Anesthetics Flashcards

1
Q

Anesthesia

A

Abolition of sensation

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2
Q

Analgesia

A

Abolition of pain

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3
Q

Triad of general anestesia

A

need for unconsciousness, need for analgesia, need for muscle relaxation

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4
Q

Inhaled anesthetic agents

A

MAC: minimum alveolar anesthetic concentration. median concentration concentration that results in immobility in 50% of pts
Nitrous oxide, halothane, isoflurane, sevoflurane/desflurane,

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5
Q

Nitrous oxide

A

Simple, linear compound. Not metabolized. Only anesthetic agent that is INORGANIC
LOW POTENCY–MAC 105% (lower the MAC, more potent the drug)
Weak anesthetic, powerful analgesic; needs other agents for surgerical anesthesia
Low blood solubility (quick recovery)

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6
Q

NO systemic effects

A

minimal effects on heart rate and BP, respiration; safe.
May cause myocardial depression in sick pts
SEs: manufacturing impurities toxic, hypoxic mixtures can be used. large volumes of gases can be used. inhibits methionine synthetase (precurser to DNA synthesis), vit B-12 metab.
Dentists, OR personnel, abusers at risk

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7
Q

Halothane

A
Volatile liquid, easily vaporized, stable and nonflammable 
Most potent inhalational anesthetic
MAC: 0.75%
efficacious in depressing consciousness
Very soluble in blood and adipose
Prolonged emergence
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8
Q

Halothane s/es

A
HALOTHANE HEPATITIS--1/10,000: fever, jaundice, hepatic necrosis, death. 
Malignant hyperthermia (more common w/ succinylcholine): Classic--rapid rise in body temp, muscle rigidity (masseter), tachycardia, rhabdo, acidosis, hyperkalemia, DIC (coagulation). Autosomal dominant. Dx: sx, increase CO2, rise in CPK levels, myoglobinuria, muscle bx. physiology: hypermetabolic state by inhibition of calcium reuptake in sarcoplasmic reticulum. tx: early detection! d/c agents, hyperventilate, give bicarb, IV dantrolene, cool pt, lasix/mannitol/fluids, ICU. prophylaxis: preop IV dantrolene
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9
Q

Isoflurane

A

Not carcinogenic
Nonflammable, pungent
Less soluble than halothane
MAC: 1.3%

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10
Q

Isoflurane systemic effects

A

Depresses respiratory drive and ventilatory responses
Myocardial depressant
Inhibits sympathetic baroreflex response
sensitizes myocardium to catecholamines (less than halothane)
PRODUCES MOST SIGNIFICANT REDUCTION IN SYSTEMIC VASCULAR RESISTANCE–coronary steal syndrome, increased ICP
Excellent muscle relaxant–potentiates effects of neuromuscular blockers

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11
Q

Isoflurane side effects

A

Little metabolism (0.2%)–low potential of organotoxic metabolites
No EEG activity
Bronchoirritating, laryngospasm

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12
Q

Sevoflurane and Desflurane

A

Low solubility in blood–produces most rapid induction and emergence
minimal systemic effects–mild resp and cardiac suppresion
few side effects
expensive

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13
Q

IN Anesthetic agents

A

Many options: muscle relaxants, opoids, nonopoids.
appealing, pleasant experience
Agents: etomidate, ketamine, propofol/fospropofol, benzadiazepines
(diazepam, lorazepam, midazolam), opiods (narcotic agonists), muscle relaxants

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14
Q

Etomidate

A

Structure similar to ketoconazole
Direct CNS depressant (thiopental) and GABA agonist
Systemic effects: little change in cardiac function, mild resp depression. decreased cerebral metabolism
ADRs: injection site, myoclonic activity, N/V (50%), cortisol suppresion

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15
Q

Ketamine

A

Structurally similar to PCP
interrupt cerebral association pathways–“dissociative anesthesia”
stimulates central sympathetic pathways
systemic effects: characteristic of sympathetic nervous system stimulation–increase HR, BP, CO. maintains laryngeal reflexes and skeletal muscle tone
ADRs: emergence can produce hallucinations and unpleasant dreams

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16
Q

Propofol/fospropofol

A

Rapid onset and short DOA. pt remembers NOTHING
Myocardia depression and peripheral vasodilation may occur–basoreflex NOT suppresed.
Propofol not water soluble, painful. Fospropofol soluble in water.

17
Q

Benzodiazepines

A

Produce sedation and amnesia
Potentiate GABA receptors–allosteric binding, bind to different site at same receptor
Slower onset and emergence
Agents: Diazepam, Lorazepam, Midazolam

18
Q

Diazepam

A

Valium
Often used as premedication or seizure activity, rarely for induction
Minimal systemic effects–resp decreased with narcotic usage
Not water soluble–venous irritation
Metabolized by liver–not redistributed

19
Q

Lorazepam

A

Ativan
Slower onset of action (10-20min). not used for induction
used as adjunct for anxiolytic and sedative properties
not water soluble–venous irritation

20
Q

Midazolam

A

Verset.
quickest onset and emergence only if used for a short period of time.
More potent than diazepam or lorazepam
Induction slow, recovery prolonged
May depress resp when used with narcotics
minimal cardiac effects
water soluble

21
Q

Benzo toxicity

A

Excessive sedation, resp depression, coma
Flumanzenil is anidote–may need repeated dosing. 0.2mg over 30 sec, wait 30 sec, then 0.3mg over 30 sec, then 0.5mg every 60 sec up to max 3mg

22
Q

Narcotic agonists

A

Opoids
Analgesia, depression of sensorium and respiration
MOA: Receptor mediated
Minimal cardiac effects–no myocardial depression. Bradycardia in large doses
Some peripheral vasodilation and histamine release–hypotension
SEs: N, chest wall rigidity, seizures, constipation, urinary retention
Agents: alfentanil, fentanyl, sufentanil, remifentanil
Naloxone is pure antagonist that reverses analgesia and resp depression w/in 30 min

23
Q

Muscle relaxants

A

MOA: occurs at the neuromuscular junction inhibition. blocks the effects of ACH at NMJ.

24
Q

Nondepolarizing muscle relaxants

A

Competitively inhibit end plate nicotinc cholinergic receptor
Short acting: rocuronium
Intermediate (15-60m): cisatracurium, vecuronium, mivacurium
long acting: pancuronium, tubocurarine.
difference–renal function
Reversal by anticholinesterase–inhibit acetylcholinesterase: neostigmine, pyridostigmine, edrophonium

25
Q

Tubocurare

A

Nondepolarizing muscle relaxant

Suppress sympathetics, mast cell degranulation

26
Q

Pancuronium

A

nondepolarizing muscle relaxants

Blocks muscarinics

27
Q

Depolarizing muscle relaxants

A

Depolarize the end-plate nicotinic receptor. fastest onset and shortest duration.
Succinylcholine–short duration d/t plasma cholinesterase. S/Es: fasiculations, myocyte rupture, potassium extravasation, myalgias; sinus bradycardia–muscarinic receptor; malignant hyperthermia

28
Q

Local anesthetics

A

MOA: reversibly blocking sodium channels to prevent depolarization. Anesthetic enters on axioplasmic side and attaches to receptor in the middle of channel
Linear molecules that have a lipophilic and hydrophilic end. Low pH–more in ionized state and unable to cross membrane. Adding sodium bicarb–more in non-ionized state.
Two groups: esters and amides

29
Q

Esters

A

metabolized by plasma cholinesterase
Shorter duration of action
Agents: chloroprocaine, procaine, cocaine, tetracaine, novacaine

30
Q

Amiides

A

metabolized by cytochrome p-450

Agents: bupivacaine, mepivacaine, lidocaine, prilocaine, ropivacaine

31
Q

Local anesthetic toxicity

A

CNS: initial lightheaded, circumoral numbness, dizzy, tinnitus, visual change. later: drowsiness, disorientation, slurred speech, LOC, convulsions. finally resp depression
Cardiovascular: myocardial depression and vasodilation–hypotension and circulatory collapse
Allergic reactions: rare, usually d/t ester and PABA reaction. Rash, bronchospasm
Prevention and tx of toxicity: primarily from IV infection or excessive dose–anticipation. Aspirate often with slow injection, ask about CNS sx, have monitors available, prepare with CPR equipment, CNS-depressant drugs, cardio drugs. ABCs
Tx: assure adequate ventilation, administer O2. Seizures–diazepam. Hypotension: Trendelenburg position (head down, legs up), IV fluids bolus, vasopressors (dopamine). dysrhythmias: as per ACLS protocol, quit agent.

32
Q

Cocaine

A

Many uses in head and neck. Strong vasoconstrictor, no need for epi
MOA: blocks sodium, prevents uptake of epi and norepi.
may lead to increased levels of circulating catecholamines–tachycardia, peripheral vasoconstriction
safe limits: 200-400mg