General Anesthetics Flashcards
Intravenous anesthetics?
Etomidate, ketamine, propofol, thiopental
Etomidate: Side Effects
Induction agent known for its
cardiovascular stability.
Contraindicated in septic shock.
Metabolism of IV general anesthetics?
Metabolism: hepatic Excretion: renal clearance
Ketamine: MOA
Antagonizes the NMDA receptor.
- Causes some areas of the brain to be
tonically excited → this central stimulation
of the sympathetic nervous system allows
for CV stability, maintained ventilation,
and increased cerebral blood flow,
intracranial pressure, and cardiac output.
Propofol: MOA
- Possesses high lipid solubility and a redistribution phase with a short half-life (t1/2α) - Powerful respiratory depressant. - Available for IV administration only.
Thiopental: MOA
- Belongs to the barbiturate drug class.
- Suppresses transmission of excitatory
NTs (e.g., acetylcholine) and enhances
inhibitory NTs (e.g., GABA). - Can create a loss of consciousness in
30 seconds.
Ketamine: Indications
- Blocks polysynaptic reflexes in spinal cord. - Inhibits excitatory NT effects in parts of the brain. - Disassociates thalamus from limbic cortex → “dissociative” anesthetic, Pt appears conscious but can’t process sensory input.
Propofol: Indications
- Rapid onset and recovery
- One of the most well-known and
highly utilized general anesthetics. - Approved for mod-deep sedation
and general anesthesia (induction +
maint.).
Thiopental: Indications
Decreases ICP - Acts as resp. and CV depressants. Decreases both CBF and ICP → reduces brain O2 consumption → helpful in neurosurgical patients. - Most used as induction agent.
Ketamine: Side Effects
Hallucinations,
nightmares
Propofol: Side Effects
Respiratory
depression,
bradycardia
Thiopental: Side Effects
Respiratory
depression,
bradycardia
Inhaled general anesthetics?
Desflurane, halothane, isoflurane, nitrous oxide, sevoflurane
Treatment for malignant hyperthermia?
Dantrolene
Dantrolene: MOA
Dantrolene is a muscle relaxant that depresses excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor and decreasing intracellular calcium concentration.
Inhaled general anesthetics: MOA
Although inhalation anesthetics are widely used, their mechanism of action is largely unknown. It is presumed that their primary mechanism is through the inhibition of glutamate receptors and enhancement of GABA neurotransmission. The site of action for these drugs likely occurs at multiple locations within the CNS. Specific brain areas including the reticular activating system (RAS), cerebral cortex, hippocampus, and spinal cord are all impacted by anesthetic agents, contributing to these drugs’ various physiologic effects.
Inhaled anesthetics: Indications
Inhalation anesthetics are used for the induction and maintenance phase of general anesthesia. These gases are administered by breathing through an anesthesia mask or endotracheal (ET) tube connected to an anesthetic machine.
What factors affect inhaled anesthetics?
The ultimate clinical effect of inhalation anesthetics depends on delivery of a therapeutic partial pressure of an agent to the CNS. This delivery is affected by properties of the agents themselves and by physiologic variables including regional blood flow, cardiac output, and ventilation.
Side effects of inhaled anesthetics?
Myocardial depression - Decreased SVR and SBP. - Volatile anesthetics create classic respiratory pattern: increased RR, decreased TV, and decreased ventilatory response to CO2 (hypercarbia). All agents cause reduced RBF and GFR. Malignant hyperthermia (MH) is a potential complication shared by all of the volatile anesthetics (and succinylcholine).
Inhaled anesthetics: Metabolism
Inhalation anesthetics undergo limited metabolism. The recovery (emergence) from these drugs is achieved by lowering the anesthetic’s concentration at the site of action (the brain). The majority of elimination occurs at the alveolus and is dependent upon same principles that facilitate induction of anesthesia.
