General Anesthetics Flashcards
(35 cards)
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
- 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)
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
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
