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Meyer-Overton Correlation

Dependent upon affinity for water or affinity for fat (fat/water partition coefficient). States anesthetics are soluble in fat


Unitary Theory

Cell membranes mostly lipid therefore majority of anesthetic effects come from effects on cell membranes


Concept of MAC

Analogous to plasma EC50 - 50% of nonparalyzed do not move with surgical stimulus. Universal measurement for inhaled anesthetic potency


Protein Centered Theory

Signaling proteins (ion channels/receptors) are the molecular site of action


Effects of Inhaled anesthetics on ligand gated ion channels

Potentiate GABA & Glycine, Inhibit Acetylcholine & glutamate


Effects of inhaled anesthetics on voltage gated ion channels

Nervous system - reduction in amplitude through sodium channels, CV system - reduction in amplitude and duration through calcium & potassium channels


Intracellular signaling mechanisms that inhaled anesthetics work on

G-protein coupled receptors, protein phosphorylation, gene expression


Cellular mechanisms of inhaled anesthetics

Hyperpolarize neurons - decrease neuronal excitability (determined by resting membrane potential, threshold potential & input resistance. Alter transmitter release presynaptic & neurotransmitter responses postsynaptic


How do volatile anesthetics enhance inhibitory synaptic transmission postsynaptically?

Potentiating ligand-gated ion channels activated by GABA & glycine, extrasynaptically by enhancing GABA receptors & leak currents, & presynaptically by enhancing basal GABA release


How do volatile anesthetics suppress excitatory synaptic transmission?

Presynaptically by reducing glutamate release (volatile agents) and postsynaptically by inhibiting excitatory ionotropic receptors activated by glutamate (gaseous agents)


Desired effects of inhalation agents

Immobility, unconsciousness, no learning/memory, sedation, neuroprotection, CV & respiratory protectants


How immobility is mediated

Probably by spinal cord NMDA receptors, requires 2.5-4X MAC needed for amnesia & unconsciousness


How unconsciousness is mediated

Hyperpolarization of thalamic sites, *dimmer, not on/off*, depends on interrupting synchronicity between multiple neural networks


How learning & memory is mediated

Possibly hippocampal & amygdala dependent (usually 0.3-0.4 MAC is enough)


How sedation is mediated in potent agents vs gases?

Potent agents probably stimulate GABA, gases (N2O & Xenon) possibly antagonize NMDA


How neuroprotection is mediated

All potent agents prevent apoptosis, decrease CMRO2 (by increasing inhibitory and decreasing excitatory transmission).


What is a neurological risk of inhaled anesthetics

Neurotoxicity- irreversible cell damage by N2O & less by potent agents


CV Effects of gases - general

Dose dependent myocardial depression, hypotension, SVR, direct negative chronotropic effects, sensitized to arrhythmogenicity, direct coronary artery vasodilation in vitron, coronary vasoconstriction in vivo


Pulmonary Effects of gases - general

Significant respiratory depression via central depression


Why are volatile anesthetics fluorinated?

Reduce or eliminate toxicity via metabolism, reduce/eliminate flammability, allow increased speed of induction and recovery from anesthesia


Basic hydrocarbon structures useful as fluorinated anesthetics include what?

ethane, methyl ethyl ether & propyl methyl ether


Most to least pungent anesthetic

Desflurane, isoflurane, halothane, sevoflurane


Potent inhaled anesthetics pulmonary effects- specifics

Decrease tidal volume in dose dependent manner (get less than adequate increase in RR & increased resting end tidal CO2). Decrease FRC, bronchodilation, increase activity of laryngeal irritant receptors and decrease activity of pulmonary irritant receptors, can adversely effect hypoxic pulmonary vasoconstriction. Effects on PVR are relatively small


Why does FRC decrease

Loss of intercostals, altered respiratory pattern, cephalad movement of diaphragm, altered thoracic blood volume


How are potent inhaled anesthetics bronchodilators

Decreases intracellular calcium concentration & reduces calcium sensitivity- Relaxes airway smooth muscle by directly depressing smooth muscle contractility- it directly effects bronchial epithelium and airway smooth muscle cells through phosphorylated myosin light chain, and indirectly inhibits reflex neural pathways.


What does an increase in pulmonary vascular resistance cause

Corresponding increase in pulmonary arterial pressure which promotes interstitial fluid transudation


When is pulmonary vascular resistance lowest

At lung volume equivalent to FRC


How do inhaled anesthetics effects hypoxic pulmonary vasoconstriction

Through vasodilation of pulmonary vascular bed and dose dependent myocardial depression, blood flow will get to the area that was restricted (such as in the case of a tumor)


Inhaled anesthetics protein binding site, effect & target

Amphiphilic site, effect: conformational flexibility/ligand binding, target: ion channels/receptors and signaling proteins


Inhaled anesthetics action potential site, effect & target

Site: Nervous system Effect: small reduction in amplitude, target: sodium channels. Site: CV system Effect: reduced amplitude & duration Target: Calcium & Potassium channels