general anesthetics Flashcards
IV anesthetics
- Barbiturates
- Propofol
- Ketamine
- Etomidate
use of inhaled anesthetics
maintenance of anesthesia after admin of an IV agent
inhaled anesthestic common features
inc perfusion of brain
bronchodilation
dec minute ventilation
rate of onset inversely correlates to blood solubility
inhaled anesthetics MOA
ligand gated ion channels
positive modulation of GABA(a) and glycine receptors
inhibition of nicotinic receptors
minimum alveolar concentration
concentration that results in immobility in 50% of pt when exposed to noxious stimulus
% of alveolar gas mixture
low for potent anesthestics
MAC values
NO = high MAC, therefore needs to be added with something else for effect
methoxyflurane = low MAC - very potent
meyer-overton correlation
potency - predict from liposolubility
high oil:gas partition = MAC decreases = high potency
rate at which concentration in anesthetic in brain is reach depends on
- Solubility of the anesthetic
- Its concentration in the inspired air
- Pulmonary ventilation rate
- Pulmonary blood flow
- Arteriovenous concentration gradient
anesthestic solubility in blood
low solubility in blood - reaches arterial blood - the anesthetic rises quickly
the more insoluble in blood, the more will be as gas
if has high blood solubility, need more anesthetic before partial pressure of anesthetic increases = arterial tension increases less rapidly
low blood:gas partition, fast or slow onset?
fast onset of anesthesia
blood:gas partition values
nitrous oxide = low ratio (low solubility in blood - fast onset)
methoxyflurane: high ratio (highly soluble in blood - slow onset)
compare oil:gas to blood:gas ratio and their potency
high potency = slow onset
high oil:gas and high blood:gas ratios - are also very potent
therefore, high potency also has slower onset
rate of induction vs anesthetic concentration vs ventilation rate vs pulmonary blood flow
inc anesthetic concentration = inc rate of induction
inc ventilation = inc rate of induction
inc pulmonary blood flow = dec rate of induction (larger volume exposed to anesthetic)
arteriovenous concentration gradient
difference reflects solubility in tissues = uptake by tissues slows onset and recovery
elimination of anesthetics
low blood and tissue solubility - recovery mirrors induction (REGARDLESS OF DURATION OF ADMIN)
high blood/tissue solubility - recovery depends on duration of administration because of fat accumulation**
anesthetic effects on CV
dec cardiac contractility = dec BP
halothane and enflurane on CV effects
dec MAP via depression on myocardium - little effect on PVR
isoflurane, desflurane, sevoflurane CV effects
vasodilation - little effect on CO
**better for pt with impaired myocardial fxn
which anesthetics to give pt w/impaired mycardial function
isoflurane
desflurane
sevoflurane
halothane CV effects with catecholamines
sensitizes myocardium to catecholamines – ventricular arrhythmias
anesthetic respiratory effects
bronchodilators and respiratory depressants
isoflurane, desflurane = pungent - not good for pt with bronchospasm
halothane, sevoflurane, NO = nonpungent
isoflurane and enflurane are most resp depressant
N2O least depressant
which anesthetics are not good for people with bronchospasms
isoflurane
desflurane
use halothane, sevoflurane, NO
anesthetics CNS effects
inc ICP
not good for pt with brain tumor or head injury
N2O inc blood flow the least
enflurane can cause tonic-clonic movements
N2O on air containing cavities
N2O exchanges with nitrogen - N2O escapes faster than nitrogen escapes
= inc volume/pressure of cavity
when should N2O be avoided
- Pneumothorax
- Obstructed middle ear
- Air embolus
- Obstructed loop of bowel
- Intraocular air bubble
- Pulmonary bulla
- Intracranial air
hepatotoxicity from anesthetics
halothane
nephrotoxicity from anesthetics
methoxyflurane - fluoride released during metabolism
malignant hyperthermia with anesthetics
- Tachycardia
- Hypertension
- Severe muscle rigidity
- Hyperthermia
- Hyperkalemia
- Acidosis
halothane and succinylcholine
AD trait = ryanodine receptor gene 1 affected (uncontrolled Ca2+ release = hyperthermia release) - depletion of O2 and ATP b/c aerobic metabolism – leads to anaerobic metabolism = lactate – hyperkalemia and myoglobinuria
main COD d/t anesthesia
dantrolene
blocks Ca2+ from sarcoplasmic reticulum
caffeine halothane muscle contracture test
establish susceptibility to malignant hyperthermia
hematotoxicity
chronic exposure to N2O dec methionine synthase = megaloblastic anemia
hazard for dentists
ultra short barbituates
thiopental
methohexital
induction of anesthesia and for short surgical procedures
dec ICP
no analgesia = may cause hyperalgesia
coughing, chest wall spasm, laryngospasm = concern for asthmatic pt
propofol
induction and maintence of anesthesia
- produces no analgesia
- metabolized in liver
- potent resp depressant
- dec ICP
- hypotension through dec PVR
fospropofol = prodrug converted to propofol in vivo
etomidate
used for anesthetic induction of pt at risk for hypotension
minimal CV/respiratory depression
- no analgesic effects
- dec ICP
- n/v
ketamine
dissociative anesthesia = catatonia, amnesia, analgesia w/w/o LOC
may involve blockade of NMDA receptors
only IV anesthetic that is both analgesic and ability to produce CV stimulation
“emergence phenomena” - sensory and perceptual illusions and vivid dreams
- reduced by incidence diazepam, midazolam, propofol
neuroleptic opioid combinations
potent opioid analgesic + neuroleptic = neurolept analgesia is established
neurolept anesthesia = addition of 65% N2O in O2
anesthetics adjuvants
benzodiazepines = anxiolytic and anterograde amnesic properties
opioids = analgesia
NM blockers = muscle relaxation
anti-emetics
anti-muscarinics = amnesic effects, prevent salivation, protect heart from bradycaria
