Anesthetics Flashcards
How does LA work
Procaine, tetracaine, lidocaine
They r esters or amides that inhibit conduction of AP across nerve fibres by blocking Na channels
Parts of LA
Aromatic part and amine chain linked by ester or amide bond
How to keep effect while minimising systemic se
Vasoconstrictors like adrenaline to decrease BF
Ph needed
LA will be ionised if hypoxic = low pH or infected so cant cross membrane
LA in neurone
Binds to voltage gated Na channels on cytoplasmic surface
State dependent so effective neurones which fire more rapidly as they bind more tightly to inactivated Na channels prolonging inactivated state (not closed but inactivated)
So no AP
Effects in small and myelinated
Greater effect as pain neurones r usually small
At greater doses stop temp touch and pressure too then loss of motor function
Ester eg LA
Cocaine and Benzocaine r surface anesthetiser for topical use only as serious se
Cocaine is only one that blocks reuptake of catecholamine so they build up causing vasoconstriction, tachycardia, arrhythmia and blocks reuptake of dopamine so euphoric
Benz can cause methemoglobinemia where hb fe 2+ to 3+ so cant transport o2= cyanosis
Tetracaine has long duration and used in spinal and corneal anaesthesia
Procaine has short duration but CNS and cardio se
Amide LA eg
Lidocaine most used, intermediate duration, used in topical and spinal
Mepivacaine intermediate duration but toxic for new borns
Bupivacaine long duration = epidural given in labour but cardio toxic and can cause myocardial depression if given in blood vessel
Metabolised by cytochrome P450 enzymes in liver at diff rates
Se of both amide and ester LA on CNS
If get in blood stream they decrease activity of inhibitory neurones = restlessness, anxiety, seizures
If higher dose decrease activity of all neurones= depression of CNS and resp depression
In CVS they decrease rate of AP on myocytes of the heart= bradycardia and decrease CO
Also vasodilation causing further HPT
General aesthetics aim
Dismiss AP in CNS
To stop Excitatory- stops glutamate binding to NMDA receptor to start an AP
Stim inhibit so more GABA binding to GABA receptors or increase sensitivity
Parenteral anesthetics
Given through vein
Lipophilic so travel to highly lipophilic tissues from blood stream stream to induce anesthetiset state before going to bloodstream to liver then kidney to excreted
Induction via single IV injection and can be used for maintenance by continuous IV infusion
Features of thiopental, midazolam, propofol, etomidate
Stimulate or increase GABA receptor sensitivity
Rapid onset 20-30 s but have shorter duration
Used for induction and maintenance in short procedures
Parenteral anaesthetics se
T-has barbiturate so CVS depression, hypotension, respiratory depression, decreases intracranial pressure, bronchoconstriction
M- benzodiazepine slower onset, longer duration and less CVS and resp depression but can cause cognitive dysfunction like amnesia, and post op resp depression but can be reversed w flumazenil
P- short duration so used in out patient surgery- CVS dep and hypotension, vasodilation, inhibit mitochondrial FA metab- propofol infusion syndrome (Bradycardia, HF, metabolic acidosis, rhabdomyolysis, fatty liver)
E- less CVS depression so used in coronary aa disease etc people risk of hypotension but causes adrenal suppression
Ketamine Parenteral
Rapid onset, longer duration
Blocks NMDA receptor
Increases cerebral bf and intracranial pressure
Stim SNS increasing BP, CO and dilation of bronchi so ok in hypo and asthma
Dissociative anaesthesia so open eyes, breathe, swallow, move involuntarily but don’t remember or feel pain
Delusions and hallucinations on waking
Inhaled anesthetics
Small therapeutic window which is close to toxic
Gases or volatile liquids given via mask or tracheal tube to alveoli to body where theres fat and it accumulates if high lipid solubility to increase potency and if higher blood solubility then bind to hb leading to slower onset and recovery
