Anesthetics Flashcards
Goals of general anesthetics (5)
Hypnosis, amnesia, analgesia, muscle relaxation, and physiologic homeostasis
All do hypnosis and amnesia.
Thiopental Delivery Timing Use Mechanism Adverse rxn Upside
IV
•Fast onset, short duration. Quickly redistributed to fat. Wake up 5 min after bolus but is in your system for many days.
•Mainly used for IV induction, but then switch to inhaled anesthetic to keep pxs asleep.
•Mechanism – enhances GABA-a receptor function
•Adverse rxn – cardiorespiratory depression
• However, decrease in cerebral metabolic rate and cerebral blood flow have protective effect.
Propofol Delivery Timing Use Mechanism Adverse rxns Upside
IV
•Fast onset, short duration, rapid elimination
•Used for IV induction and maintenance, as well as conscious sedation
•Mechanism – enhances GABA-a receptor function
•Adverse rxns – cardiorespiratory depression and pain on injection
• However there is less nausea / vomiting compared to thiopental.
• Cerebral protection
Etomidate Delivery Timing Use Mechanism Adverse rxns Upside
IV
•Fast onset, short duration, semi-rapid elimination
•Used for IV induction
•Mechanism – enhances GABA-a receptor
•Adverse rxns – myoclonus during onset, adrenal suppression, pain on injection
• However, there is minimal cardiorespiratory depression and good cerebral protection
Ketamine Delivery Timing Use Mechanism 2 odd features Effects on CV system Adverse rxn Precaution
IV
•Fast onset, longer duration, semi-rapid elimination
•Used for IV / IM induction of anesthesia, as well as analgesia
•Blocks NMDA receptor → analgesia
•Dissociative – pxs may have eyes open, may be moving or have rigid muscles. But don’t respond to external stimuli. Not true hypnosis. Still don’t remember though.
•Catalepsy (waxy rigidity, purposeless movements)
•Acts as CV stimulant (activates sympethetics). Maintains spontaneous ventilation and bronchodilation.
•No cerebral protection (increases cerebral metabolic rate and blood flow)
•Adverse rxn: Post-op dysphoria – pxs wake up w/ hallucinations. Tx w/ benzos.
•Precaution - Don’t give to pxs w/ ICP or risk of ischemia
3 main volatile anesthetics
Use
Mechanism
Adverse rxns
Isoflurane, Sevoflurane, and Desflurane
Used for both induction and maintenance
•Mechanism - Enhance GABA-a receptor → hypnosis / amnesia. Na, Ca, K channels → analgesia and skeletal muscle relaxation
•Adverse rxns
• Malignant hyperthermia – may be fatal
• Mutations in EC coupling proteins → increased myoplasmic Ca
• Hypermetabolism → rigidity (even w/ NMJ blocker), heat, CO2, acidosis, rhabdomyolysis (may cause kidney damage), hyperkalemia
• Tx – DC anesthetic, cooling, hyperventilate to remove CO2, IV dantrolene (blocks Ca release from SR)
Other adverse rxns:
• CV depression
• Respiratory depression – rapid shallow breaths (opposite of opioids)
• Increase ICP – decrease metabolic rate but increase cerebral blood flow
• Bronchodilation may inhibit mucociliary clearance
• Airway irritation / cough (Des > Iso > Sevo)
How do you treat malignant hyperthermia?
DC anesthetic, cooling, hyperventilate to remove CO2, IV dantrolene (blocks Ca release from SR)
N2O
Mechanism
Use
- Mechanism – Blocks NMDA receptors → analgesia.
* Use - Often combined w/ other drugs to get full hypnosis w/ faster onset.
Local anesthetics
Use
Mechanism
2 main types w/ metabolism and way to distinguish
Use - Sensory block, motor block, and sympathetic block (vasodilation)
•Mechanism - Blocks AP generation. Main target is V-gated Na channel – Enters axoplasm through cell membrane and blocks Na channel via inside of cell. Can’t block from outside.
•2 main types
• Amides – hydrolyzed by plasma esterases → PABA, which may cause anaphylactic rxns in some pxs. Amides always have 2 I’s in the name
• Esters – metabolized in the liver. No PABA. Esters only have 1 I in the name. Only used on the skin.
Acid / base effects on local anesthetics
Tertiary amines can accept a proton.
•Commercial forms are acidic b/c it’s more stable. Acidic form is the active form.
•Once injected into tissue, some gets unprotonated, which is good b/c then it can diffuse across membranes, getting into axons and blocking Na channels from the inside. This can be hastened by adding more base.
2 main adverse rxns of local anesthetics
Systemic toxicity and methemoglobinemia
Injection into which 2 sites (not counting vessels) are biggest risk for systemic toxicity of local anesthetics?
Intercostal and epidural areas
Sxs of systemic toxicity
Lightheadedness, circumoral paresthesias, tinnitus, NV, tremors, confusion, seizures, CV depression, coma, respiratory arrest, or death
Which local anesthetic is highly cardiotoxic?
Bupivucaine
Treating systemic toxicity
- Support w/ airway, benzos for seizures, and ACLS (advanced care life support) for arrythmias / CV collapse.
- Lipid emulsion soaks up local anesthetic that is circulating in blood and is eliminated slowly. Reverses toxicity.
