CA Blum, M.D.

Anesthesia of the Surgical Patient

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

AnesthesiaEmbodies control of three great

concerns of humankind: ConsciousnessPainMovement.

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 pharmacokineticsdifferent rates of drug entry into

the circulation based on admin route (IV, sublingual, IM, SubQ)

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).

Elimination – Varies widelySome drugs:

Excreted unchangedDecomposed by plasma enzymesDegrated by liver

Take homeResponse to drugs varies widely

AgeWeightSexPregnancy, Disease state, Drug interactionsGenetic factors

“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”

ABSITE Pearls

Sublingual and rectal drugs do not pass through liver firstSo no “first pass effect”First-pass effect concentration 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

Pharmacodynamics

What the drug does to the bodyHow plasma concentration of

drug translates into effect on body

Depends on biologic variability, receptor physiology, and clinical evaluations of the actual drug.

VocabularyAgonist: causes a response. (full/partial)Antagonist: blocks an agonist Additive effect: effect is sum of partsSynergistic effect: effect greater than sum of

partsPotency: dose required for effect.Efficacy: power to produce a desired effect.Dose-response curves compare dose and

pharmacologic effectEffective 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.

Anesthesia Written Boards

Local AnestheticsLocal anesthetics block nerve

conduction by stabilizing sodium channels in their closed state, preventing action potentials from propagating along the nerve.

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.

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

durationLess local anesthetic absorbed in

bloodstream – reducing toxicityAvoid epi in nose – toes – fingers - hose

Local Anesthetic ToxicityCNS – 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.

Calculations1 % = 10mg/ml1% lidocaine = 10mg/ml30ml = 300mg70kg person (toxic dose 5mg/kg)

70 x 5 = 350 mg toxic dose

Anesthesia Sim LabTable UpTable DownHead UpHead Down

Anatomy

Spinal AnesthesiaInjected 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%

Epidural AnesthesiaLocal anesthetics are injected into the epidural

space surrounding the dural sac of the spinal cord

Achieves analgesia from 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 relaxationAnxiolysis, amnesia, or sedation must be attained by

supplemental IV administration of other drugsComplications are similar to those of spinal

anesthesia

EpiduralBigger needle, accidental dural puncture

often results in severe headacheBlood patch in epidural space

General AnesthesiaA triad of three major and separate

effects: unconsciousness (and amnesia)analgesiamuscle relaxation

A combination of IV and inhaled drugs

Intravenous agentsProduces unconsciousness and amnesia

- frequently used for the induction of GABarbiturates (sodium thopental), Benzodiazepines (versed), Propofol, Etomidate, Ketamine.

BarbituratesFast actingDecreased cerebral blood flow and

metabolic rateHypotension

PropofolVery rapid on and offAmnesia and sedations NO ANALGESIAProfound hemodynamic effects –

HYPOTENSIONRespiratory DepressionDecreased cerebral blood flow

PropofolGA 100 – 200 mcg/kg/minIcu 5-50 mcg/kg/minComes 10mg/cc, 1mg = 1000mcg therefore

1ml =10,000mcg5cc = 50,000mcg = 50mgInduction dose = 2mg/kg (70kg = 140mg)

KetamineDissociation (cataleptic state, amnesia and

analgesia)NO RESPIRATORY DEPRESSIONHallucinations, increased secretions,

increased cerebral blood flowCONTRAINDICATED IN HEAD INJURYGood for Kids

EtomidateFewer hemodynamic changes, fast actingContinuous infusion can lead to adrenal

insufficiency

BenzodiazepinesHepatically metabolizedAnticonvulsantAmnesticAnxiolyticRespiratory depression NOT analgesicFlumazenil – competitive inhibitor may

cause seizures and arrythmias, contraindicated in pts with elevated ICP or status epilepticus

AnalgesiaNarcotic – morphine (histamine release,

constipation), demerol (seizures), codeine, fentanyl (80x stronger than morphine)Act on mu receptorsProfound anagesia, respiratory depression,

no cardiac effects, blunt sympathetic response

Metabolized by liver, excreted by kidnedNARCAN

Non-narcoticToradolKetamine

Neuromuscular Blocking AgentsDepolarizing – Succinylcholine – fast, short

actingRapid onset and offsetHyperkalemia ( not for burns, renal failure, SCI)

Non-depolarizing – inhibit NMJ compete with ACHPancuronium – long actingRocuronium, vecuronium, – intermediateReversed by neostigmine, edrophonium, Block ACETYLCHOLINESTERASE Increase

ACH

ParalyticsDiaphragm – last muscle to go down, first

to recoverNeck and face muscles – first to go down,

last to recover

Inhalational AgentsProvides 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

Halothane – doesn’t smell bad, good for kids, HEPATITIS

Enflurane - seizures

Mallampati Classification

ASA ClassI – healthyII – 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)

Malignant HyperthermiaMH 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 predispositionTriggering agents include all volatile

anesthetics and the depolarizing muscle relaxant succinylcholine

Treatment must be aggressive and begin as soon as a case of MH is suspectedStop all volatile anesthetics and give 100%

O2Hyperventilate the patient up to three

times the calculated minute volumeBegin infusion of dantrolene sodium

2.5mg/kg IVRepeat as necessary to titrate for clinical

signsContinue dantrolene for atleast 24 hoursGive bicarbonate to treat acidosis if

dantrolene ineffectiveTreat hyperkalemia with insulin, glucose,

and calciumContinue to monitor core temperature