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