Anesthetics Flashcards
Types of anesthetics
inhaled, parenteral, local
Two important properties that drive onset, extent and duration
lipid solubility (determines potency, protein binding and DOA), Ionization constant
General anesthesia should always include
sleep induction, loss of pain responses, amnesia, skeletal muscle relaxation, loss of reflexes
Inhaled anesthetics
Ether, Nitrous oxide, Haltothane (Fluothane), Enflurane (Ethrane), Desflurane (Suprane), Isoflurane, Sevoflurane (Ultane)
Inhaled anesthetic MOA
activate K channels, block Na channels to increase cellular threshold for firing, decreases neuronal activity
Inhaled anesthetic ADRs
increases ICP, post op N/V, malignant hyperthermia: tachy, HTN, hyperkalemia, muscle rigidity, associated with sudden and massive release of Ca
What is used to treat malignant hyperthermia
dantrolene and fluids
Parenteral anesthetics
Ketamine, Etomidate (Amidate), Proprofol (Diprivan), short acting barbituates (sodium pentothal), benzodiazepines
Katamine is mostly used
in animals and some in dental procedures
Etomidate (Amidate) is used for
short term sedation (10 min)
Proprofol (Diprivan) is used
regularly in hospt setting for procedures and continuous infusions in ICUs
Parenteral anesthetics can also be used for
signal conduction alteration (arrhythmias)
Parenteral anesthetic MOA can make them dangerous
if inadvertently given IV when intended to be given locally
Local anesthetics MOA
blockade of voltage gated Na channels in a manner that is use-dependent, oftentimes given with a agonist such as epi with goal of vasoconstriction of microvascular to reduce blood flow to area and minimize wash out
Local anesthetic can be given with
dexamethasone (corticosteroid) with the thought that it will increase duration by 50%
How can local anesthetic toxicities be reversed
with use of IV lipid to remove anesthetic from sight of action
Effects of local anesthetics
Nerves- dec conduction, vascular smooth muscle- vasodilation, heart- decrease excitability, reduce pacemaker activity, prolong ERP up to and including death in severe toxicity, CNS-increased excitability
Local anesthesthics tend to affect
small myelinated neurons 1st, at higher concentration, they will block signal transduction through myelinated neurons
The more lipophillic the anesthetic the…
more potent w/ faster onset
Order of local anesthetic blockade
pain, sensation of temperature, touch/pressure, motor function, reversal/recovery is the opposite
Classes of local anesthetics
Esthers- Procaine (Novocaine), tetracaine (pontocaine), Benzocaine; Amides- Lidocaine (Xylocaine), mepivacaine (Carbocaine), Bupivacaine (marcaine), Ropivacaine (Naropin)
Topical administration
Benzocaine*** (only indication), Lidocaine, Tetracaine, used for diagnostic, procedures
Infiltration administration
lidocaine, procaine, bupivacaine, local application, injection
Nerve block administration
Bupivacaine, ropivacaine, drug is injected or catheter inserted for infusion to cluster of neurons (femoral, sciatic)
Epidural administration
burivacaine, ropivacaine, injected directly into CSF, usually childbirth or abnormal surgeries, allows for complete blockade of large # of neurons
Local anesthetic ADRs
CNS- sedation, restlessness, nystagmus, convulsions, CV- cardiac block, hypotension, arrythmias, vasodilation, allergic rxns- more common with esthers
Local anesthetic toxicity
mostly related to inadvertent IV infusion via INTRAVASCULAR catheter or inadvertant IV injection, always aspirate before injecting to confirm placement; HTN, tachy, excitability
Lidocaine
dental anesthesia, available as 1%, 2% in combo w/ epi, keep perservatives in mind, dose needed depends on area and duration needed, usually 2 hrs
Bupivacaine (marcaine), Ropivacaine (Naropin)
most common for epidural or nerve blocks post op (femoral or sciatic), different anesthesia providers will use different concentrations, opioids added w/ epidurals
Long lasting local anesthetics
Tetracaine (Pontocaine), Bupivacaine (Marcaine), Ropivacaine (Naropin)
