Flashcards in Inhalation Anesthetics Deck (63):
Two major measurable effects of inhaled anesthetics (for research purposes)
1. Immobility in response to surgical stim
2. amnesia to intraop events
minimum alveolar concentration of anesthetic required to inhibit movement on surgical incision in 50% of patients
mech of action of immobility for NO
activates descending noraderenergic pathways from periaquaductal gray matter in brainstem
- these pathways inhibit nociceptive input to DH of spinal cord
MOA of amnestic effects of inhaled anesthetics
involves amygdala, hippocampus, cortex (most likely)...
MOA of CNS depression of inhaled anesthetics
1. Enhance function of inhibitory ion channels (= hyperpolarization via Cl or K+ mediated GabaA and glycine receptors)
2. Block function of excitatory ion channels (prevents depolarization, prevents positive charge ions via NMDA or Na channels)
State of NO at room temp? other inhaled anesthetics?
NO = gas
inhaled anesthetics = liquid at room temp
What anesthetics cause nephrotoxicity after prolonged anesthesia?
methoxyflurane --> inorganic floride
Sevoflorane/Halothane --> Compound A
How can you prevent nephrotoxicity with Sevoflorane?
Limit low fresh gas flow (<2L/min) to less than 2 MAC hours of Sevoflorane
How do you avoid carbon dioxide absorbent reaction w/ inhaled anesthetics? Which anesthetic is usually the culprit?
Sevoflorane causes most exothermic rxns
1. maintain adequate hydration in CO2 absorbent
2. change regularly
3. turn fresh gas flow down/off on unattended machines
4. limited fresh gas flow during anesthesia
5. change absorbant when in doubt
How can you measure the RELATIVE potency of inhaled anesthetics?
MAC = minimum alveolar concentration of anesthetic required to prevent movement on surgical incision in 50% of patients
Describe the response curve of MAC re movement on surgical incision
SD of MAC is 10%
50% not move with 1 MAC
95% not move with 1.2 MAC
99% not move with 1.3 MAC
Which variables do NOT affect MAC
duration of anesthesia
Factors that INCREASE MAC (5 min.)
1. Drugs (amphetamine, cocaine, ephedrine, chronic EtOH)
2. Age (highest 6 mo)
3. Electrolytes (hypernatremia)
5. Red Hair
Factors that Decrease MAC?
2. Age (Elderly)
3. Electrolytes (Hyponatremia)
Drugs that DECREASE MAC?
1. IV anesthetics (propofol, etomidate, ketamine, dexmedetomidine)
3. Ethanol (acute use)
4. Local anesthetics
6. amphetamines (chronic use)
MAC of Isoflorane
MAC of Halothane
MAC of Desflurane
MAC of Sevoflorane
MAC of nitrous oxide
Blood gas coefficent of inhaled anesthetics (smallest to largest)
Factors that effect transfer of anesthetic from machine to alveoli
Pi (inspired partial pressure)
breathing system characteristics (absorb into plastic, etc)
Factors effecting transfer from alveoli into blood
BG partition coefficient
alveolar-venous partial pressure difference
Factors effecting transfer anesthetic from blood to brain
Blood-brain partition coefficient
Cerebral blood flow
art-vein partial pressure difference
High Pi----> help or hurt increase in Palv
Neccessary to have high PI initially to ofset uptake into blood
accellerates induction of anesthesia
How should you change Pi as time increases at induction
Need to decrease Pi to match decreasing uptake to maintain a constant/optimal Pbr
If PI maintained constant, PA would progressively increase
What is the second gas effect?
ability of large volume gas uptake of one gas (first gas) to accelerate the rate of increase of the PA of a concurrent administered gas (second gas) = 2nd gas effect
Example: initial large vol uptake of NO accelerates uptake of companian gasses (volatile anesthetics and oxygen). PaO2 increases by about 10%
How does the second gas effect work?
increased flow of both gasses
concentration of the second gas in a smaller lung volume=concentrating effect
How does alveolar ventilation effect PA?
increased Va (hyperventilate) = more rapid rate of increase of PA and more rapid induction
hypoventilation = decreased rate and slower induction
How does hyperventilation and controlled ventilation increase induction speed? What should you do about it?
1. Increase Va (ventilation)
2. Decrease venous return by hypervent = slow CO = decreased uptake into blood (quicker rise of PA)
this can result in overdose--> LESSON- decrease PI when switching from spontaneous to controlled ventilation to adjust for this change
Higher = more soluble, large amount of inhaled anesthetic needs to be dissolved before blood/alvoli are in equilibrium = LONGER ONSET
Lower= less soluble, less amount needed for equilirium =QUICKER ONSET
Brain-blood coefficients are measured how?
in a time constant....complete equilibriation of any tissue with Pa = 3x time constants
Brain-blood coefficient of isoflurane? total equilibriation?
total time = ~10-15 min (x3 time coefficient)
Are des/sevoflurane and NO more or less soluble in brain than iso?
less soluble = 2 min time coefficient (6 min total equilibriation)
Which anesthetic interacts with methionine synthase?
What does it do and why do we care?
methionine synthase regulates B12 and folate metabolism...decrease can increase homocysteine and increase risk of vascular/cardiac disease/sequela
Why is it important not to give NO to someone with a pneumo?
NO blood gas coefficient 34x greater than nitrogen (main component of normal ambient air)
Causes increased volume of distensible air space or pressure of non-distensible air space.
75% NO doubles pneumothorax volume in 10 min
Closed ptx is a contraindication to NO
How does CO affect induction speed?
Low CO = less uptake = faster induction (pts in shock = quicker induction)
Faster CO (fear) = more uptake = slower induction
How do shunts affect induction speed?
R->L cardiac shunt slows induction speed (dilutional effect of shunted blood with no anesthetic)
L->R cardiac shunt (AV fistula, etc) offsets dilutional component of R to L.
How does dead-space (wasted ventilation) effect induction speed?
It doesn't effect it.
Principle effect is production of difference between PA and Pa of anesthetic (similar to difference between observed end tidal PCO2 and PaCo2).
What is the importance of the PA-PV ratio?
reflects tissue uptake of inhaled anesthetics
tissues with more blood flow equilibriate rapidly with Pa
3x time constant = Pv = PA for anesthetic (PI and PA difference narrows)....decrease PI at this time to maintain a constant PA
How does anesthesia recovery differ from anesthesia induction?
1. absence of a concentration effect (PI cannot be less than zero)
2. variable tissue concentrations at start of recovery
3. metabolism effect on rate of decrease in PA
Does time of exposure to anesthetics matter more if it is a soluble or non-soluble anesthestic?
soluble= will take longer to unload high tissue concentrations (i.e. isoflurane)
Which anesthetics does metabolism matter for?
Define context sensitive half time
the dependency of elimination of inhaled anesthetics on 1. length of administration ("context")
2. solubility of inhaled anesthetics in blood/tissue
Define diffusion hypoxia
hypoxia that occurs after NO administration in patients given fresh gas (but no oxygen)
NO takes up so much of alveolar space at discontinuation that PAO2 dilutes to the point of PaO2 decreasing
GIVE PTS O2 AFTER NO
Effect of inhaled anesthesia on MAP
major changes that cause this?
sevo/des/isoflurane = (dec SVR > dec CO)
halothane = dec CO > dec SVR
How can you minimize MAP effects of inhaled anesthetics?
Co-administer NO (increase MAP)
HR effect of iso/des/sevoflurane?
Which anesthetics have greatest effect?
Isoflurane (0.25 MAC) >> Desflurane (1 MAC) > Sevoflurane (1.5 MAC)
How can you attenuate HR effects of desflurane?
b blocker, opioids, time
NOT nitrous oxide
Does a rapid or slow increase in desflurane have greater circulatory effects?
Faster change = bigger change
slow the rate of increase, attenuate with opioids/b-blockers
similar effect not seen with other anesthetics
Inhaled anesthetics that effect cardiac contractility?
Halothane (induction alone in children, or + NO in adults)
sevoflurane (1 MAC in adults)
INhaled anesthetic that can predispose to dysrhythmia?
what increases this risk?
increased with catecholamines, hypercarbia
Which anesthetic increases QTc? What should you do to prevent issues?
Give B blocker
How do inhaled anesthetics effect ventilation?
Increase RR, decrease Vt = maintain minute ventilation (with more dead space)
inefficient ventilation = increase PaCO2
What happens to PaCO2 responsiveness?
Blunted, resulting in apnea
Effect of inhaled anesthetics on airway resistance
- bronchodilate (mostly when bronchoconstriction already present)...minimal effect clinically in normal airway
Not the case with NO
Whcih anesthetic has modestly increased airway resistance in smokers?
Which anesthetics would you pick for inhalation induction? Why?
Halothane or Sevoflurane = smell nice and aren't irritating to airway
Do inhaled anesthetics effect cerebral vascular responsiveness to PaCO2?
NO effect on cerebral blood flow and CMRO2?
- increased CBF, increase CMRO2 (small)
CBF/CMRO2 effect of halothane/isoflurane/sevoflurane/desflurane?
CBF- increase (if MAC > 0.6)
1 MAC CBF predominantes
ICP effect of inhaled anesthetic
increase with all anesthetic > 1 MAC