general anesthesia Flashcards
name the three stages for general anesthesia
induction, maintenance, recovery
name the three routes of administration
endotracheal/inhalation
intravenous
oral
endotracheal/inhalation route of administration
Blood volume completely passes through the lungs
• Re-breathing is facilitated by the carbon dioxide absorber
intravenous route of administration
Continuous and bolus dosing
• Route for supportive medications
oral route of administration
Pre-operative for pediatric patients
• To sedate the patient before placing intravenous lines
therapeutic monitoring
End tidal anesthetic concentration • Bispectral index • Level of sedation • Richmond agitation and sedation scale • Ramsey’s scale • Level of paralysis • Train of four
toxic monitoring
Vital signs • Blood pressure, heart rate and rhythm, temperature, oxygen saturation • Laboratory • Blood gas arterial • Blood gas venous • Electrolytes
mechanism of action for inhaled anesthetics
Block excitatory responses
• N-methyl D-aspartate (NMDA) receptors antagonist
decrease binding and action of glutamate, the main
excitatory neurotransmitter
• Blocking nicotinic acetylcholine receptors to reduce the
response to noxious stimuli
Potentiate inhibitory transmitters
• Activating glycine channels
• Activate GABAa
Two-pore-domain K+ channels in the neuronal cell membrane are activated leading to hyperpolarizing and delayed transmission
what does the uptake of inhaled anesthetics depend on?
Depends on:
• Solubility in body tissue (partition coefficients)
• The potential reservoir for soluble gases is
large and will be filled more slowly
• More soluble–>more likely to stay in the blood (high blood:gas partition
coefficient) = Slower onset
• Less soluble (low blood:gas partition
coefficient) = Faster onset
- Cardiac output
- Alveolar-venous partial pressure difference
nitrous oxide
Produces sedation and analgesia
• NMDA receptor antagonism and activation of two-poredomain K+ channels
• Concentrations between 20-50%
• Poor solubility in blood and other tissues leads to
quick equilibration
• Rapid induction and rapid emergence
• Low potency leads to little utility as a sole anesthetic
• Can be combined with other gases to quicken induction
• MAC of 105%
dont really give it in the hopsital. more in the abulatory setting
halogenated gases
Share similar mechanisms of action
• All can be combined with nitrous oxide to facilitate quicker
induction
• Advantages over earlier drugs such as diethylether
◼ Well tolerated
◼ Lower blood:gas solubility coefficient
◼ Non explosive
• Dose dependent decrease in cardiac output and blood
pressure
• Not analgesic
comparison of inhalation anesthetics
The more soluble an anesthetic is in blood, the more of it must be dissolved in blood to raise its partial pressure in the blood
Halothane
Slow induction and slow recovery
• Lowest cost of halogenated gases
• Cardiac effects
Direct myocardial depressant
Predictable decrease in arterial blood pressure of 20-
25 mmHg
Sensitizes the myocardium to epinephrine and
circulating catecholamines –>Ventricular arrhythmias
Decreases auto-regulation in end organs, decreased
perfusion to gut, liver, and kidneys
• Bronchodilator: May be used in resistant status asthmaticus
• Some metabolism by the liver, may cause oxidative stress
and potential hepatic necrosis
more about halothane
Due to side effect profile compared to other agents:
• Little utility as a general anesthetic in the U.S.
• May be used globally in low resource areas
• Some utility as a treatment for asthma
Desflurane
Very low blood:gas, rapid induction and recovery
• Irritating to airway so not often used for induction
• Cardiac effects
Decreased blood pressure due to decreased systemic
vascular resistance
Does not subside with duration of anesthesia
Increased heart rate due to sympathetic stimulation
• Respiratory effects
Decreased ventilation, increased carbon dioxide retention, potential laryngospasm
