupuis, R Martin, JP Tetrault. Atracurium and vecuronium interaction with gentamycin and tobramycin. Can J Anaesth. 1989;36(4):407-11.
Katzung BG, Walter M, Harrah Marvin D. The interactions of d-Tubocurarine with Antiarrhythmic drugs. Anesthesiology October 1970;33(4).
Matsuo S, Rao DBS, Chaudry I, Foldes FF. Interaction of muscle relaxant and local anesthetics at the neuromuscular junction. Anesthesia & Analgesia. September/October 1978;57(5).
Saarnivaara L, Ertama P. Interactions between lithium/rubidium and six muscle relaxants. A study on the rat phrenic nerve-hemidiaphragm preperation. Des Anaesthesist. 1992;41(12):760-764.

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May 10, 2016

AnesthesiaExam Podcast For Board Review and Practice Management Updates TEXT the word ANESTHESIAEXAM to the number 33444 For more information, CME credit and MOCA and Primary Board Prep,For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,Go to AnesthesiaExam.comFor Basic and Advanced Anesthesia Exam Review, Go to ABAStagedExams.com For CRNA Board Prep, go to CRNABoardPrep.com For the Pediatric Anesthesiology Board Review, Go to PedsAE.com David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medicaal Center and AABP Pain ManagmentFor evaluation and treatment of a Paianful Disorder, go to www.AABPPain.com718 436 7246DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment. You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional. Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

Validity of the Straight-Leg Raise Test for Patients With ...

www.jmptonline.org

Validity of the Straight-Leg Raise Test for Patients With Sciatic Pain With or Without Lumbar Pain Using Magnetic Resonance Imaging Results as a Reference Standard

Baastrup’s disease (kissing spines syndrome): a pictorial ...

www.ncbi.nlm.nih.gov

Pathogenesis. Baastrup’s disease is a term referring to close approximation of adjacent spinous processes due to general degenerative changes of the spine.

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Dr. Rosenblum Discusses the management and treatment of

Femoral Neuropathy

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For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medical Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

Frontera: Essentials of Physical Medicine and Rehabilitation, 2nd ed.

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Apr 19, 2016

Dr. Rosenblum Discusses the management and treatment of

Hip OA and anesthetic management

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AnesthesiaExam Podcast

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For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medical Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPai

Pain Management and is the Director of Pain Management at Maimonides Medical Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

Frontera: Essentials of Physical Medicine and Rehabilitation, 2nd ed.

https://www.hss.edu/professional-conditions_anesthesia-analgesia-for-total-knee-hip-replacement.asp

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Dr. Rosenblum discusses a patient who was injured by and IED and developed RSD, and PTSD.

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For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,

For the Pediatric Anesthesiology Board Review, Go to PedsAE.com

David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medical Center and AABP Pain Managment

For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com

718 436 7246

DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment.

You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional.

Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

References

http://emedicine.medscape.com/article/1819950-overview#a2

http://www.mayoclinic.org/diseases-conditions/post-traumatic-stress-disorder/basics/symptoms/con-20022540

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Chronic post operative pain, abdominal pain, phrenic nerve block, the splanchnic nerve block and the TAP Block all discussed.

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Multiple Sclerosis- Free Version 0

Mar 29, 2016

Multiple Sclerosis for the Anesthesia Boards

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Lumbar Degenerative Disc Disease for the Anesthesia Boards 0

Mar 24, 2016

Dr. Rosenblum Discusses the management and treatment of

Lumbar DDD

PainExam Podcast

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References

Frontera: Essentials of Physical Medicine and Rehabilitation, 2nd ed.

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Volatile Anesthetics for the Anesthesia Boards 0

Mar 15, 2016

halothane
Effects on CNS	Do not cause retrograde amnesia or prolonged impairment of intellectual function. Cerebral metabolic oxygen requirement are decreased parallel with drug induced decreases in cerebral activity. Drug induced increases in cerebral blood flow may increase intra cranial pressure in patients with space occupying lesion. Volatile anesthetics produce an imprecision in the control of thermoregulatory responses at the level of the anterior hypothalamus. It produces shivering like activity during emergence. (1)
Effects on circulation	Halothane sensitizes the heart to catecholamines It is liable to cause cardiac arrhythmias, occasionally fatal, particularly if hypercapnia has been allowed to develop. Arrhythmias are very common in children anesthetized with halothane. Halothane depresses cardiac index and myocardial contractility in patients with congenital heart disease. (2) Halothane causes reduction in heart rate and hypotension during anesthesia. It has no effect in bronchomotor tone. (3) 1.0 MAC enflurane, halothane and isoflurane mildly disrupt coronary blood flow (CBF) autoregulation, increasing CBF out of proportion to myocardial demands. These anesthetics do not affect maximal CBF or coronary vascular reserve. (4) Volatile anesthetics alter tissue excitability by decreasing the extent of gap junction-mediated cell-cell coupling and by altering the activity of the channels that underlie action potential. The magnitude of the effect of halothane on channel open time isleast for Cx40-like channels and greatest for heteromeric channels. (5)
Effects on neuromuscular function	It is a potent trigger to malignant hyperthermia It relaxes uterine smooth muscles and this may increase blood loss during delivery or termination of pregnancy. Halothane should not be used in patients with neuromuscular disease like Duchenne muscular dystrophy. These patients show evidence of muscle damage with increased serum creatinine kinase concentration and myoglobinuria.
Effects on renal function	Halothane anesthesia does not affect early post operative renal functions. (6)
Effects on hepatic function	Repeated exposure of halothane can result in severe liver injury.This halothane hepatitis is the result from the metabolism of halothane to triflouroacetic acid via oxidative reactions in the liver. Halothane has more deleterious effect on liver blood flow , interferes with liver cell ability to absorb and excrete indocyanine green (ICG). (7)
Effects on hematologic and immune systems	A study on the effect of halothane on division of cultured, murine bone-marrow cells showed that halothane caused a dose-dependent depression of growth rate ranging from a minimal effect at 0.5% to almost total inhibition at 2.0%. Halothane exposure results in increased number of IgG secreting cells as well as the circulating 7S serum agglutinins. (8)
Minimum alveolar concentration and pressures	Oil: gas partition coefficient = 224 Blood: gas partition coefficient = 2.3 MAC = 0.75 vol % Vapor Pressure 244 mmHg (at 20 Deg C) 288 mm Hg (at 24 Deg C)
Trace concentrations, O.R. pollution, personnel hazards	Halothane should be used with caution in patients with Phaechromocytoma, Renal failure, Pre existing liver disease, Myasthenia gravis
Advantages	Pleasant odor Slower induction and recovery
References: Farber NE, Poterack KA, Kampine JP, Schmeling WT. The effects of halothane, isoflurane and enflurane on the thermoregulatory responses in the neuraxis of cats. Anesthesiology 1994 Apr;80(4): 879-91. Rivenes SM, Lewin MB, Stayer SA, Bent ST, SchoeniqHM, McKenzie ED, Fraser CD, Andropoulos DB. Cardiovascular effects of sevoflurane, isoflurane, halothane and fentanyl-midazolam in children with congenital heart disease: an echocardiographic study of myocardial contractility and hemodynamics. Anesthesiology 2001 Feb;94(2):223-9. Van den Berg AA, Honjol NM. effects of heart arte, blood pressure and bronchomotor tone of halothane, enflurane and isoflurane in young fit patients. Middle East J Anesthesiol 1993 Oct;12(3): 271-86. Hickey Robert F, Sybert Peter E, Verrier Edward D, Cason Brian A. Effects of Halothane, Enflurane and Isoflurane on coronary blood flow autoregulation and coronary vascular reserve in the canine heart. Anesthesiology Jan 1988; 6(1). Ding Sheng He, Janis M Burt. Mechanism and selectivity of the effects of halothane on gap junction channel function. Circulation Research. 2000;86:e104-e109. Saricaoqlu, Akinci SB, Oc B, Kanbak M, Akbulut B, Celebioqlu B. The effects of halothane, isoflurane, sevoflurane and propofol infusion on renal function after coronary artery bypass surgery. Middle East J Anesthesiol 2006 Jun;18(5):955-64. Gelman Simon, Fowler Kathryn, Smithg Lloyd R. Liver circulation and function during isoflurane and halothane anesthesia. Anesthesiology December 1984; 61(6). Puing NR, Elena GA, Barragan J, Comba JO, Amerio N. Halothane associated enhancement of the secondary immune response to sheep erythrocytes in mice: cell transfer studies. Acta Anaesthesiol Scand. 1993 Oct;37(7):647-51.

Isoflurane
Effects on CNS	Isoflurane causes an increase in cerebral blood flow at deeper levels of anaesthesia, (1·5%), and this may give rise to an increase in cerebral spinal fluid pressure. Where appropriate, this can be prevented or reversed by hyper-ventilating the patient before or during anaesthesia. Isoflurane must be used with caution in patients with increased intracranial pressure Several incidence of postoperative convulsive disorder have been reported after isoflurane anesthesia. If seizures occured after anesthesia, volatile anesthesia itself may not be the cause. (1) 2% isoflurane given immediately after hypoxic ischemia, reduce brain infarct volume in short term as well as brain atrophy and neurobehavioural effects in the long term. (2)
Effects on circulation	Isoflurane is a powerful systemic and coronary arterial dilator. The phenomenon of "coronary steal" means that isoflurane should be used with caution in patients with coronary artery disease. In particular, patients with subendocardial ischaemia might be anticipated to be more susceptible. Isoflurane preserve cardiac index in patients with congenital heart disease. (3) Most appropriate isoflurane dose level is 1.5% v/v yielding stable mean arterial pressure (MAP) and heart rate (HR) with minute to minute variability in MAP and HR of <11%. (4)
Effects on respiration	Isoflurane is a profound respiratory depressant, this effect being accentuated by narcotic premedication or concurrent use of other respiratory depressants. No change in respiratory rate occurs with isoflurane at increasing alveolar concentration whereas at each level of anesthesia, inspiratory time is significantly reduced. (5)
Effects on GI function	Salivation and tracheo-bronchial secretions may be stimulated in children but pharyngeal and laryngeal reflexes are quickly diminished. Gastrointestinal motility is 50% reduced 120 min after the isoflurane anesthesia. (6)
Effects on neuromuscular function	Isoflurane produces sufficient muscle relaxation for some intra- abdominal operations. Isoflurane is compatible with all commonly used muscle relaxants, the effects of which may be markedly potentiated by isoflurane. The effect is most notable in non-depolarising agents, thus lower doses should be used in the presence of isoflurane. The effect of non-depolarising muscle relaxants can be counteracted by administering neostigmine as this has no effect on the relaxant properties of isoflurane. Interaction of rocuronium and volatile anesthetics results in augmentation of the neuromuscular block but does not significantly affect duration of or recovery from the block. (7) 0.95% isoflurane and 1.70% sevoflurane augments and prolongs the neuromuscular block produced by vecuronium, pancuronium and atracurium to a similar degree. (8)
Effects on hepatic function	Isoflurane causes frequent increase in the level of liver enzymes like Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), glutamyl transpeptidase (GTP). (9) Repeat anaesthesia with isoflurane within a short period of time should be approached with caution since the risk of hepatotoxicity is not fully understood. Caution should be exercised when administering isoflurane to patients with pre-existing liver disease.
Other system	Repeated exposure to isoflurane at anaesthetic concentrations has no effect on fertility, pregnancy or delivery. The viability of the offspring was unaffected.
Biotransformation; reaction with CO2 absorbants; toxicity	Isoflurane has been reported to interact with dry carbon dioxide adsorbents during closed circuit anaesthesia, to form carbon monoxide. Inhalation of carbon monoxide may lead to formation of significant levels of carboxyhaemoglobin in exposed patients.
Minimum alveolar concentration and pressures	MAC = 1.15 vol % Vapor pressure 238 mm Hg 31.7 kPa (at 20 deg C) 295 mm Hg 48.9 kPa (at 25 deg C) 367 mm Hg 48.9 kPa (at 30 deg C) 450 mm Hg 60.0 kPa (at 35 deg C) Blood gas partition coefficient = 1.4 Oil: gas partition coefficient = 98
Trace concentrations, O.R. pollution, personnel hazards	Isoflurane causes postoperative cognitive dysfunction (POCD) Isoflurane induce apoptsis and accumulation and aggregation of amyloid beta protein Adverse effects of isoflurane are hypotension, respiratory depression and arrhythmias It has pungent odor (not suitable for children) Broncho-irritant
Advantages	Stable cardiac rhythm Rapid onset/ recovery Minimal metabolism- low tox potential Excellent muscle relaxant
References: J Kurata, T Adachi, S Nakao, M Murakawa, T Shichino, M Shibata. Sevoflurane, enflurane and isoflurane have no persistent effects on central nervous system in cats. British Journal of Anesthesia. 1996;76:721-725. ZhouY, Lekic T, Fathali N, Ostrowski RP, Martin RD, Tang J, Zhang JH. Isoflurane posttreatment reduced neonatal hypoxic-ischemic brain injury in rats by the sphingosine-1-phosphate/ Phosphatidylinositol-3-kinase/Akt pathway. Stroke.2010;41:1521-1527. Rivenes SM, Lewin MB, Stayer SA, Bent ST, SchoeniqHM, McKenzie ED, Fraser CD, Andropoulos DB. Cardiovascular effects of sevoflurane, isoflurane, halothane and fentanyl-midazolam in children with congenital heart disease: an echocardiographic study of myocardial contractility and hemodynamics. Anesthesiology 2001 Feb;94(2):223-9. Christakis Constantinides, Richard Mean and Ben J Janssen. Effects of isoflurane anesthesia on cardiovascular function of the C57BL/6 Mouse. ILAR J 2011;52:e21-e31. Murat I, Chaussain M, Hamza J, Saint-Maurice C. The respiratory effects of isoflurane, enflurane and halothane in spontaneously breathing children. Anesthesia 1987 Jul;42(7):711-8. Torjman MC, Joseph JI, Munsick C, Morishita M, Grunwald Z. Effects of isoflurane on gastrointestinal motility after brief exposure in rats. Int J Pharm 2005 Apr 27;294(1-2): 65-71. Wulf H, Ledowski T, Linstedt U, Proppe D, Sitzlack D. Neuromuscular blocking effects of rocuronium during desflurane, isoflurane and sevoflurane anaesthesia. Can J Anaesth 1998 Jun;45(6):526-32. LEH Vanlinthout LHDJ Booij, Van Egmond, EN Robertson. effect of isoflurane and sevoflurane on the magnitude an dtime course of neuromuscular block produced by vecuronium, pancuronium and atracurium. British Journal of Anesthesia. 1996;76:389-395. Tomoki Nishiyama, Takeshi Yokoyama, Kazou Hanaoka. liver function after sevoflurane or isoflurane anesthesia in neurosurgical patients. Can J Anaesth 1998;45(8): 753-756.

Sevoflurane
Effects on CNS	Sevoflurane raises intracranial pressure Sevoflurane had minimal effect on intracranial pressure (ICP) and preserved CO2, responsiveness in patients with normal ICP. Rare cases of seizures have been reported in association with sevoflurane use. Sevoflurane suppresses the background central nervous system electrical activities in a dose dependent manner, leaving the reactive capabilities facilitated at deep anesthesia. (1)
Effects on circulation	During the maintenance of anaesthesia, increasing the concentration of sevoflurane produces dose-dependent decreases in blood pressure. Excessive decrease in blood pressure may be related to depth of anaesthesia and in such instances may be corrected by decreasing the inspired concentration of sevoflurane. Sevoflurane has not been associated with untoward cardiovascular changes in volunteers and patients undergoing elective surgery and may have less potent effects on the vascular smooth muscle. (2) Autonomic nerve activity is attenuated by sevoflurane. Parasympathetic input to the heart by respiration is suppressed following apperance of isoelectric EEG. (3) Sevoflurane uptake is higher in patients with higher cardiac output. (4)
Effects on respiration	Sevoflurane causes respiratory depression which increase as anesthesia is deepened Sevoflurane is a suitable agent for induction under spontaneous respiration with higher concentrations in pediatric anesthesia. (5) Sevoflurane produce more profound respiratory depression at high MAC. (6)
Effects on GI function	Deep sedatioj with inhaled sevoflurane for pediatric outpatient gastrointestinal endoscopy is as safe as conventional sedation technique, potentially less expensive, increases endoscopy unit productivity and eliminates the inconvenience associated with obtaining intravenous access in children. (7)
Effects on neuromuscular function	Use of sevoflurane can cause malignant hyperthermia. The syndrome may include non-specific features such as muscle rigidity, tachycardia, tachypnoea, cyanosis, arrhythmias and unstable blood pressure. Treatment includes discontinuation of triggering agents (e.g. Sevoflurane), administration of intravenous dantrolene sodium, and application of supportive therapy. Renal failure may appear later, and urine flow should be monitored and sustained if possible. Use of sevoflurane has been associated with very rare increases in serum potassium levels that have resulted in cardiac arrhythmias and death in children during the postoperative period. The condition has been described in patients with latent as well as overt neuromuscular disease, particularly Duchenne muscular dystrophy.
Effects on renal function	Sevoflurane should be used with caution in patients with renal insufficiency No significant renal effects are seen with low flow or high flow sevoflurane. (8)
Effects on hepatic function	Sevoflurane can be administered to patients with normal or mild-to-moderately impaired hepatic function. Use of sevoflurane in patients with severe hepatic dysfunction has not been investigated. Very rare cases of mild, moderate and severe post-operative hepatic dysfunction or hepatitis with or without jaundice have been reported from post marketing experiences. Clinical judgement should be exercised when sevoflurane is used in patients with underlying hepatic conditions or under treatment with drugs known to cause hepatic dysfunction. Sevoflurane at concentrations less than 2.0 MAC preserves hepatic arterial blood flow, total hepatic O2 delivery and the O2 delivery to consumption ratio. (9)
Effects on hematologic and immune systems	Transient increases in serum inorganic fluoride levels may occur during and alter Sevoflurane anaesthesia. Generally, concentrations of inorganic fluoride peak within 2 hours of the end of sevoflurane anaesthesia and return within 48 hours to pro-operative levels.
Biotransformation; reaction with CO2 absorbants; toxicity	Sevoflurane produces low levels of Compound A (pentafluoroisopropenyl fluoromethyl ether (PIFE)) and trace amounts of Compound B (pentafluoromethoxy isopropyl fluoromethyl ether (PMFE)), when in direct contact with CO2 absorbents. Levels of Compound A Increase with:- increase in canister temperature; increase in anaesthetic concentration; decrease in gas flow rate and increase more with the use of Baralyme rather than Soda lime. The exothermic reaction that occurs with sevoflurane and CO2 absorbents is increased when the CO2 absorbent becomes desiccated, such as after an extended period of dry gas flow through the CO2 absorbent canisters. Rare cases of extreme heat, smoke and/or spontaneous fire in the anesthesia machine have been reported during sevoflurane use in conjunction with the use of desiccated CO2 absorbent. An unusually delayed rise or unexpected decline of inspired sevoflurane concentration compared to the vaporizer setting may be associated with excessive heating of the CO2 absorbent canister.
Minimum alveolar concentration and pressures	MAC = 2.1 vol % MAC of sevoflurane decrease with age and with the addition of nitrous oxide Vapor pressure 157 mm Hg 22.9 kPa (at 20 deg C) 197 mm Hg 26.3 kPa (at 25 deg C) 317 mm Hg 42.3 kPa (at 36 deg C) Blood gas partition coefficient = 0.68 Oil: gas partition coefficient = 47
Trace concentrations, O.R. pollution, personnel hazards	Frequent adverse effects of sevoflurane are nausea and vomiting Other adverse effects are: in adults, hypotension; in elderly, hypotension and bradycardia; in children, agitation and increased cough. Less frequent adverse events associated with sevoflurane administration were; agitation, somnolence, chills, bradycardia, dizziness, increased salivation, respiratory disorder, hypertension, tachycardia, laryngismus, fever, headache, hypothermia, increased SGOT. Occasionally reported adverse effects associated with the administration of sevoflurane administration include : arrhythmias, increased LDH, increased SGPT, hypoxia, apnoea, leukocytosis, ventricular extrasystoles, supraventricular extrasystoles, asthma, confusion, increased creatinine, urinary retention, glycosuria, atrial fibrillation, complete AV block, bigeminy, leucopenia. Allergic reactions, such as rash, urticaria, pruritus, bronchospasm, anaphylactic or anaphylactoid reactions have also been reported. As with all potent inhaled anaesthetics, sevoflurane may cause dose-dependent cardiorespiratory depression. Convulsions may occur extremely rarely following sevoflurane administration, particularly in children. There have been very rare reports of pulmonary oedema.
Advantages	Fast induction/ recovery High potency (least soluble) Non irritating vapor
References: Osawa M, Shingu K, Murakawa M, Adachi T, Kurata J, Seo N, Murayama T, Nakao S, Mori K. Effects of sevoflurane on central nervous system electrical activity in cats. Anesth Analg. 1994 Jul;79(1):52-7. Ebert TJ. Cardiovascular and autonomic effects of sevoflurane. Acta Anaesthesiol Belg. 1996;47(1):15-21. Itsuo Nakatsuka, Ryoichi Ochai, Junzo Takeda. Changes in heart rate variability in sevoflurane and nitrous oxide anesthesia: effects of respiration and depth of anesthesia. Journal of Clinical Anesthesia. May 2002;14(3):196-200. JFA Hendrickx, AAJ Van Zundert, AM De Wulf. Sevoflurane pharmacokinetics: effect of cardiac output. British Journal of Anesthesia. 1998;81:495-501 Mori N, Suzuki M. Sevoflurane in pediatric anesthesia: effects on respiration and circulation during induction and recovery. Pediatr Anaesth. 1996;6(2):95-102. M Yamakage,K Tamiyamd, Dai Horikawa, K Sato, A Namikimd. Effects of halothane and sevoflurane on the pediatric respiratory pattern. Pediatric Anesthesia. January 1994;4(1):53-56. Montes RG, Bohn RA. Deep sedation with inhaled sevoflurane for pediatric outpatient gastrointestinal endoscopy. J Pediatr Gastroenterol Nutr. 2000 Jul;31(1):41-6. Bito Hiromichi, Ikeuchi Yukako, Ikeda Kazuyuki. Effects of low flow sevoflurane anesthesia on renal function: comparison with high flow sevoflurane anesthesia and low flow isoflurane anesthesia. Anesthesiology 1997;86(6):1231-1237. Frink Edward J, Morgan Scott EBS, Coetzee Andre, Conzen Peter F, Brown Burnell R. The effects of sevoflurane, halothane, enflurane and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs. Anesthesiology January 1992;76(1).

Desflurane
Effects on CNS	Desflurane causes dose dependent decrease in cerebrovascular resistance and cerebral metabolic rate of oxygen consumption (CMRO2). (1) It is a cerebral arteriolar dilator Desflurane cause cerebral vasodilation and may result in change in intracranial pressure in vulnerable patients, however if adequate hyperventilation and depth of anesthesia are maintained, it is safe to use desflurane. (1) With desflurane anesthesia, there is increase in activity in the midbrain at surgical end tidal anesthetic concentration. (2)
Effects on circulation	Use of desflurane causes tachycardia Increase in desflurane concentration increase the sympathetic and renin angiotensin system activity and cause transient increase in arterial blood pressure and heart rate. It also causes a transient increase in plasma AVP concentration. (3) 6% desflurane significantly prolongs QTc interval in children with normal QTc interval undergoing inguinal herniorraphy. (4)
Effects on respiration	It causes airway irritability and laryngospasm at concentration greater than 10 vol %. Desflurane causes respiratory depression at concentration higher than 1 MAC due to decrease in tidal volume. So, it should be avoided at high concentration in infants and chuildren with spontaneous ventilation. (5) There is dose dependent decrease in tidal volume and increase in respiratory rate, arterial carbon dioxide tension, dead space/tidal ventilation ratio, and intrapulmonary shunt fraction. (6) Desflurane does not affect respiratory resistance at 1 MAC, but at 1.5 MAC it causes significant increase in both total and airway resistance with return to baseline values after discontinuation. (7)
Effects on GI function	Desflurane maintain the esophageal barrier pressure (BrP = Lower esophageal sphincter pressure - gastric pressure). Hence, it can be used in patients with high risk of regurgitation. (8)
Effects on neuromuscular function	In susceptible individuals, desflurane may trigger a skeletal muscle hypermetabolic state leading to high oxygen demand and the clinical syndrome known as malignant hyperthermia. The clinical syndrome is signaled by hypercapnea, and may include muscle rigidity, tachycardia, tachypnea, cyanosis, arrhythmias, and/or unstable blood pressure. Some of these nonspecific signs may also appear during light anesthesia: acute hypoxia, hypercapnia, and hypovolemia.
Effects on renal function	Concentrations of 1-4% desflurane in nitrous oxide /oxygen have been used in patients with chronic renal or hepatic impairment and during renal transplantation surgery. Because of minimal metabolism, a need for dose adjustment in patients with renal and hepatic impairment is not to be expected. Desflurane does not aggravate renal impairment in patients with preexisting renal insufficiency. (9)
Effects on hepatic function	Use of desflurane may cause sensitivity hepatitis in patients who have been sensitized by previous exposure to halogenated anesthetics Better post operative hepatic tests and INR are seen using desflurane in living donors undergoing right hepatectomy. (10)
Effects on hematologic and immune systems	It has the most rapid onset and offset among the volatile anesthetic drugs used for general anesthesia due to its low solubility in blood.
Biotransformation; reaction with CO2 absorbants; toxicity	Desflurane has been shown to react with the carbon dioxide absorbent in anesthesia circuits to produce detectable levels of carbon monoxide through degradation of the anesthetic agent. The CO2 absorbent, Baralyme, when dried, is most culpable for the production of carbon monoxide from desflurane degradation, although it is also seen with soda lime absorbent as well. Dry conditions in the carbon dioxide absorbent are conducive to this phenomenon, such as those resulting from high fresh gas flows
Minimum alveolar concentration and pressures	MAC = 6 vol % Vapor pressure 672 mm Hg 88.5 kPa (at 20 deg C) 804 mm Hg 107 kPa (at 24 deg C) Blood gas partition coefficient = 0.42 Oil: gas partition coefficient = 19
Trace concentrations, O.R. pollution, personnel hazards	Very pungent Irritating to airways Laryngospasm Expensive Desflurane is a green house gas and contributes to global warming. Adverse effects associated with use of desflurane include arrhythmia, myocardial ischemia, vasodilation; hepatitis; agitation, diziiness; dyspnea, hypoxia;increased creatinine phosphokinase level; myalgia and pruritis
Advantages	Rapid onset/recovery High potency (least soluble) Even less metabolism
References: WL Young. Effects of desflurane on the central nervous system. Anesthesia & Analagesia. 1992;75(4):S32-7. DJA Vaughan, C Thornton, DR Wright, JR Fernandes, P Robbins, C Dore, MD Brunner. Effects of different concentrations of sevoflurane and desflurane on subcortical somatosensory evoked responses in anesthetized, non stimulated patients. Br J Anaesth. 2001;86(1):59-62. Weiskopf RB, Moore MA, Eqer EI, Noorani M, McKay L, Chortkoff B, Hart PS, Damask M. Rapid increase in desflurane concentration is associated with greater transient cardiovascular stimulation than with rapid increase in isoflurane concentration in humans. Anesthesiology 1994 May;80(5):1035-45. Aypar E, Karaqoz AH, Ozer S, Celiker A, Ocal T. The effects of sevoflurane and desflurane anesthesia on QTc interval and cardiac rhythm in children. Paediatr Anaesth. 2007 Jun;17(6):563-7. Behforouz N, Dubousset AM, Jamali S, Ecoffey C. Respiratory effects of desflurane anesthesia on spontaneous ventilation in infants and children. Anesth Analg. 1998 Nov;87(5):1052-5. Warltier DC, Pagel PS. Cardiovascular and respiratory actions of desflurane: is desflurane different from isoflurane? Anesth Analg. 1992 Oct;75(4 Suppl):S17-29. V. Nyktari, A papaioannou, N. Volakakis, A lappa, P Margaritsanaki, H Askitopoulou. Respiratory depression during anesthesia with isoflurane, sevoflurane and desflurane: a randomized clinical trial. Br J Anaesth 2011. D Chassard, JP Tournadre, KR Berrada, B Bryssine, P Bouletreau. Effect of halothane, isoflurane anbd desflurane on lower esophageal sphincter tone. British Journal of anesthesia. 1996;77:781-783. Litz RJ, Hubler M, Lorenz W, Meier VK, Albrecht DM. Renal responses to desflurane and isoflurane in patients with renal insufficiency. Anesthesiology 2002 Nov;97(5):1133-6. Topark HI, Sahin T, Aslan S, Karahan K, Sanli M, Ersoy MO. Effects of desflurane and isoflurane on hepatic an drenal functions and coagulation profile during donor hepatectomy. Transplant Proc. 2012 Jul-Aug;44(6):1635-9.

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Nitrous Oxide for the written and oral Anesthesia Boards 0

Mar 8, 2016

N2O
Effects on CNS	Mild depression of central nervous system (cerebral cortex) in conjunction with physiological levels of O2 (greater than 20%) Sensations depressed (sight, hearing, touch and pain ) It offers both hypnotic and analgesic characteristics. It decreases the propofol consumption and does not reduce the remifentanil consumption when given by a closed loop automated controller to maintain a similar Bispectral index (BIS) (1) In view of the limited evidence of human studies and the sufficient evidence of experimental studies, there is a significant association between exposure to nitrous oxide and Parkinson's disease. (2) Nitrous oxide exerts analgesia by inhibition of N-methyl-D-aspartate receptors. However, nitrous oxide anesthesia was not associated with decreased opioid administration, pain, or incidence of moderate to severe pain in the early postoperative phase. (3)
Effects on circulation	Blood pressure remains stable with only slight decrease Cutaneous vasodilation No changes in heart rate and cardiac output The pulmonary vascular resistance is increased due to constriction in pulmonary vascular smooth muscle, so nitrous oxide should be avoided in patients with pulmonary hypertension. (4) Nitrous oxide result in less depression of cardiac index when given with isoflurane than when given with halothane. (5)
Effects on respiration	Changes (drop) in rate and depth more likely due to anxiolytic effects Non irritating to pulmonary epithelium Slight elevation in resting respiratory minute volume at 50%/50% Nitrous oxide causes decrease in tidal volume and increase in respiratory rate. it also causes reduction in ventilatory response to hypoxia and hypercapnia. It decrease tracheal mucociliary flow and neutrophil chemotaxis. This may increase post operative complication. (4)
Effects on GI function	No clinically significant effect, unless there is a closed space (obstruction) N/V rarely seen unless hypoxia present
Effects on neuromuscular function	No direct relaxation of skeletal muscle Anxiolytic effects help relaxation Administration of nitrous oxide may increase motor activity with clonus and opisthotonus even in clinically used concentration.
Effects on hepatic function	It can be used in hepatic dysfunction
Effects on hematologic and immune systems	Long term exposure (greater than 24 hours) can produce transient bone marrow depression. Repeated use of nitrous oxide, particularly during lengthy procedures, may precipitate megaloblastic anemia and spinal cord degeneration. (4)
Other system	Uterine contractions not inhibited Pregnancy is a relative contraindication (avoid in first trimester) Nitrous oxide provided less effective pain relief than epidural anesthesia in labor pain management. (6)
Minimum alveolar concentration and pressures	Oil: gas partition coefficient = 1.4 Blood: gas partition coefficient = 0.47 MAC (%) = 105
Trace concentrations, O.R. pollution, personnel hazards	It is a compressed liquefied gas, an asphyxiation risk, and a dissociative anesthetic. Acute toxicity: N/V Exposure to Nitrous oxide causes short term decrease in mental performance, audio-visual ability and mental dexterity. Long term exposure can cause vitamin B12 deficiency, numbness, reproductive side effects (in pregnant females)
Advantages	No odor Fast induction and recovery Minimal cardio pulmonary depression Good analgesic
Clinical implications	general anesthesia obstetrics pain management (4)
References Liu N, Le Guen M, Boichut N et al. Nitrous oxide does not produce a clinically important sparing effect during closed-loop delivered propofol-remifentanil anaesthesia guided by the bispectral index: a randomized multicentre study.Br J Anaesth. 2014 Jan 31. Mastrangelo G, Comiati V, dell'Aquila M, Zamprogno E. Exposure to anesthetic gases and Parkinson's disease: a case report. BMC Neurol. 2013 Dec 9;13:194. Duma A, Helsten D, Brown F, Bottros MM, Nagele P. The effect of nitrous oxide anesthesia on early postoperative opioid consumption and pain.Reg Anesth Pain Med. 2014 Jan-Feb;39(1):31-6. Amelia Banks, Jonathan G Hardman. Nitrous Oxide. Contin Edus Anaesth Crit Care Pain (October 2005) 5(5): 145-148 MS McKinney, JPH Fee. Cardiovascular effects of 50% nitrous oxide in older adult patients anesthetized with isoflurane or halothane. British Journal of Anesthesia. 1998; 80: 169-173. Likis FE, Andrews JC, Collins MR, Lewis RM, Seroogy JJ, Starr SA, Walden RR, McPheeters ML. Nitrous oxide for the management of labor pain: a systematic review. Anesth Analg. 2014 Jan;118(1):153-67. AnesthesiaExam Podcast For Board Review and Practice Management Updates TEXT the word ANESTHESIAEXAM to the number 33444 For more information, CME credit and MOCA and Primary Board Prep, For more information, CME credit and MOCA and Primary Anesthesiology Board Prep, Go to AnesthesiaExam.com For Basic and Advanced Anesthesia Exam Review, Go to ABAStagedExams.com For CRNA Board Prep, go to CRNABoardPrep.com For the Pediatric Anesthesiology Board Review, Go to PedsAE.com David Rosenblum, MD specializes in Pain Management and is the Director of Pain Management at Maimonides Medical Center and AABP Pain Managment For evaluation and treatment of a Painful Disorder, go to www.AABPPain.com 718 436 7246 DISCLAIMER: Doctor Rosenblum IS HERE SOLELY TO EDUCATE, AND YOU ARE SOLELY RESPONSIBLE FOR ALL YOUR DECISIONS AND ACTIONS IN RESPONSE TO ANY INFORMATION CONTAINED HEREIN. This podcasts is not intended as a substitute for the medical advice of physician to a particular patient or specific ailment. You should regularly consult a physician in matters relating to yours or another’s health. You understand that this podcast is not intended as a substitute for consultation with a licensed medical professional. Copyright © 2015 QBazaar.com, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, recording or otherwise, without the prior written permission of the author.

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Opiates and Renal Failure- Free Version 0

Feb 2, 2016

Discussed in this Podcast

Renal Failure

Morphine

Fentanyl

Codeine

Buprenorphine

Oxycodone

Alfentanil

AnesthesiaExam Podcast

For Board Review and Practice Management Updates TEXT the word

ANESTHESIAEXAM to the number 33444

For more information, CME credit and MOCA and Primary Board Prep,

For more information, CME credit and MOCA and Primary Anesthesiology Board Prep,