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49 Cards in this Set
- Front
- Back
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General anesthesia
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Pharmacologically induced state causing unconsciousness, amnesia, analgesia, suppression of surgical stress response and muscle paralysis. These are reversible and cause loss of memory of immediate events and loss of awareness. This eliminates perception and physiological reactions to painful stimuli (leads to better outcomes).
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Coma
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"Coma is a profound or deep state of unconsciousness. An individual in a state of coma is still alive but unable to move or respond to his or her environment" - NIH
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Mechanism of General Anesthesia
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All components of GA can be produced by a volatile anesthetic but with different dose dependancies. To complicate things further, dose response relationship is dependent on the amount of surgical stimulation.
(if you take a healthy volunteer and give them anesthesia , this will not correlate with the OR as there is no surgical stimulation) |
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Actions on CNS
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Significant action on brain and spinal cord. (Spinal anesthesia can be admin in the canal and is made heavier than the CSF so that it settles to the bottom, the higher the level goes, the more sedated the patient gets, even before touching the brain) (animal preps with brain separated have proven this)
-hypnotic effects probably at brain, absence of mov't probably at spinal cord |
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Effects on nerve conduction?
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Inhalational anesthetics are unlikely to affect axonal conduction, however, may effect synaptic transmission
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Membrane effects--The Myer-Overton hypothesis
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GA are thought to effect lipid content of plasma membranes, reversal at high pressures, linear relationship of anesthetic potency to lipid solubility. However, there are substances that are very lipid soluble but not very good anesthetics. Also, the high atmospheric pressure is a stimulation, much like surgical stimulation.
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Modified Myer-Overton
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Anesthetic agents have preferential solubilities for specific regions of the lipid membrane, this may induce an intense lateral pressure causing distortion of membrane protein such as ion channels
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Actions on presynaptoc and postsynaptic
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-presynaptically: prevention of NT release, increase reuptake, action on voltage gated ion channels
-postsynaptic: inhibition of ligand gated channels on postsynaptic membrane |
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Advantages of inhalational anesthetics
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easy administration, elimination via lungs, little metabolism with most agents to toxic or active substances (you essentially get the drug back unchanged). Very good at blunting the surgical stress response.
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Uptake of inhalational IA
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Anesthetic is delivered as a gas to the lung.
IMPORTANT: alveolar partial pressure = partial pressure of anesthetic gas in the brain |
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Tissue uptake of IA
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Have to compete with uptake by the tissues, this slows the rise of alveolar concentration and slows induction. The factors effecting alveolar concentration: solubility of gas in blood, alveolar blood flow (CO), partial pressure diff between alveolar blood and venous blood.
Graph shows that more solubility equals slower speed of induction. Are there gas bubbles in the brain? Lol no. One exception, NO, which expand any gas pocket |
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Tissue distribution
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Highly perfused vessel rich group is first to take up anesthetic and first to fill, muscle group is not well perfused so uptake is slower, higher volume is slow to fill, fat group has perfusion nearly equal to muscle but much higher solubility, vessel poor group has insignificant uptake.
(shut off anesthetic but the vessel rich group does not go to zero, this is because there is residual anesthetic in the fat and muscle group and this then enters the vessel rich group) |
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Minimum alveolar concentration
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Necessary to have a standard way to describe anesthesia dose. MAC = alveolar concentration necessary to prevent movement in 50% of pts. in response to a standard stimulus (so we def want to be above MAC)
NO has a terrible MAC, so why use it? Because MACs are additive, NO goes on and comes off quickly so we like to use it |
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Local anesthetics
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Drugs that produce a transient loss of sensory, motor, and autonomic function in a discrete portion of the body. Mechanism of action: most bind to the sodium channel in the inactivated state, preventing channel activation, blocking sodium influx with depolarization, the result being that an action potential is not propagated.
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Local anesthetic, two main classes
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Esters and the amides
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Systemic effects of local anesthetics
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Have the potential to effect Na channels throughout the body, if accidentally administered into the vasculature.
-Cardiovascular effects at low doses have anti arrhythmic effects, and at high doses may cause bradychardia and heart block -brain effects at lower doses causes excitement and seizures, at higher doses leads to CNS depression and coma and death. -should recognize and treat, hit with benzodiazapene, and then antidote |
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Modern anesthesia
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Balanced anesthesia: the rational combination of anesthetic and adjuncts, maximize beneficial clinical effects, minimize dangerous side effects, greater control of anesthetic level, rapid emergence with greater post op lucidity
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Stages of anesthesia (like with ether in the old days)
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-Stage 1: sedation, amnesia, analgesia
-Stage 2: loss of consciousness, excitement, -DANGEROUS, instability, airway hyperactivity -Stage 3: surgical anesthesia -Stage 4: OVERDOSE, medullary suppression, cardiovascular collapse (IV agents help us get from 1 to 3 as soon as possible) |
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IV Induction agents (hypnotics)
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-Isopropylphenol: propofol
-Barbiturates: Thiopental -Carboxylated imidazole: Etomidate -Phenycyclidine: Ketamine, the strange actor -Benzodiazapines: Diazepan, common sedative |
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What would the ideal IV drug be like?
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Easy to use, water soluble, long shelf life, small volume (10-20cc), onset in one arm brain circulation time, inactivated by rapid metabolism to inactive metabolites, no side effects, and real cheap. Sadly, this does not exist. The ones we have today fall short in various respects.
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What would happen if you dosed an IV anesthetic the same way an inhaled agent?
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Not a good idea, done originally and killed many patients
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Redistribution of IV anesthetic
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Plays a major role, metabolism and elimination generally play a minor role, unless large doses are used for long durations
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Context sensitive half time
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The time it takes for the concentration of the drug to fall to half in the central compartment after various infusion times. Half time of the drug will depend on the context in which it is given. Prolonged administration of drug saturates redistribution sites.
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Metabolism and elimination
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Liver metabolism and Renal elimination
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Mechanism of action (IV anesthetic)
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-Interaction with GABAa receptor (Barbs, benzos, propofol)
-some have mixed actions, ex. NMDA receptor antag Ketamine |
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Induction doses
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Recommendations are weight based, and based on healthy patients, so considerations should be taken for sicker patients
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Physiological effects
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-Cardiovascular effects: usually little to no effect, but ketamine is the strange actor as it kicks out stored endogenous catecholamines and so increases cardiac effects
-Respiratory effects: most result in respiratory depression, ketamine no effect -CNS effects: decreased cerebral blood flow and decreased oxygen requirements, lower metabolic rate, and ketamine does the opposite (terrible idea for trauma patients) -EEG changes: awake is high freq low ampl, anesthesia will make it look like they're brain dead -seizure activity: most have anti seizure activity, ketamine will cause seizures, important for shock therapy -obstetrics: thiopentol is used, works well with no fetal effect, for emergency c-section need anesthesia |
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Misc effects
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-thiopental: contraindicated in acute intermittent porphyria, histamine release, slight increase in blood glucose
-methohexital: hiccups, twitching -etomidate: painful injection, suppression of adrenal function -propofol: opisthotonos, pain on injection -ketamine: nystagmus, mydriasis, emergence rxns, salivation (foaming at the mouth) -midazolam: anterograde amnesia -diazepam: pain on injection |
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Propofol, special consideration
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-supports bacterial growth, studies have shown, patients can potentially get septic and die.
-it was expensive when it came out, so ppl tried to save it, now they have bacteriostatic treatments -Fospropofol, water soluble pro-drug, lag b/w bolus and clinical effect, may have increased safety for non-anesthesiologists |
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Etomidate, special considerations
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-useful for its hemodynamic stability
-some adrenal suppression |
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Ketamine, special consideration
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-strange actor, pts will almost look like they're awake, has profound analgesic effects
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Dexmedetomidine
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Induces a sleep-like state, patient is arousable, acts as alpha-2 AR agonist, has some cardiac protective effects
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Pharmacodynamics of propofol
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Rapid acting hypnotic agent, CNS effects primarily thru GABAa receptorm enhances chloride conductance causing hyperpolarization, also inhibits glutamate action at NMDA receptors
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Chemistry of Propofol
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insoluble in water, 1% emulsion in interlipid, discard after 6hrs after opned
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CNS and propofol
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Probably neuroprotective, vasoconstriction decreases cerebral blood flow and ICP, has anti convulsive properties
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Unique effects of propofol
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Sedative effects at low doses, effective at reducing airway reflexes, small dose has antiemetic effect (good for chemo pts.)
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Reparatory effects of propofol
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Dose dependent decrease in ventilatory drive, dec tidal volume, minute vent, and increased PaCO2, at induction doses apnea occurs for a few minutes (this is how people die on propofol)
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Cardiovascular system effects of propofol
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Decreases systemic BP, myocardial depressant effect, blunts barostatic effect, reduced venous and arterial systemic vascular resistance (preload and afterload), exaggerated in older pts. with CVD
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Adverse effects of propofol
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Pain on injection, no superior technique, ?lidocaine with tourniquet?
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Allergies with propofol
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Does not cause histamine release, no egg albumin or soy protein, allergic rxn is unlikely and rarely seen in practice
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Pharmacokinetics of propofol
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Very lipid soluble, rapid onset of effect under 1 minute, and rapid redistribution, 3-8 mins
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Clinical uses of propofol - induction of anesthesia
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Most common induction agent, dose must be tailored to patient, on emergence patients achieve recovery milestones quickly with less hangover and elevated mood, occasional euphoria (abuse potential? almost always used for going to sleep actaully)
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Propofol, using it to maintain anesthesia
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Can be used to maintain anesthesia as an infusion, part of TIVA, context sensitive half time makes this attractive. In malignant hyperthermia pts. this is an excellent option.
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Sedation with propofol
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Can be titrated for sedation, but it becomes very easy to stack the dose and get into trouble, very easy to overshoot. Long term administration linked to propofol infusion syndrome, a rhabdomyolysis, metabolic acidosis, cardiac and renal failure, then fatal
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Levels of sedation and effects
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-Minimal (anxiolysis)
-Moderate/analgesia -Deep -General ***You should be able to rescue the pt. from the next level of sedation |
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Target controlled infusion of propfol
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PK/PD monitored administration, computer controlled pump to maintain targeted effect site concentration
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BiS machine
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Monitors EEG channels, 0=no brain activity and 100=awake state, the goal for general anesthesia is 40-60, a reading takes about 20 seconds. This could be great in conjunction with the computer controlled administration.
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Where do we want to be on the dose response curve?
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We want to be where the smallest amount of drug gives us the biggest effect, it allows us the most control. It is of course a double edged sword, most control = easy to go wrong. It is important to monitor closely and possibly use more forgiving agents.
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The SedaSYS system
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First computer assisted sedation system, monitors and administers anesthesia. It will probably prevent stacking of doses.
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