Anesthesia-Surgery-EM Phase II Pharm Final- TCC 1-3-23 (1).pptx

Anesthesia-Surgery-EM Phase II Pharm Fina

1. Pharmacology II Anesthesiology / Surgery / Emergency Medicine Stephen A.  Vitkun , M.D., M.B.A., Ph.D. SUNY Distinguished Teaching Professor Professor of Anesthesiology, Vice-Chair Professor of Pharmacological Sciences Professor of Health Sciences Department of Anesthesiology SUNY at Stony Brook Stony Brook, N.Y.  11794-8480 1/3/23 (Asa) Peter Viccellio , MD, FACEP Professor and Vice Chairman Department of Emergency Medicine Associate Chief Medical Officer HSC, Level 4, Rm 050 101 Nicolls Road Stony Brook, NY 11794-8350

2. Quiz Question #1 Which medication is not paired with its appropriate use/indication A) Midazolam- Amnesia B) Fentanyl- Analgesia C) Succinylcholine- Neuromuscular blockade D) Propofol - Analgesia 2

3. Quiz Question #2 True or False Sugammadex is a competitive inhibitor or Rocuronium and Vecuronium FALSE 3

4. Quiz Question #3 Lidocaine toxicity is best described as: A) Cardiac toxicity followed by CNS collapse B) Infrequently causing seizures C) Progressive CNS symptoms progressing to arrhythmia and cardiac arrest D) Rarely encountered due to the large doses required to produce toxicity 4

5. Quiz Question #4 Which medication is not paired with its appropriate indication: A) Octreotide- Upper GI Bleeding B) Beta Blockade- Anti-arrhythmic and infarct size reduction C) Octreotide- Oral sulfonylurea poisoning D) Naloxone- Propofol reversal 5

6. Quiz Question #5 True or False Anaphylaxis is an IgE mediated severe allergic reaction while Anaphylactoid Reactions are produced by histamine release from non-immune mediated activation of mast cells. TRUE 6

7. 7 Pharmacology – Anes /Surgery Breakout Room Purpose: Today, We will discuss clinical cases related to anesthesia/surgery and emergency medicine. Our primary focus will be the clinical pharmacology of the drugs. In addition, we will have a clinically focused discussion in order to provide a perspective of the use of the drugs in clinical situations and hopefully, some Clinical Pearls.

8. Stuff to think about Precision in ordering Interactions and side effects Lexicomp Sanford or Hopkins ID app Spend time to learn doses of commonly used drugs Look up everything else 8

9. Helpful links Radiopaedia.org : excellent resource for learning to read radiology Life in the Fast Lane : litfl.com (emergency medicine and critical care focus, especially good EKG library) Wikijournalclub.org : library of reviews of landmark papers in medicine, also available as App on your phone Mdcalc.com online calculators for many common medical scores, calculations EMCRIT online resource for emergency medicine and critical care Sanfords or Hopkins ID manual

10. Case I – The Appendectomy You are the Anesthesia Resident on call and you get a call from your colleague in the ER. There is a 35 y/o man with acute appendicitis and the surgeon wants to bring him to the OR for a laparoscopic appendectomy. He has a history of HTN (takes HCTZ). Physical exam is remarkable for abd tenderness and rebound. He weighs 80 Kg and is 5ft 11inches tall. 11

11. What Else Do You Want to Know? Some Selected Items you might want to Know (Besides Complete Hx and General Physical (Focus on Heart/Lungs)): Potential Ease/Difficulty Intubating Last PO Ingestion / “Full Stomach” Considerations? Your Plan for Anesthesia? What are the Options (if any)? 12

12. The Airway Assessment Physical Exam Mallampati Score ROM Neck / TMJ / Dentition /ULBT (Upper Lip Bite Test) Concerns? Why is Difficult Intubation a Concern in this Case 13

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15. General Anesthesia When thinking about the Drugs, Consider the “Pharmacodynamics” – “Choosing the Right Drug for the Right Purpose” - General Anesthesia: Amnesia (Benzodiazepines) Analgesia (Opioids) Anesthesia (Absence of All Sensation) Induction and Maintenance Propofol / Etomidate / Ketamine / Others / Inhalational Anesthetics Muscle Relaxation (NMBs) Hemodynamic Stability – “Balanced” Anesthesia, Normally NOT “ Pressors ” 15

16. Case I - Induction General Anesthesia - Induction What is Rapid Sequence? Why Do We Do It (Or Not Do It) in This Case? We Will Use Propofol/Fentanyl/Midazolam for Induction Drugs – Other Choices? Why? What About NMBs? Succinylcholine? Rocuronium? Vecuronium? Others? Concerns when Paralyzing a Patient? 16

17. 17 “Anesthesia” Absence of All Sensation - Unconsciousness Induction Agents Pentothal, Etomidate , Ketamine , Propofol (Pictured) Opioids, Benzodiazepines, Others Maintenance of Anesthesia Inhalational Anesthetics, Opioids, Benzos May Be TIVA (total IV) or Combination of Gases (Inhalational) and IV Drugs.

18. Neuromuscular Blocking Drugs Pharmacology Depolarizing (Succinylcholine) Non-Depolarizing (Rocuronium / Vecuronium / Pancuronium / Atracurium /Others) What Drug(s) Do You Choose? Why? What are the Risks / Benefits of Your Choices? 18

19. NMB Pharmacology Succinylcholine: Depolarizing – Produces random action potentials at Neuromuscular end plate. Leads to Fasciculations (May then cause post-op arthralgia and myalgias). Other side effects include Sinus Brady, Sinus arrest, Hyperkalemia, increased intraocular pressure, increased gastric pressure, trismus, triggering agent of MH. 19

20. NMB Pharmacology Non-Depolarizing NMBs Rocuronium, Vecuronium, Atracurium, Cis-Atracurium (Medium Duration) Pancuronium , Doxacurium (Long-Acting) Mivacurium, Rapacuronium (Short-Acting – not used in clinical practice) NMBs block ACH Receptors at the Neuromuscular Endplate without causing an action potential (non-depolarizing, leading to flaccid paralysis. 20

21. Antagonism of NMBs (“Reversal ”) At the End of the Anesthetic, we need to terminate the action of the NMB. This can now be done by Competitive Antagonism or Non-Competitive Methods: What are the Differences Between Competitive and Non-Competitive (+/-)? Which Antagonists are Competitive / Non-Competitive? 21

22. Antagonism of NMBs Competitive Antagonists: Anticholinesterases Edrophonium Neostigmine Physostigmine Side-Effects: Bradycardia Anti- Muscarinics Atropine Glycopyrrolate 22

23. Non-Competitive Antagonism of NMBs Sugammadex : Antagonizes steroidal NMBs Rocuronium and Vecuronium What is the Significance? Why is this Clinically Important 23

24. Advantages of Sugammadex For a Competitive Antagonist, there must be a sub-maximal agonist concentration or they will not work, not so for non-competitive agonists as they do not compete for the receptor sites. Sugammadex binds Rocuronium (or Vecuronium) directly and the complex is inactive. 24

25. Case I – Take Aways Full Stomach Patients Need RSI RSI Has Increased Risk – Increased Concerns About Ability To Intubate/Ventilate Airway Assessment Must Be Able to Ventilate when Giving NMBs. New Antagonist – Sugammadex – Significant Advantages! 25

26. Case II- Local Anesthetics 26 You are in the middle of a busy shift when you receive a call from EMS that they are 10 minutes out with a cardiac arrest. The patient is a 52-year-old male who was being prepped for a hip procedure at an outpatient surgery center. He received a fascia iliaca nerve block w/ lidocaine and shortly thereafter developed generalized seizures. He then became hypotensive and progressed to an asystolic arrest.

27. Question True or False: The percent concentration of a solution refers to the amount of grams of that compound per deciliter. TRUE 27

28. Lidocaine Local anesthetics are routinely used in the emergency department and elsewhere for acute pain relief and procedures. Common applications: wounds/suturing nerve blocks topical applications (IV placement, etc.)

29. How local anesthetics work Desired effects are achieved by inhibiting pain-sensing peripheral nerve fibers through a blockade of intracellular sodium channels. This inhibits neuron firing and prevents pain signals from reaching the brain. As serum concentrations rise, the sodium channel blockade will also start to alter nerve conduction of other organ systems, specifically the myocardium and brain.

30. How we use them

31. Regional nerve blocks

32. Back to our case! You are in the middle of a busy shift when you receive a call from EMS that they are 10 minutes out with a cardiac arrest . The patient is a 52-year-old male who was being prepped for a hip procedure at an outpatient surgery center. He received a fascia iliaca nerve block w/ lidocaine and shortly thereafter developed generalized seizures . He then became hypotensive and progressed to asystole arrest.

33. Local Anesthetic Systemic Toxicity (LAST) Injection of local anesthetic into the systemic circulation Rapid absorption of local anesthetic injected into a highly vascular area Use of local anesthetic doses in excess of the maximum dose (typically occurs with multiple subcutaneous injections)

34. Toxicity/Side effects CNS excitation-related symptoms will occur first as the anesthetics block CNS inhibitory pathways.

35. How do we treat LAST Prevention of toxicity Know & calculate maximum doses of local anesthetic agent prior to use Always aspirate prior to injection to ensure drug is not delivered intravascularly Ask patient about symptoms after injection Consider serial repairs of large or multiple wounds to minimize chance for toxicity Basic Management Start treatment early; don’t wait for CV findings! Stop injection or infusion of agent Establish IV access if not already present Continuous cardiac monitor Aggressive supportive care ABC’s

36. Management continued Consider epinephrine to augment cardiac output and improve peripheral vascular tone Consider bicarbonate infusion for severe acidosis High-quality CPR in arrest Manage seizures w/benzodiazepines over propofol as (propofol is a cardiac depressant) Controlling seizures and preventing hypoxia should be a top priority Lipid emulsion therapy “Lipid sink” – Intra-arterial lipids rapidly bind the lipophilic anesthetic and extract it from the target tissues

37. Local Anesthetics What are the Different Types of Local Anesthetics? How Do They Work? There are Other Drugs that May Be Added to Local Anesthetics – Why? Epinephrine Methylparaben What are the Toxic Effects of Local Anesthetics 37

38. Local Anesthetics What is the Concentration of 1% Lidocaine? 2%? Besides ”Local” Injection/Infiltration, What Other Types of Anesthesia May Be Provided with Local Anesthetics? 38

39. 39 Local Anesthetics Clinical Uses: “Local” Infiltration Anesthesia Regional Anesthesia Digital Blocks Wrist Blocks Axillary Blocks Spinal (Sub-Arachnoid) Blocks Epidural Blocks Others Chronic Pain Management Therapy

40. 40 Spinal Anesthesia I

41. 41 Epidural Anesthesia

42. 42 Types of Local Anesthetics Amides Esters

43. 43 Local Anesthetics - Pharmacology Amide Type Lidocaine (Xylocaine) Prilocaine ( Citanest ) Mepivacaine ( Carbocaine , Polocaine ) Bupivacaine (Marcaine, Sensorcaine ) Etidocaine ( Duranest ) - Trade Names in Parentheses

44. 44 Local Anesthetics - Pharmacology Ester Type: Procaine (Novocain) Chloroprocaine ( Nesacaine ) Tetracaine ( pontocaine )

45. 45 Local Anesthetics - Pharmacology “Ester” type local anesthetics have an ester linkage in the chemical structure “Amide” type local anesthetics have an amide linkage in the chemical structure - C - O - O -NH - C - O

46. 46 Local Anesthetic Nomenclature All Local Anesthetics are: ......... - caine In the Generic Name, If there is an “- i -” before the “- caine ”, then it’s an Amide For Example” LIdocaine - Amide BupIvacaine - Amide Procaine - Ester Cocaine - Ester Xylocaine - Amide (It’s a Brand Name)

47. 47 Allergic Reactions to Local Anesthetics Incidence is Low with Esters and Very Low with Amides “Allergic Reactions” may Occur in Response to: Epinephrine added to the Anesthetic Solution Preservative (Methylparaben) in Multi-Dose Vials

48. 48 Use of Epinephrine in Local Anesthetics Vasoconstriction Decreases Blood Flow and Delays Absorption/Prolongs Action Allows Use of Lower Doses of Anesthetic in Areas of Higher Blood Flow Decreases Chance of Toxicity (Lower Doses) Realize - Patient’s may Experience Reactions to the Epinephrine (Tachycardia, Palpitations, Hypertension, Nervousness). The “Flight-or-Fight” Response DO NOT Use Epinephrine in Areas of “Terminal” Blood Supply (Fingers, Toes, Nose, etc.)

49. Local Anes – Max Amounts? Difficult to Determine as There is Some Dependence on the Use – SubQ infiltration vs. Major Nerve Block, etc. General Risks are From Systemic Absorption (or Accidental IV injection) My Numbers – Lidocaine 5-7mg/kg and Bupivicaine 2-3mg/kg. Local Anesthetics must be treated with respect! They can be lethal! Always aspirate first!!! 49

50. Know your doses!

51. Intralipid Rescue from Bupivicaine Overdose Local Anesthetic Toxicity - The role of intralipid (Not Propofol) Pharmacology Local Anesthetics block open Na + Channels Speed of onset related to pKa Duration of action related to protein binding Potency related to lipid solubility Toxicology Toxicity associated with blockade of neuronal and cardiac voltage-gated sodium channels. Potent local anesthetics such as bupivacaine can also disrupt metabotropic and ionotropic signal transduction. They can also inhibit each of the four components of oxidative phosphorylation - i.e. substrate transport, electron transport, proton motive force maintenance and ATP synthesis. 51

52. Case III – Oral Sulfonylurea OD An 8 y/o girl is brought in by her mom after being found unresponsive. Her grandfather’s dose of glipizide (Glucotrol) which he left on his nightstand is missing. She is transported to the ED. She had 2 glucose levels that were less than 40, and she is drowsy. She has been started on a dextrose infusion. What next?

53. Octreotide Octreotide: mimics natural somatostatin pharmacologically, though it is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone. 53

54. Octreotide What is the management of sulfonylurea-induced hypoglycemia, and how does octreotide treat it? Can present with delayed hypoglycemia after ingestion despite having initial normal blood glucose levels and receiving treatment. Food and IV glucose can also delay onset of hypoglycemia. After recognizing hypoglycemia you can start with IV dextrose and feed the patient. An “amp” of D50W provides 25 gm of dextrose. The patient must eat as soon as decontamination phase ends (lavage, activated charcoal),the pt. is awake, alert, and has no nausea/vomiting.

55. Dosing The recommended dose for octreotide Children : 1 – 2 mcg/kg up to 50 mcg SC or IV Q6 hrs Adults: 50 – 100 mcg SC or IV every 6-12 hrs The SC route is preferred IV dextrose infusion should be gradually tapered off. Best to feed the patient if possible.

56. Question True or False: Octreotide binds to pancreatic beta cells to close K+ channels resulting in increased insulin secretion. FALSE 56

57. Octreotide for Sulfonylurea OD Octreotide prevents rebound hypoglycemia after tx of sulfonylurea overdose with dextrose. Mimics somatostatin, octreotide suppresses the secretion of gastrin, cholecystokinin, growth hormone, glucagon, and insulin. Voltage-gated calcium channels on pancreatic beta cells are bound by G-protein-coupled somatostatin-2 receptors (octreotide binds to the somatostatin receptors, the calcium channels close, preventing the influx of calcium and subsequent secretion of insulin).

58. Dougherty, P.P., Klein-Schwartz, W. Octreotide’s Role in the Management of Sulfonylurea-Induced Hypoglycemia.  J. Med. Toxicol .   6,  199–206 (2010). https://doi.org/10.1007/s13181-010-0064-z

59. Octreotide Tumors (carcinoid syndrome) Bleeding varices (reduces portal venous pressure and splanchnic blood flow) Radiolabeling (nuclear medicine) Acromegaly Hypoglycemia ( tx . of sulfonylurea OD)

60. Case IV- Opioids A 31 year-old male presents to the ED BIBEMS after he was found unresponsive in a nearby park by his friends. He is only producing agonal respirations. Pupils are slightly less than 2mm and minimally reactive. EMS informs you that his friends think he may have “taken something” but stated they aren’t sure what is was.

61. Opioids

62. Common opioids *

63. Naloxone (Narcan) Naloxone is a lipophilic compound that acts as a non-selective and competitive opioid receptor antagonist.

64. Naloxone (Narcan) First dose: 0.4mg IV/IM followed by 1mg in 3 minutes if no response. Then double the dose q3mins until targets are reached as outlined above. Targets of naloxone dosing: RR>12 SpO2 >90% EtCO2 <45 EVALUATE FROM THE DOOR

65. Side Effects Naloxone has little to no effect if opioids are not present. In people with opioids in their system, it may cause: increased sweating nausea restlessness trembling vomiting flushing Headache In rare cases, naloxone has been associated with rhythm changes, seizures, and pulmonary edema.

66. Question True or False: The following opioids are listed appropriately in order of increasing potency….. Morphine<Fentanyl<Hydromorphone FALSE 66

67. Opioid Equivalency 1mg of hydromorphone ( dilaudid ) ~ 6.666mg of morphine Problems with codeine

68. Opioid Equivalency

69. Case V- Chest Pain A 78-year-old male presents to the ED complaining of chest pain. He states he was watching TV when his pain started. He describes the pain as “tightness & pressure” over the left chest that started 30 minutes prior to arrival.  The pain radiates to the left arm with some nausea but no vomiting. He states that it’s not better or worse with position and isn’t reproducible if you press on his chest. He adds that he usually gets this pain with exertion and it is typically relieved with his home nitroglycerin.

70. Acute Coronary Syndrome EKG ABC’s Aspirin Chest X-ray IV Monitor Labs (troponin)

71. Acetylsalicylic acid (aspirin) M orphine - used for refractory pain with caution – some evidence of interactions with antiplatelet agents causing impaired platelet inhibition and an association with worsened clinical outcomes.  O xygen- now only given if O 2 sats <90% N itrates - Don’t give with pre-load dependent MIs (right sided and inferior wall Mis) A spirin – (324mg chewed) blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes Inhibition of COX-1 results in the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan).

72. Acetylsalicylic acid (aspirin)

73. Anti-platelets https://images.app.goo.gl/RyrV3qBfV8PFeXbKA Pharmacolcogy Animation 2021 Mechanism

74. GP IIb / IIIa Inhibitors After plaque rupture in the coronary artery, tissue factor in the lipid-rich core is exposed and forms complexes with factor VIIa to generate factor Xa . relatively low concentrations of factor Xa leads to production of large amounts of thrombin, with deposition of fibrin strands and activation of platelets.

75. Back to our case! This patient was successfully treated by PCI and 2 stents were placed. He was subsequently sent home on a…. beta-blocker ACE inhibitor and a statin. 3 weeks after discharge he presents to his PCP with muscle aches.

76. Statins, Beta blockers, ACE inhibitors ACE inhibitors: Improved survival – early effect on limitation of infarct expansion, attenuation of the remodeling process , reduction of the neurohumoral impact on the heart, and increases in collateral flow to the peri -infarct ischemic area. Beta-blockers: Reduce the size of the infarct in patients who do not receive fibrinolytic therapy. They also reduce the incidence of ventricular ectopy and fibrillation. (reduction of oxygen consumption of the myocardium by lowering the heart rate, blood pressure, and myocardial contractility). Statins: Help to lower bad cholesterol and stabilize plaques, all patients with an acute MI should be started on high-potency statin therapy and continued indefinitely.

77. Frequently changing and hotly contested statin guidelines

78. Side effects on our patient How statins cause muscle pain is not fully understood. One theory is that statins may affect a protein in muscle cells, which decreases muscle growth. Another is unregulated calcium leaks may cause damage to muscle cells, potentially leading to muscle pain and weakness.

79. Statin induced myopathy Common complaints, especially in the lower body, include: cramps heaviness stiffness Symptoms of rhabdomyolysis include: severe muscle pain throughout the entire body dark urine muscle weakness kidney damage Get a CPK level!

80. Case VI- Sedation An anxious lady, 24 years old is coming to the OR for a breast biopsy. She is otherwise healthy but has a FHx of breast ca in her mother and an aunt. She is normal height and weight, last PO ingestion was 8 hours ago. The planned anesthetic is local anesthesia with sedation. 80

81. What is Sedation? What Drugs Are Used? What are the Goals of Sedation? What are the Potential Problems Associated with Sedation? Are There any Antidotes (antagonists) to Sedation/sedative drugs? 81

82. Case VI Continued The Patient’s anxiety continues and more sedation is needed. It is provided in Divided Doses. The Pulse ox now drops from 98% to 85% over about 30 seconds. The patient is unarousable. What Do You Do? What are Your Thoughts? Patient Does Not Appear to Be Breathing 82

83. Sedation Sedation is Part of the Continuum from Anxiolysis to General Anesthesia. Sedation may be light, moderate (old term – “Conscious Sedation”) or Deep. Sedation is Best Defined as “Amnesia and Analgesia” as This Then Suggests the Drugs we Should Use: Benzodiazepines and Opioids. Goals: Cloud Memory, Relieve Anxiety and Minimize Pain while maintaining Spontaneous Respiration and Hemodynamic stability. 83

84. 84 Amnesia Benzodiazepines Diazepam (Valium) Midazolam (Versed) Anterograde Amnesia Little Analgesia Sometimes Referred to as Sedatives or Tranquilizers

85. Benzodiazepines Binds GABA-A Receptor-Chloride Ion Channels and Facilitate GABA actions. Multiple Physiological Effects: Sedation, Hypnotic, Anesthesia, Anticonvulsant, Muscle Relaxation, Respiratory and Cardiac Function Prolonged Use may Lead to Psychological and Physiological Dependence Used to Treat: Anxiety, Insomnia, Seizures, Ethanol Withdrawal, Muscle Relaxation in Some Neuromuscular Disorders Some Psych Issues Antagonism – Flumazenil – Good For Antagonism of Sedative Effects – Less Reliable in Treatment of Respiratory Depression! Shorter Half Life! – Potential to “ Rebenzodiapinize ” = Respiratory Depression 85

86. 86 Analgesia Analgesics in Anesthesia Primarily Opioids Morphine Fentanyl (Pictured) Sufentanil Remifentanil Intravenous NSAIDs - Ketorolac, Caldolor , Others IV Acetaminophen (Tylenol) - Ofirmev

87. Opioids Derived from Opium (Poppy Seeds) – Morphine Act at Opioid Receptors (Mu, Kappa, Delta) Affinity for Different Receptors Leads to Partial Agonists Agonist Binding to specific G-Protein Coupled Receptors in Brain/Spinal Cord Modulates Pain Perception Comparative IV Doses: Morphine 1.0 mg - Hydromorphone 0.2mg - Fentanyl 10 ug Clinical Effects: Analgesia, Euphoria, Sedation, Respiratory Depression, Miosis, truncal Rigidity, N/V, Bradycardia, GI (Constipation), Biliary Tract Spasm (Sphincter of Oddi), Uterine (Prolonged Labor), Pruritus (itching), Cough Supression , Reduced Shivering (Meperidine), Other Effects Antagonism – Naloxone (Narcan) - *Shorter Duration of Action* Potential to “ Renarcotize ” = Respiratory Depression 87

88. Anesthesia Safety From Monitoring, Vigilance and Understanding of Side-Effects of the Drugs Administered The Bottom Line – RESPIRATORY DEPRESSION! Some Safety in “Sedation” if Benzos and Opioids are Used – Direct Antagonism by Naloxone and/or Flumazenil Not so With Propofol! – No Direct Antagonist means the Antagonist is “Tincture of Time”. Must Oxygenate and Ventilate until Respiration Returns! A Case in Point… 88

89. Date: June 15, 2009 Patient: Michael Jackson Time Dose Drug Drug Class 1 1:30 AM 10 mg Diazepam (Valium) Long-acting benzodiazepine 2 2:00 AM 2 mg Lorazepam (Ativan) Short to medium-acting benzodiazepine 3 3:00 AM 2 mg Midazolam (Versed) Ultra-short acting benzodiazepine 4 5:00 AM 2 mg Lorazepam (Ativan) Short to medium-acting benzodiazepine 5 7:30 AM 2 mg Midazolam (Versed) Ultra-short acting benzodiazepine 6 10:40 AM 25 mg Propofol (Diprivan) Short-acting (IV) hypnotic agent Patient finally went to sleep. About 2 min later the patient was no longer breathing. Efforts at CPR proved fruitless. (*) Information taken from coroner’s preliminary toxicology findings. Prescription Drug Abuse

90. Question True or False: Propofol, Fentanyl, and Midazolam share a greater safety profile for use in sedation due to the availability of antagonists for each of them. FALSE 90

91. Sedation – Take Aways Safest if Performed with Benzodiazepines and Opioids (Meets Goals of Amnesia and Analgesia) Propofol Sometimes Used Too – Problem is that there is NO Direct Antagonist (only Tincture of Time). Must Be Able to Support the Airway Antagonists – Naloxone and Flumazenil Have Shorter Half-Lives than the Benzos or Opioids they reverse Patients Should Be Monitored For at Least 2 Hours After Receiving Naloxone or Flumazenil 91

92. Case VII – The ”Hip” Patient A hip 50 year old male is brought to the OR for a scheduled Right Hip Replacement. He has no PMHx, NKDA, negative FHX. He gets an IV (LR at 150ml/ hr ) and his Ancef 1gm IV pre-op Abx is started in OR holding. 15 Minutes Later he is brought to the OR and monitors are placed. 92

93. Case VII Continued The Initial BP is 76/48, HR 118 When Placing the monitors, the Anesthesiologist listens to the lungs with a stethoscope – the Patient is Wheezing and says he feels dizzy and his throat feels weird. He has no Hx of Asthma. What Do You Do? What are Your Thoughts? 93

94. Case Variation: What if the patient were allergic to Ancef and the Surgeon asked for 1 gram of Vancomycin pre-op and it was administered IV over 20 minutes (the time from the holding area to the OR) Would you have any concerns? What would you look for? BP and HR are as given, patient appears flushed? 94

95. Case Questions How Would you Treat the BP? What Are Your Options? Why? What is on Your Differential Diagnosis for the Case and the Variation? 95

96. Sympathetic Receptor Sub-Types 96

97. 97

98. 98

99. Anaphylaxis vs. Anaphylactoid Anaphylaxis is a Severe Allergic Reaction. It is IgE mediated. In contrast, Anaphylactoid Reactions are non-immune mediated reactions related to the rate of administration of a drug. They result from mast cell activation and resultant histamine release. The Vancomycin Reaction (anaphylactoid) is sometimes called “Red Man Syndrome” Remember, The Common Initial Presentation of Anaphylaxis is that the Patient is Unaware of their Allergy. 99

100. Post Case Review (On Your Own) What are the Signs of Anaphylaxis What is the Treatment Protocol for Anaphylaxis Here are Some of the Basics: 100

101. Anaphylaxis Symptoms: Bronchospasm Facial /Laryngeal Edema – Risk of Airway Compromise Hypotension Nausea / Vomiting /Diarrhea 101

102. Anaphylaxis Initial Treatment ABCDE (Airway, Breathing, Circulation, Disability, Exposure) Establish IV Access Ensure Clear Airway / Give Suppl. Oxygen Monitor BP / HR Closely Epinephrine 0.5 mg IM (repeat in 5 mins) Antihistamines Steroids (Hydrocortisone 100mg IV) Consider Securing Airway if Necessary 102

103. Epi note IM in the thigh has 5-6 times the absorption and serum levels compared with EITHER IM or SQ epi in the arm 103

104. Do You Know? Post-Session Questions 1) Difference between competitive and non-competitive antagonists? 2) Can you provide a clinical example? 3) Can you name the different types of local anesthetics and give an example of each? 4) What are the Toxicities of Local Anesthetics? 104

105. Do You Know? 5) How do you assess a patient’s airway 6) What is a Rapid Sequence Induction? How does it differ from a routine induction? 7) What are the differences between depolarizing and non-depolarizing NMBs? Can you give an example of each? 105

106. Do You Know? 8) What are the antagonists for benzodiazepines and narcotics? What are the potential problems with their use? 9) Difference Between Anaphylaxis and Anaphylactoid Reactions 10) When asked to Get a Local Anesthetic Drug, what is the difference between ”Plain”, “Multi-use”, ”Single Use”, ”MPF”, ”with Epinephrine”. It says 1.5%, How many mg/ml? 106

107. 107 References/Readings Pardo, M, Miller, R. BASICS OF ANESTHESIA (7thEd). Elsevier, 2018 Brunton, L. Goodman & Gilman’s: THE PHARMACOLOGICAL BASIS OF THERPEUTICS (13thEd). McGraw Hill, 2018 Marcucci , C., Gierl , B., Kirsch, J. AVOIDING COMMON ANESTHESIA ERRORS (2ndEd). Wolters Kluwer, 2020

108. Thank You!!! 108