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Flashcards in General Anesthetics Deck (35):

Balanced anesthesia

Combo of Intravenous drugs and inhale drugs
-use favorable properties of each agen while minimizing their adverse effects
(Gen anesthetics + NM blocking agents, local anesth, and analgesics)


Monitored anesthesia care

Sedation -based
-diagnostic and/or minor therapeutic surgical procedures
-w/out gen anesthesia
-midazolam (premed): anxiolytics, amnesia and mild sedation
-titrated propofol infusion: moderate to deep levels of sedation
-added potent opioids analgesia or ketamine (min discomfort)


Conscious sedation

-pt retains ability to maintain patent airway; responsive to verbal commands
-BDZ and opioid analgesics (fentanyl) in conscious sedation protocols have adv of being rev by specific Rc antagonist drugs (flumazenil and naloxone, resp)


Deep sedation

Light state of gen (IV) anesthesia (decreased consciousness from which put not easily aroused)
-loss of protective reflexes; inability to maintain patent airway; lack of verbal responsiveness to surgical stimuli
-IV agents: sedative hypnotics (propofol and midazolam) sometime in combo w/ opioids analgesics or ketamine


ICU sedation

Pts require mechanical ventilation for prolonged periods
-sedative hypnotic drugs and low doses of IV anesthetics


Where is the primary focus of anesthetic in neurons?

The synapse


At the organ level, what does the effect of anesthetics result from?

-strengthening inhibitor or diminishing excitation w/in CNS
-excitatory transmission is impaired more strongly than inhibitor effects are potentiated


What are the primary inhibitory ion channels that are considers candidates of action?

Cl- (GABAa and glycine rcs)
K+ channels (K2P, Kv, KATP channels)


What are the excitation ion channel targets?

NAChRs and M
-EAA (AMPA, kainite, NMDA Rcs)
-5HT2 and 3 Rcs


Describe volatile anesthetics

Halothane, enflurane, isoflurane, desflurane, sevoflurance
-low Vapor pressure; high boiling pt = liquid at rt


Describe gaseous anesthetics

Nitrous oxide
-high vapor pressures and low boiling points
Gas at RT


What are the keys to determining the kinetics of the inhaled anesth?

(1) uptake form alveoli inot the the blood and distribution
(2) partitioning into the effect compartments (CNS)


What is the driving force for uptake of inhaled anesthetics?

Alveolar concentration


What determines how quickly the alveolar concentration changes?

(1) inspired concentration (partial pressure)
(2) alveolar ventilation
(Increases I either will increase the rate of rise in the alveoli and will accelerate induction


Partial pressure in the alveoli is expressed as..

Alveolar concentration (FA)/ inspired concentration (FI)
-faster the ratio approaches 1, the faster anesthesia will occur during an inhaled induction


Define blood: gas coefficient

Refines the relative affinity of an anesthetic for the blood compared with that of inspired gas (blood solubility)


Describe the relationship between the coeffiecent values (blood solubility) and rate of anesthesia onset

Inverse relationship between coefficient values and rate of anest onset
-agents with low blood sol (nitrous oxide, desflurane) reach high arterial pressure rapidly --> rapid equil w/ brain and fast onset
-high blood sol (halothane)--> slow onset


Describe the brain: blood coefficient

All agents are more soluble in the brain than the blood


What are the factors that control uptake of inhaled anesthetics?

Solubility, Cardiac output, alveolar-venous partial pressure difference


What is the effect of increased pulmonary blood (CO) have on uptake of inhaled anesthetics?

Increase the uptake of anesthetic and decrease rate by which by which FA/FI rises -> decrease rate of induction of anesthesia (FA decreases bc increased pulmonary blood flow dilutes the drug in alveoli)


What effect will an increase in CO and pulomanry blood flow have on uptake of inhaled anesth in blood?

Increase uptake into blood; distributed and disturbed into all tissues. (Not just CNS)
--> slower rise is partial pressure in the blood dye to a greater volume of distribution


What I s the anesthetic partial pressure difference between alveolar and mixed venous blood dependent on?

Uptake of the anesthetic by tissues (including non-neuronal tissues)


What is the effect of a slower rate and extent of tissue uptake of inhaled anest?

Greater the difference in anesthetic gas tensions between arterial and venous blood --> more time to achieve equilibrium with brain tissue
Note: anesthetics must be carried from the tissues to the lungs for primary elimination, Larger A-V concentration differences means less drugs are returning for elimination (increase awakening time)


What effect does the increase in rate and depth of ventilation has on the concentrations of inhaled anesthetics in the blood?

Increase concentrations in blood
-depression of respiration slows onset of anesthesia of inhaled anesthetics if ventilation is not manually or mechanically assisted


What does increasing pulmonary blood flow (CO) do to the rate of increase in arterial concentration of inhaled anesthetics?

Slows the rate of increase bc a larger volume of blood is exposed to the anesthetic
-blood capacity increases and the anesthetic concentration rises slowly (reverse is true)


Elimination of inhaled anesthetics

Those that are insol in blood and brain are eliminated at faster rates than more soluble anesthetics


What is the major route of elimination from the body of inhaled anesthetics?

-some agents are metabolized by the liver


What is the effect of duration of exposure to inhaled anesthetics on the recovery time?

Accumulation of anesthetics in muscle, skin, and fat increases w/ prolonged exposed (esp in obese Pts), and blood tension may decline slowly during recovers as the agent is slowly eliminated from these tissues


What is the exception to the idea that recovery may be rapid with more soluble inhaled anesth following a short period of exposure?

Recovery is slow after prolonged administration of halothane or isolflurane


Inhaled anesthetics: describe MAC (minimal alveolar concentration)

Describes anesthetic potency; concentration of inhaled anesthetics that prevents movement in response to surgical stimulation in 50% of subjects (measure of potency ED50)


What dose a MAC value of greater than 100% indicate?

Even if 100% of the inspired air at barometric pressure is the anesthetic, the MAC would still be less than 1 and other agents must be supplements to achieve full surgical anesthesia (i.e. Nitrous oxide)


What are the four stages of increasing depth of CNS depression?

(1) stage of analgesia: both analgesia and amnesia are produced at the end of stage 1
(2) stage of excitement: delirious, irregular respiration, reg breathing at end of stage
(3) stage of surgical anesthesia: reg breathing---> apnea
(4) stage of medullary depression: severe depression of the gasometer center in the medulla as well as respiratory center


What is a reliable indication that stage III has been achieved in increasing CNS depression (Inhaled anesthetics )?

Loss of responsiveness to painful stimuli (trap muscle squeeze) and the reestablishment of regular breathing


What effect does Inhaled anesthetics have on CV system?

Inhaled voliti


What are the component changes in behavior or perception involved in the anesthetic state?

Unconsciousness, amnesia, analgesia, attenuation of autonomic reflexes to noxious stimulation, immobility in response to noxious stimulation (sk m relaxation)
-none of the currently available agents when used alone can achieve all five desired effects