Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
66 Cards in this Set
- Front
- Back
|
general anesth state
|
analgesia
amnesia loss of consciousness suppression of sensory and autonomic reflexes skeletal mm relaxation |
|
|
administration of general
|
IV or inhalation
|
|
|
balanced anesth
|
several drugs used in combination:
*IV agents used (more rapid) to begin *NMJ blocking agents used for paralysis *analgesic |
|
|
Stage 1
|
Analgesia - loss of pain
Is conscious and conversational |
|
|
Stage II
|
Excitement - delirium and violent
combative behavior, rise in BP, RR AVOID this with THIOPENTAL IV |
|
|
Stage III
|
Surgical anesthesia - UNCONSCIOUS
Regular RR until complete cessation of spontaneous respiration. EYE reflexes decrease until dilated and fixed. |
|
|
Stage IV
|
Medullary depression - NO EYE
movement, severe resp center and vasomotor center, resp ARREST, cardiac ARREST, w/o resp support, death |
|
|
inhaled anesth gases
|
N20 (nitrous oxide)
|
|
|
inhaled anesth halogenated hydrocarbons
|
Me HIDES
Methoxyflurane Halothane Isoflurane Desflurane Enflurane Secoflurane |
|
|
Inhaled aneths use
|
*maintain anesthesia AFTER IV agent
*rapid elimination *DO NOT cause postoperative respiratory depression |
|
|
Inhaled anesth PK
|
MORE LIPOPHILIC, MORE POTENT (direct relationship)
MORE soluble in blood, the LONGER it will take to WORK (inverse relationship w/induction) RECOVERY is d/t redistribution FROM the BRAIN |
|
|
Inhaled anesth mech
|
Direct interaction w/LIGAND gated ion channels
*POSITIVE modulation of GABA *POSITIVE modulation of GLYCINE *INHIBITION if NICOTINIC receptors |
|
|
MAC def
|
Minimum alveolar concentration that
results in immobility in 50% of patients when exposed to noxious stimuli (surgical incision). Expressed as a % of the alveolar gas mixture |
|
|
MAC characteristics
|
LOW MAC for POTENT anesth
large MAC for less potent anesth MAC does not explain SLOPE of DOSE-RESPONSE CURVE *DRC are STEEP for inhalational anesth |
|
|
MAC steep curve
|
steep anesth curve allows a MAC of
1 to fail to respond 50% but 1.1-1.3 has 95% fail to respond |
|
|
MAC properties
|
*MACs are ADDITIVE
*Nitrous can be used as a "carrier" gas and lessen the amount of other gases (VHH) *LEAST POTENT have a HIGH MAC *NITROUS has the HIGHEST MAC of the inhaled anesth so nitrous is LEAST POTENT *METHOXYFL has the LOWEST MAC so it is the MOST POTENT only need 0.16 for 50% not to respond |
|
|
Meyer-overton correlation
|
*Potency can be predicted from
liposolubility MORE LIPO, MORE POTENT |
|
|
L (oil:gas)
|
*Measure of LIPO solubility
*POTENCY increases as solubility in OIL increases *As L (oil:gas) INCREASES, MAC DECREASES, POTENCY INCREASES |
|
|
Partition coefficients
|
ratio in oil vs ratio gas = L (oil:gas)
Oil:gas of 0.5 = given that partial pressure is equal, the concentration of anesth in lipid is 50% that present in gas. MORE POTENCY, MORE OIL |
|
|
When is equil achieved with inhalation anesth?
|
When the partial pressure of the
anesth gas is equal in the 2 tissues. When a person has breathed an inhalational anesth for a sufficiently long time that all tissues are equil, the partial pressure of the anesth in ALL tissues will be equal to the partial pressure of the anesth in the inspired gas BUT while the pp may be equal in all tissues, the concentration of the anesth in each tissue will be different (since different tissues have different densities) |
|
|
What does induction require?
|
Induction requires the brain partial
pressure to equal MAC Induction requires the transfer of anesth from the alveolar air to the blood and then the brain |
|
|
What does the induction rate depend on?
|
SOLUBILITY of the anesth
CONCENTRATION in INSPIRED AIR PULMONARY VENTILATION RATE PULMONARY BLOOD FLOW CONCENTRATION GRADIENT b/t ARTERIAL and VENOUS BLOOD |
|
|
What is the L(blood:gas)?
|
Useful index of solubility in blood compared to air
|
|
|
Why is blood solubility important?
|
Anesth w/LOW blood solubility
diffuses from lung to arterial blood, few molecules are needed to raise its pp, therefore ARTERIAL TENSION RISES QUICKLY BLOOD GAS A GOOD INDICATION of ITS INDUCTION RATE RAPID INDUCTION = LOW SOLUBILITY |
|
|
What about high solubility in blood?
|
More molecules of anesth will dissolve
in the blood before the pp changes significantly, and the arterial tension of the gas increases slowly |
|
|
what is the relationship between blood
solubility and rate of rise arterial tension? |
A LOW: BLOOD GAS partition
coefficient determines a FASTER ONSET of ANESTHESIA |
|
|
examples of L(blood:gas)
|
NITROUS: 0.47, INSOLUBLE, FAST ONSET
METHOXYF: 12.0 VERY SOLUBLE, SLOW ONSET The HIGHER the coefficient, the slower the induction time as the anesth needs to saturate the blood before it can escape into pp. HALOTHANE: 2.3 (so 2.3x more halothane in the blood than in gas) NITROUS: 0.47 (so half the concentration in blood than in gas) |
|
|
So to bring it all together?
|
POTENCY:
LARGE OIL:GAS LARGE BLOOD:GAS SLOW ONSET (ONSET can be further delayed with INCREASED PULMONARY BLOOD FLOW) |
|
|
Pulmonary blood flow
|
caused by increased cardiac output
which slows the rate of rise in arterial tension due to an increase in volume of blood being exposed to anesthetic and blood capacity increases and tension rises slowly |
|
|
what about tissue absorption?
|
uptake by tissues also slows down onset of tension rise
|
|
|
Elimination
|
reverse of uptake
|
|
|
elimination for poorly soluble
|
*low blood and tissue soluble anesth
elimination should mirror induction, regardless of administration *high blood and tissue solubility recovery will be a fxn of duration of anesth administration **d/t anesthetic accumulated in fat will prevent blood (and therefore) alveolar partial pressures from falling rapidly |
|
|
examples of elimination
|
NITROUS: not soluble in blood or
fat, so steep drop in pp, and recovery is almost immediate HALOTHANE: accumulates in fat, like a depot, so recovery takes a while METHOXYF: BIG DEPOT in tissues, so elimination will be a function of how long you gave it for and how long it had to accumulate which can take hours to recover |
|
|
CARDIO effects of inhaled anesth
|
decrease BP moderately
ENU and HALO: myocardial depressants that decrease CO ISO, DES, SEVO: peripheral vasodilation NITROUS: almost no CVS effects HALOTHANE and ISO: sensitize mycardium to arrhythmogenic effects of catecholamines (still mild) |
|
|
RESP effects of inhaled anesth
|
ALL except Nitrous:
DECREASE tidal volume INCREASE RESP RATE DECREASE in MINUTE VENTILATION ALL including Nitrous ALL are RESPIRATORY DEPRESSANTS (which is to reduce response to CO2) Nitrous is the least depressant ISO and ENF are the MOST depressant |
|
|
RESP effects of inhaled anesth cont.
|
*depress mucocilliary function
*prolonged may lead to pooling of mucous and atelectasis (and infections) *bronchodilation (can be used to tx active wheezing and status asthmaticus) |
|
|
BRAIN effects of inhaled anesth
|
*soluble agents reduce resistance
in cerebral vasculature *increase cerebral blood flow * NOT GOOD w/increased intracranial pressure (head injury or brain tumor) *Nitrous increases blood flow the LEAST |
|
|
OTHER effects of NITROUS
|
*exchanges with NITROGEN BUT
FASTER than NITROGEN ESCAPES so INCREASE in VOLUME or PRESSURE |
|
|
NITROUS CI
|
Contraindicated in:
pneumothorax obstructed middle ear air embolus obstructed bowel intraocular air bubble pulmonary bulla intracranial air |
|
|
NITROUS AE
|
HEMATOXICITY
*prolonged exposure decreases methionine synthase activity and causes megaloblastic anemia *occupational hazard for dental staff |
|
|
HALOTHANE AE
|
SEVERE LIFE-THREATENING
HEPATOTOXICITY NO Tx Liver transplant |
|
|
METHOXYF AE
|
NEPHROTOXICITY
d/t FLUORIDE released during metabolism |
|
|
Malignant Hyperthermia
|
FATAL
AD GENETIC DISORDER of SKELETAL MM Triggered by VOLATILE anesth (NOT NITROUS) and depolarizing skeletal mm relaxants such as SUCCINYLCHOLINE |
|
|
Malignant Hyperthermia sx
|
tachy
HTN mm rigidity hyperthermia hyperK acidosis A MAIN COD d/t ANESTHESIA |
|
|
Malignant Hyperthermia genetic
|
AD
Ryanodine receptor RYR-1 gene 25 causal mutations for MH INCREASE in FREE Ca+ from the SR in mm cells MM stays contracted LACTIC ACID BUILD UP Muscle becomes "pickled" |
|
|
Malignant Hyperthermi tx
|
*DANTROLENE: blocks Ca release
from SR *LOWER TEMP *RESTORE electrolyte and acid-base |
|
|
Caffeine-Halothane mm contracture test
|
*to determine MH suceptibility
*part of mm samples tx w/HALOTHANE *abnormal mm twitches way out of the normal conduction *other part of mm samples tx w/CAFFEINE *abnormal response is any response >0.2 gm from 2 mM caffeine (normal mm only change at 4, 8, and 32 nM caffeine) |
|
|
IV anesth drugs
|
BB POKE
Barbituates Benzodiazepines Propofol Opioids Ketamine Etomidate |
|
|
IV anesth use
|
*used to initially achieve anesthesia
*sedate patients w/mechanical ventilation in the ICU |
|
|
Ultra-short acting barbituates
|
*effects are terminated by
REDISTRIBUTION from brain to other tissues 1. brain, liver, kidneys then 2. muscles, skin then 3. fat *elimination by hepatic metabolism |
|
|
THIOPENTAL use
|
BARBITUATE
*ultra short acting *induction *short surgical procedures |
|
|
BENZODIAZEPINES
|
*diazepam, lorazepam, midazolam
used as ADJUVANTS *PREMEDICATION, reduce anxiety |
|
|
Drug to accelerate recovery from benzos
|
FLUMAZENIL
can be used as a rescue antidote too |
|
|
OPIOIDS use
|
*IV morphine fentanyl sufentanil
alfentanil remifentanil ANALGESIA |
|
|
OPIOIDS AE
|
INCREASE chest wall RIGIDITY
*impair ventilation POSTOP RESP DEPRESSION *requires assisted ventilation *admin of NALOXONE |
|
|
How is neurolept anesthesia achieved?
|
fentanyl+droperidol (neuroleptic) =
NEUROLEPT ANALGESIA ADD 65% NITROUS (N20) = NEUROLEPT ANESTHESIA All by IV |
|
|
PROPOFOL
|
similar rate to barbituates
recovery is faster ambulate sooner vomiting is uncommon (antiemetic) induction and maintenance popular for DAY SURGERY |
|
|
ETOMIDATE
|
Minimal cardio and resp depression
Common N, V, pain, myoclonus Adrenocortical supression w/ inhibition of steroid generation and decreased hydrocortisone after a single dose |
|
|
KETAMINE
|
*dissociative anesthesia
catatonia, amnesia, analgesia w/o loss of consciousness *similar to PCP *CAN GIVE DIAZEPAM to reduce the PCP-like illusions, vivid dreams *may block NMDA receptor for memory and learning *ONLY ONE THAT PRODUCES CV STIMULATION ***can be used for patients in shock for that reason NOT common in US |
|
|
BENZO as adjuncts
|
ANXIOLYTIC
ANTEROGRADE AMNESIC properties |
|
|
Opioids as adjuncts
|
ANALGESIA
|
|
|
NM blockers as adjuncts
|
MUSCLE RELAXATION
|
|
|
H1 as adjuncts
|
PREVENT ALLERGIC RXNs
|
|
|
H2 as adjuncts
|
REDUCE GASTRIC ACIDITY
|
|
|
ANTIEMETICS as adjuncts
|
prevent ASPIRATION of STOMACH
CONTENTS |
|
|
ANTIMUSCARINICs as adjuncts
|
AMNESIC
PREVENT SALIVATION PREVENT BRONCHIAL SECRETIONS PROTECT HEART from BRADY caused by INHALATION agents and NM blockers |
