Week 7 Local and general anesthesia Flashcards Preview

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Flashcards in Week 7 Local and general anesthesia Deck (20)
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What are the two major types of local anesthetics?

1. Ester: procaine, cocaine, chloroprocaine, tetracaine
2. Amides: lidocaine, bupivacaine (have "i" in 2nd syllable of name)


Where do local anesthetics work?

-at binding site on voltage gated Na+ channels in neuronal cell membranes, on nerve axons
-on inner side of membrane channel
-blockade of transmission of action potentials


How do local anesthetics work?

-uncharged (lipophilic) molecules have greater solubility across the plasma membrane
-charged molecule is active component to bind to sodium channel
-charged:uncharged ratio of drug is important
-pka>7.4, greater proportion of molecule in cationic/protonated form
-bicarbonate can be given to local anesthetic sln to change pH and pKa ratio. Increases amount of neutral form to enable local anesthetic molecule to cross the membrane.
-when pKa is high, there is delay in onset


How is local anesthetic nerve conduction blockage determined by fiber diameter, myelin, and function?

-nerve conduction is faster with greater nerve diameter and myelin
-need higher dose Cm (min concentration of local anesthetic) for greater nerve diameter
-sequence of clinical effects (which nerves affected first): Type C nerve fibers (dull pain, temp, touch), Type B (pre gang autonomic), Type C (proprioception, large and small motor, touch, pressure, muscle tone, pain, temp


What is the sequence of clinical effects following local anesthetic administration?

1. Autonomic nervous system blockade: vasodilation
2. sensory anesthesia: pain, temp, touch, pressure
3. Skeletal muscle paralysis: motor blockade


What factors impact the systemic absorption during local infiltration and nerve plexus block when administrating local anesthesia?

1. Dose
2. physicochemical properties of drug
3. use of epinephrine-cause vasoconstriction to localize and prevent migration of anesthetic molecules
4. Site of injection and local tissue blood flow
5. protein binding, the more lipid soluble the drug, the great the degree of protein binding


How are local anesthetics metabolized and eliminated?

-esters: hydrolysis in the plasma
-amide: hepatic metabolism by Cyt P450


What are some adverse effects of local anesthetics?

-CNS: circumoral numbness, facial tingling, restlessness, vertigo, tinnitis, slurred speech, seizures
-Cardiovascular system: hypotension, myocardial depression (from blockade of cardiac sodium ion channels)
-ECG changes-PR interval prolongation and widened QRS complex


How can CNS or CV toxicity due to local anesthetics be treated?

Lipid rescue=lipid emulsion administered which enables a "lipid sink" extraction of these lipophilic local anesthetic molecules to reduce the effective plasma concentration


What is the state of anesthesia?

The following occurs:
-loss of consciousness
MAC=minium alveolar concentration, used to measure immobility


What are the anatomic sites of action of general anesthetics?

-brainstem-hypothalamic/thalamic network
-cerebral cortex


What are the molecular targets general anesthetics?

1. inhibitory neurotransmitters: glycine, GABA-->potentiation of GABA A and glycine activity (Cl- conduction leading to hyper polarization)
2. Excitatory neurotransmitters: NMDA-->inhibition of excitatory glutamate and NMDA receptors
3. Inhibition of Na, Ca, and K+ channels in cell membranes


How do volatile anesthetics get to the brain?

-volatile anesthetics are liquid at room temp, vaporized in machine and carried by oxygen
-they diffuse through alveolar-arterial membrane (uptake)
-transported to brain in circulation
-brain, heart, lung, kidneys are vessel rich group due to high volume of blood to these organs


Describe the uptake of volatile anesthetics.

-uptake=movement of anesthetic molecules into the lung and will move into the lungs until the partial pressure in alveoli=that in blood
-insoluble agents-alveolar concentrations rise faster and induction faster since taken up by blood less readily
-Blood/gas coefficient: the lower the greater the anesthetic's insolubility, the faster the onset


How is the potency of a general anesthetic measured?

by MAC=minimum alveolar concentration
-indicates the relative value/amount of anesthetic given


How are general anesthetics metabolized/eliminated?

Elimination though the lungs. reversal of Pbrain-->Parterial-->Palveoli. Metabolism is negligible.


What are the CNS effects of general anesthetics? general CV and pulmonary effects?

-CNS obtundation
-decreased cerebral metabolic rate (CMRO2)
-increase cerebral blood flow through vasodilation
-increased intracranial pressure with MAC>1
-decreased activity in the CV and pulmonary system


What is the mechanism of intravenous general anesthetics?

-alteration of synaptic function of GABA or NMDA neurotransmitters
-propofol decreases rate of GABA dissociation
-ketamine is a NMDA receptor antagonist
-etomidate has enhanced GABA binding to receptors


Describe the pharmacokinetics of intravenous anesthetics.

1. Distribution:
-highly lipid soluble distribute to VRG (vessel rich group)
-degree of protein binding can decrease distribution
2. Redistribution:
-termination of clinical effect, movement of IV agent from site of action to less perfused peripheral compartments, followed by metabolism and elimination
3. Metabolism and Elimination
-Metabolized by liver enzymes and eliminated by kidneys
-measured by half lives


What are the effects of intravenous anesthetics on CNS, CV, and pulmonary systems?

-propofol, etomidate, barbiturates, and benzodiazepines are CNS, CV, and pulmonary depressants
-ketamine on CNS and CV organs are stimulatory

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