Anesthesia of the Surgical Patient

1. Anesthesia of the Surgical Patient CA Blum, M.D.

2. Pharmacology • Local anesthetics • Epidural / Spinal • IV Agents • Analgesics • Paralytics • Inhalational Agents • Classifications • Malignant Hyperthermia

4. Anesthesia • Embodies control of three great concerns of humankind: • Consciousness • Pain • Movement.

5. Pharmacokinetics • What the body does to the drug –describes relationship bw DOSE and CONCENTRATION • Involves: Absorption, Distribution, Elimination • Route of Administration affects Absorption and therefore pharmacokinetics • different rates of drug entry into the circulation based on admin route (IV, sublingual, IM, SubQ)

6. Distribution – delivery from the circulation to the tissues. • Molecular size, capillary permeability, polarity, and lipid solubility, protein and tissue binding. • The fluid volume in which a drug distributes is termed the volume of distribution (Vd).

7. Elimination – Varies widely • Some drugs: • Excreted unchanged • Decomposed by plasma enzymes • Degrated by liver

8. Take home • Response to drugs varies widely • Age • Weight • Sex • Pregnancy, • Disease state, • Drug interactions • Genetic factors

9. “The most important monitor in the operating room is the anesthesiologist, who continously assesses the patient’s response and adjusts the doses of anesthetic agents to match the surgical stimulus”

10. ABSITE Pearls • Sublingual and rectal drugs do not pass through liver first • So no “first pass effect” • First-pass effectconcentration of a drug is greatly reduced before it reaches the systemic circulation. • Zero order kinetics – constant amount of drug elimated regardless of dose • 1st order kinetics – constant amount of drug elimanted regardless of dose

11. Pharmacodynamics • What the drug does to the body • How plasma concentration of drug translates into effect on body • Depends on biologic variability, receptor physiology, and clinical evaluations of the actual drug.

12. Vocabulary • Agonist: causes a response. (full/partial) • Antagonist: blocks an agonist • Additive effect: effect is sum of parts • Synergistic effect: effect greater than sum of parts • Potency: dose required for effect. • Efficacy: power to produce a desired effect. • Dose-response curves compare dose and pharmacologic effect • Effective dose (ED50) desired effect in 50% of the gen pop. • Lethal dose (LD50) death in 50% of animals to which it is given. • Ratio of the lethal dose and effective dose, LD50/ED50, is the therapeutic index.

13. Anesthesia Written Boards

14. Local Anesthetics • Local anesthetics block nerve conduction by stabilizing sodium channels in their closed state, preventing action potentials from propagating along the nerve.

15. Amides and Esters. • Amides: Lidocaine, bupivacaine, ropivacaine • have in common an amide • all have ‘I’ in first part of name • Lidocaine has a more rapid onset and is shorter acting than bupivacaine; however, both are widely used for tissue infiltration, regional nerve blocks, and spinal and epidural anesthesia.

16. Esters: Cocaine, tetracaine, and benzocaine have an ester linkage – • Increased incidence of allergic reactions. • Epinephrine is a vasoconstrictor, reduces local bleeding, and keeps local anesthetic in the nerve proximity for a longer period of time. • Faster; Block Quality improved, longer duration • Less local anesthetic absorbed in bloodstream – reducing toxicity • Avoid epi in nose – toes – fingers - hose

17. Local Anesthetic Toxicity • CNS – tinnitus, slurred speech, seizures, and unconsciousness • CV - hypotension, increased P-R intervals, bradycardia, and cardiac arrest • NEURO FIRST! • Toxic dose Lidocaine 5 mg/kg • Infected tissue hard to anesthetize 2ndary to acidosis.

18. Calculations • 1 % = 10mg/ml • 1% lidocaine = 10mg/ml • 30ml = 300mg • 70kg person (toxic dose 5mg/kg) • 70 x 5 = 350 mg toxic dose

19. Anesthesia Sim Lab • Table Up • Table Down • Head Up • Head Down

20. Anatomy

21. Spinal Anesthesia • Injected directly into the dural sac surrounding the spinal cord (subarachnoid space, where CSF lives) • Possible complications include hypotension, especially if the patient is not adequately prehydrated • High spinal block requires immediate airway management • Spinal headache is related to the diameter and configuration of the spinal needle, and can be reduced to approximately 1%

22. Epidural Anesthesia • Local anesthetics are injected into the epidural space surrounding the dural sac of the spinal cord • Achieves analgesiafrom the sensory block, muscle relaxation from blockade of the motor nerves, and hypotension from blockade of the sympathetic nerves as they exit the spinal cord • Provides only two of the three major components of anesthesia—analgesia and muscle relaxation • Anxiolysis, amnesia, or sedation must be attained by supplemental IV administration of other drugs • Complications are similar to those of spinal anesthesia

23. Epidural • Bigger needle, accidental dural puncture often results in severe headache • Blood patch in epidural space

24. General Anesthesia • A triad of three major and separate effects: • unconsciousness (and amnesia) • analgesia • muscle relaxation • A combination of IV and inhaled drugs

25. Intravenous agents • Produces unconsciousness and amnesia - frequently used for the induction of GA • Barbiturates (sodium thopental), • Benzodiazepines (versed), • Propofol, • Etomidate, • Ketamine.

26. Barbiturates • Fast acting • Decreased cerebral blood flow and metabolic rate • Hypotension

27. Propofol • Very rapid on and off • Amnesia and sedations NO ANALGESIA • Profound hemodynamic effects – HYPOTENSION • Respiratory Depression • Decreased cerebral blood flow

28. Propofol • GA 100 – 200 mcg/kg/min • Icu 5-50 mcg/kg/min • Comes 10mg/cc, 1mg = 1000mcg therefore 1ml =10,000mcg • 5cc = 50,000mcg = 50mg • Induction dose = 2mg/kg (70kg = 140mg)

29. Ketamine • Dissociation (cataleptic state, amnesia and analgesia) • NO RESPIRATORY DEPRESSION • Hallucinations, increased secretions, increased cerebral blood flow • CONTRAINDICATED IN HEAD INJURY • Good for Kids

30. Etomidate • Fewer hemodynamic changes, fast acting • Continuous infusion can lead to adrenal insufficiency

31. Benzodiazepines • Hepatically metabolized • Anticonvulsant • Amnestic • Anxiolytic • Respiratory depression • NOT analgesic • Flumazenil – competitive inhibitor may cause seizures and arrythmias, contraindicated in pts with elevated ICP or status epilepticus

32. Analgesia • Narcotic – morphine (histamine release, constipation), demerol (seizures), codeine, fentanyl (80x stronger than morphine) • Act on mu receptors • Profound anagesia, respiratory depression, no cardiac effects, blunt sympathetic response • Metabolized by liver, excreted by kidned • NARCAN • Non-narcotic • Toradol • Ketamine

33. Neuromuscular Blocking Agents • Depolarizing – Succinylcholine – fast, short acting • Rapid onset and offset • Hyperkalemia ( not for burns, renal failure, SCI) • Non-depolarizing – inhibit NMJ compete with ACH • Pancuronium – long acting • Rocuronium, vecuronium, – intermediate • Reversed by neostigmine, edrophonium, • Block ACETYLCHOLINESTERASE  Increase ACH

34. Paralytics • Diaphragm – last muscle to go down, first to recover • Neck and face muscles – first to go down, last to recover

35. Inhalational Agents • Provides all three characteristics of GA: unconsciousness, analgesia, and muscle relaxation • A dose-dependent reduction in MAP (myocardial depression) • Minimum alveolar concentration (MAC) - measure of anesthetic potency = smallest conc of agent at which 50% will not move w incision • Small MAC  MORE lipid soluble = MORE POTENT • Speed of induction INVERSELY PROPORTIONAL to solubility • Nitrous FAST but HIGH MAC = LOW POTENCY

36. Halothane – doesn’t smell bad, good for kids, HEPATITIS • Enflurane - seizures

37. Mallampati Classification

38. ASA Class • I – healthy • II – mild disease without limitation (controlled HTN, DM, obesity, older age) • III – severe disease (angina, previous MI, moderate COPD) • IV – severe constant threat to life (unstable angina, renal failure, severe COPD) • V- moribund (rutured AAA, saddle PE)

39. Malignant Hyperthermia • MH is a life-threatening, acute disorder, developing during or after general anesthesia • Defect in calcium metabolism  muscle excitation • 1st sign = incrase in end tidal CO2, fever, tachcardia, rigidity, acidosis, hyperkalemia, cardiac arrest, rise in temperature is often a late sign of MH • genetic predisposition • Triggering agents include all volatile anesthetics and the depolarizing muscle relaxant succinylcholine

40. Treatment must be aggressive and begin as soon as a case of MH is suspected • Stop all volatile anesthetics and give 100% O2 • Hyperventilate the patient up to three times the calculated minute volume • Begin infusion of dantrolene sodium 2.5mg/kg IV • Repeat as necessary to titrate for clinical signs • Continue dantrolene for atleast 24 hours • Give bicarbonate to treat acidosis if dantrolene ineffective • Treat hyperkalemia with insulin, glucose, and calcium • Continue to monitor core temperature