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Neuro Drugs > General Anesthetics > Flashcards

General Anesthetics Flashcards

1
Q

Balanced anesthesia

A

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)

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2
Q

Monitored anesthesia care

A

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)
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3
Q

Conscious sedation

A
  • nonanesthesiologists
  • 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)
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4
Q

Deep sedation

A

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
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5
Q

ICU sedation

A

Pts require mechanical ventilation for prolonged periods

-sedative hypnotic drugs and low doses of IV anesthetics

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6
Q

Where is the primary focus of anesthetic in neurons?

A

The synapse

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7
Q

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

A
  • strengthening inhibitor or diminishing excitation w/in CNS

- excitatory transmission is impaired more strongly than inhibitor effects are potentiated

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8
Q

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

A

Cl- (GABAa and glycine rcs)

K+ channels (K2P, Kv, KATP channels)

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9
Q

What are the excitation ion channel targets?

A

NAChRs and M

  • EAA (AMPA, kainite, NMDA Rcs)
  • 5HT2 and 3 Rcs
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10
Q

Describe volatile anesthetics

A

Halothane, enflurane, isoflurane, desflurane, sevoflurance

-low Vapor pressure; high boiling pt = liquid at rt

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11
Q

Describe gaseous anesthetics

A

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

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12
Q

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

A

(1) uptake form alveoli inot the the blood and distribution

2) partitioning into the effect compartments (CNS

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13
Q

What is the driving force for uptake of inhaled anesthetics?

A

Alveolar concentration

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14
Q

What determines how quickly the alveolar concentration changes?

A

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

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15
Q

Partial pressure in the alveoli is expressed as..

A 
Alveolar concentration (FA)/ inspired concentration (FI) 
-faster the ratio approaches 1, the faster anesthesia will occur during an inhaled induction
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16
Q

Define blood: gas coefficient

A
17
Q

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

A

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
18
Q

Describe the brain: blood coefficient

A

All agents are more soluble in the brain than the blood

19
Q

What are the factors that control uptake of inhaled anesthetics?

A

Solubility, Cardiac output, alveolar-venous partial pressure difference

20
Q

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

A

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)

21
Q

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

A

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

22
Q

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

A

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

23
Q

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

A

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)

24
Q

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

A

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

25
Q

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

A

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)

26
Q

Elimination of inhaled anesthetics

A

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

27
Q

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

A

Lungs

-some agents are metabolized by the liver

28
Q

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

A

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

29
Q

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

A

Recovery is slow after prolonged administration of halothane or isolflurane

30
Q

Inhaled anesthetics: describe MAC (minimal alveolar concentration)

A

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

31
Q

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

A

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)

32
Q

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

A

(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

33
Q

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

A

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

34
Q

What effect does Inhaled anesthetics have on CV system?

A

Inhaled voliti

35
Q

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

A

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

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