Test 3: General Principles of Inhaled Anesthetics (pt 2) Flashcards
What is Stage 1 of Anesthesia?
Analgesia.
-Patient is conscious and rational
-Perception of pain is diminished
-Ex: Monitored anesthesia care (MAC) cases
-Patient may drift off, but should come back easily.
What is Stage 2 of Anesthesia?
Delirium/Agitation.
-Patient is unconscious, but body responds reflexively and irrationally to stimuli.
-Usually fast with induction but longer with emergence
-Patients may hold their breath, but airway reflexes are intact, pupils are dilated, eyes are not conjugated.
-Don’t extubate during this
What is Stage 3 of Anesthesia?
Surgical Plane of Anesthesia
-Increasing degrees of muscle relaxation
-Loss of pharyngeal reflexes (patient is unable to protect airway)
-HR and RR slow -> Apnea
What is Stage 4 of Anesthesia?
Medullary Depression (vasomotor center in the medulla and respiratory center in the brainstem)
-Cardiovascular and Respiratory collapse
-Can lead to death
What is the Ventilation Effect?
The faster and more deeply a patient breathes or is ventilated, the faster the patient loses consciousness at the start of anesthesia and emerges at the end.
-INH agents move down a concentration gradient
-Anesthetic uptake slows throughout the procedure as the tissue compartments become saturated (gradient changes)
Increasing minute ventilation (RR and Tidal Volume) will do what to the onset/offset of anesthetic effects?
The faster and deeper a patient breathes: (can increase minute ventilation: RR and VT)
-Speeds the onset/offset of anesthetic effects
-Speeds induction
-Speeds emergence
How are gases eliminated?
They are ventilated out.
How does poor lung function or V/Q mismatch affect INH agents?
-Prolonged onset and emergence.
-Rapid-acting (low blood/gas solubility) agents are affected by these deficits to a greater extent than are slower-acting (high blood/gas solubility) drugs.
-These decreases in speed can be partially compensated for by increasing the concentration of insoluble (fast) agents or increasing ventilation with soluble (slow) drugs.
What populations have poor lung function or V/Q mismatch that will prolong onset/emergence?
-COPD, Pulmonary Fibrosis, Kyphosis, Obesity/pregnancy
What is the Concentration Effect?
During the first minutes of gas administration, a higher concentration of the drug than necessary for maintenance (above MAC), or a loading dose, is delivered to speed initial uptake. This is commonly referred to as overpressuring or the concentration effect.
-Beware of side effects (hypotension)
-Works better with slower agents and not as good with faster acting agents.
How does concentration of an INH agent affect the onset of action?
Higher concentration = faster onset of action.
How do you calculate FA (Alveoli Fractional %)?
Ex: 10% agent and 90% O2. 50% of agent flows down conc gradient into the blood. Left with 5% agent and 90% O2. 5/95 = 5.3% in the alveoli. This is how you arrive at FA (Alveoli fractional %). Agent present in the alveoli.
What is the Second Gas Effect?
Simultaneous administration of a relatively slow agent such as isoflurane and a faster drug such as nitrous oxide (in high concentrations) can speed the onset of the slower agent. This is known as the second-gas effect.
-Increases uptake on the Alveolar Side. Fills alveoli, pushing the slow agent across.
-N2O acts as a carrier, pulling the slower agent in and moving it faster.
-MOA is unknown
-Works well with a slower agent, but has less of an effect on a faster agent.
-Can be used during emergence also to rapidly eliminate volatile agents by eliminating N2O
How does increases in CO affect the onset of action of INH agents?
The higher the CO, the faster the INH agent is carried away from the lungs.
-Slows the rise of the brain and the lung concentration
Katzung:
An increase in pulmonary blood flow (ie, increased cardiac output) will increase the uptake of anesthetic, thereby slowing the rate by which FA/FI rises and decreasing the rate of induction of anesthesia. The increased uptake of anesthetic into the blood caused by increased cardiac output will be distributed to all tissues. Since cerebral blood flow is well regulated and maintained relatively constant at clinical anesthetic concentrations, the increased anesthesia uptake caused by increased cardiac output will predominantly be distributed to tissues that are not involved in the site of action of the anesthetic.
The majority of blood/agent leaving the lungs is normally distributed where?
To the Vessel Rich Group (VRG)
-Heart, liver, kidneys, brain
-10% of body weight, but gets 75% of CO.
-Also called the Central Compartment.
The longer the anesthetic is delivered, the greater the perfusion to all body parts
Where does Nitrous Oxide diffuse to?
Air containing cavities in the body.
-Normally these cavities are rich in Nitrogen, which is 34 times less soluble than N2O.
-If the space is expandable, it will increase in volume.
What are examples of expandable air cavities to avoid N2O with?
-air embolism
-pneumothorax
-acute intestinal obstruction
-intraocular air bubbles produced by sulfur hexafluoride gas injection,
-pneumoperitoneum
Avoid in trauma situations.
What equipment is air filled and could expand during N2O anesthesia?
-ETT cuff
-LMA cuff
-Pulmonary Artery Catheter balloon
What will occur in rigid air-containing spaces with N2O Diffusion?
Rigid air-containing spaces will undergo an increase in pressure.
-This includes tympanic membrane grafting after tympanomastoid procedures and intracranial air during diagnostic or surgical intracranial procedures.
75% Nitrous Oxide will do what with a Pneumothorax?
Double it in 10 min
Triple it in 30 min
Rate of induction is faster in adults or children?
Children go to sleep faster than adults
-Uptake is faster (The child’s higher alveolar ventilation specifically related to their increased respiratory rate accounts for this effect.)
-INH agents are less blood soluble in children (they want to go into the tissues)
How does MAC Change with Neonates and Infants?
-Neonates: Decreased MAC (first 28 days of life)
-Infants aged 6 months have a MAC 1.5-1.8 times higher than a 40 year old.
How does emergence differ in pediatrics?
-Reactions and agitation can occur.
-Robust stage 2 phase that can persist even through stage 1 (delirious/agitated
-Risk factors: preschool age 2-5 years, separation anxiety, and post-op pain.
-Tx with propofol, Fentanyl, Ketamine, or Precedex. Remove stimulating things.
How does Obesity affect the uptake of INH agents?
NO Clinical effect on uptake.
-Longer procedures = inc deposition of anesthetics into fat and may prolong recovery.
-Higher fat stores. After >4 hr procedures, gases are really saturating fat compartment. Wakeup/emergence is prolonged. Gases hang on tightly and don’t want to come off (especially Iso)
