Inhaled Flashcards
what is mAC
The concentration that will produce the absence of movement in 50% in response(Movement) to a noxious stimulus
For or the Volatile anesthetic, what is the Effect site
The Brain and spinal cord
What determines the reservoir size and the alveolar conc,?
solubility
Determines how the anesthetic will partition itself between the blood phase and air phase when equilibrium is reached
what is Equillibruim in VA
state of equal partial pressures NOT concentration
How does solubility affect onset and emergence
The lower sol the faster the onset and the shorter the duration. context-sensitive halftime comes in here….the lower solubility will have a quicker wake-up and quicker time to get out of the system.
what will be the impact of low hct on the onset of VA
The clinical impact of a lower HCT a faster induction. Remember lower solubility results in more agent in gas phase than blood phase. This results in faster uptake.
what are the 2 factors that need to equilibrate for induction to happen?
Alveola concentration and set inspired conc
How can we tell the brain conc
expired conc will reflect what the brain conc is.
how do we control the inspired conc
by the machine setting
what are the parameters we use to determine conc of a VA
Atmospheric pressure
The vapor pressure of the agent
What factors of the breathing circuit affects the rise in FA
Volume of tubing
Solubility of tubing
Flow rate of gas in the machine
What do we use PA(Pressure in the alveoli) to estimate
Depth of anesthetic
Recovery from Anesthetic
Potency of anesthetic
How do we over the volume in the breathing circuit that mat uptake the anesthetic
Increase the conc at induction and reduce it after equilibration
How does RR affect induction
High rate fast induction
Low rate slow induction
How does FR affect induction between adults and kids
Adult FRC larger, slow induction
Kids FrC smaller,fast induction
whats the optimal factors between alveoli ventilation and FRC
Increase Ventilation
SMall FRC
which of the agents equilibrate faster between FA/FI
least soluble agents
Explain what the parts of the FA/FI curves represent?
The steep rise represents the least soluble agents’ initial rise.
First knee rep the Vessel rich group uptake
2nd knee rep the muscle rich group uptake, which is about 4-8mins after induction
Long-tail represent the fat group uptake
Initial steep rise: a-v difference = 0 as no agent occupies the alveoli –>no uptake
The difference in curves of the low soluble and high soluble are?
Low soluble have a steep curve
High soluble have a flat curve
The highest ratio of FA/FI can go is?
1
what makes nitrous equilibrate faster than the DES
Concentration effect
The degree to which alveolar concentration is decreased depends on what?
% of uptake into blood and tissue
Uptake of the Volatile Anesthetic into the blood is determined by
- The solubility of the agent…Higher solubility..higher uptake
- Cardiac Output…Higher CO__higher Uptake/ less induction
- A-v (Alveolar to venous) pressure differences
How can we overcome the impact of tissue uptake and the effects of high solubility on induction and maintenance
Impact of uptake can be overcome by Overpressure….giving an initial high conc
To overcome the effects of high solubility you can give a higher maintenance dose.
How does solubility impact Emergence
The lower the B/G solubility coefficient, the shorter time emergence will take
Higher solubility- slower time to awaken (emergence)
Between the most soluble agents and the higher soluble agent which agent do we need to turn off first upon emergence
The most soluble agents need to be off first
how does CO affect induction
…dec co…induction up
Inc co…induction down(gives greater opportunity for soluble agents to go into reservoir)
what’s the rationale of how inc CO slow induction
by carrying away either more or less anesthetic from the alveoli. Increased CO means more blood is exposed to VA= more is dissolved in blood if it is a soluble agent and this will increase the time to induction or equilibration (Pa=PA=PBr).
what’s the rationale for how dec co speed up induction
A decreased CO speeds induction because there is less uptake to oppose input. Not really an issue with a poorly soluble anesthetic. Because the induction is rapid regardless
Does cardiac output have negative or positive feedback, explain
positive feedback,
because of the lower the cardiac output the faster the induction, which in turn depresses cardiac output more and drives the depth of induction even deeper.
does CO affect high soluble or low soluble anesthetic most
High soluble
In what situation will the alveolar conc be equal to the arterial conc
If there are no ventilation-perfusion abnormalities
what does the a-v difference indicate
Uptake of anesthetics by the tissue
what is time constant
amount of anesthetic that can be dissolved in the tissue /tissue blood flow
in relation to time constant how long do we need for an anesthetic to equilibrate
For volatile agent equilibration between the Pa and the Pbr it will depend on the anesthetic’s blood gas solubility and requires 5-15 minutes (3-time constants
what is 1 time constant and 3 time constant
63 and 95% respectively
How long would fat equilibration take
Fat has an enormous capacity to hold anesthetics combined with low blood flow can take 24-48 hours before their equilibration with the fat.
Name the 4 tissue groups, the mass distribution, and Co distribution
VRG—9% mass,75% Co (Brain ,liver ,kidney,lungs)
MRG__50% mass,18% blood flow
Fat rich group—-19% mass,7% Co
Vessel poor group–22% mass,none to minute blood flow.
what are the components of the alveolar tension curve
B/G Solubility will influence knee height
Tissue/Gas solubility influences tail
why does the anesthetic pressure curves for muscle and fat rise and fall more slowly
The anesthetic partial pressures in both muscle(red line)and fat(orange line)rise and fall much more slowly, because muscle and fat compartments represent much larger effective volumes (see Fig. 20.2) and have lower blood flow than the vessel-rich group.
why does the anesthetic pressure in fat continues to rise after anesthetic delivery stops
as long as partial pressure in alveolar gas (and arterial blood) is greater than that in the fat compartment.
when do vessel rich group and muscle rich group equilibrate
Vrg equilibrates in 5-10min
MRG equilibrates in 5-15mins
when should we start bringing down the overpressure of VA, that is the Fi
at 1-1.3Mac
The FI will need to be decreased with time as the VRG equilibrates (in 5-10 min) and further decreases when MRG equilibrates in 5-15mins
The effects of increasing ventilation are most visible with highly soluble or less soluble VA?
Highly soluble
Why does increasing FA in less soluble anesthetic will not make that much of an effect?
: N20 -low solubility -FA rises rapidly to FI even at alveolar ventilation 2L/min–> FA/FI curve not capable of further rise no matter what the ventilation inc is.
Increasing ventilation or resp rate, will this result in a negative or positive feedback effect? in spontaneously ventilating patients
Negative feedback effects
In SPONTANEOUSLY ventilating patient- as % inspired inc, ventilation is depressed and FA/FI decreases (the FA does not rise because the patient is not ventilating well)
Protective against overdose
How can the breathing circuit affect PA and how do we overcome it?
- Volume of circuit (decreases rate of rise FA/FI – overcome with high flow rates at induction >5L/min
- Plastic/rubber components can absorb anesthetic (slow induction) and then re-introduce anesthetic into the circuit during wash-out (slow emergence)
How do the Alveola ventilation and FRC ratio affect induction and whats the optimal setting
The greater the alveolar ventilation/FRC ratio = faster the induction (neonates induction very fast ratio = 5:1)
Decrease FRC and Increase Alveolar ventilation= Faster induction
2x increase in co what will be the effect on uptake
this will decrease uptake, hence faster induction
Increase vent 2x and increase co 2x will have what effect on Fa/Fi and in what conditions might this happen
Increase Fa/fi and faster induction, anything that increases metabolism, fever.
what are examples of Ventilation/perfusion Abnormalities
EX: COPD, bronchial intubation, single-lung, PE, surgical retraction, vasodilators
Right to Left shunt… example - Main Stem Intubation- one lung ventilated, both perfused
What effects does a right to left shunt have on VA
Right to left shunts have the diluting effect of the shunted blood on the partial pressure of anesthetic in the blood combined with blood coming from ventilated alveoli will decrease the Pa and slow the induction of anesthesia.
Which group of anesthetic does right to left shunt have the most effects
less soluble group
. In this case, a right to left shunt actually slow induction more for a less soluble agent compared with a soluble one. This happens because uptake of a soluble anesthetic offsets dilutional effects of shunted blood on the Pa
If a patient has a right to left shunt which group of anesthetics should be used
More soluble group to offset the dilutional effect of The shunt
whats concentration effects and what can cause this
Results when a large volume of gas is absorbed–> 2 results:
remaining residual gas in lung is concentrated as volume decreases
inspired ventilation increases which adds more anesthetic (the negative pressure created by the uptake draws more gas into the lung)
For agents with a high concentration which is Nitrous
Body has no nitrous…creates a large gradient,the drive takes a huge vol,vol deficit left and whats left behind is conc albeit lower volume.
whats the second gas effects
Occurs when N2O is used in combination with a second gas
Reduction in volume and replacement of N2O–> increases concentration and amount of any gas given concomitantly with the N2O which was absorbed in a large volume.
The increase FA of a second gas is greater @ 70% N2O than 50% N2O…(speed induction will happen)
The FA of a gas increase more rapidly when N2O given as 2nd gas than when given alone
The higher the concentration of nitrous, the higher the effect of 2nd gas due to the conc of the small vol by 2nd gas after nitrous is pulled out. And also increase in the tracheal inflow.
The CONCENTRATION EFFECT is due to 2 factors:
Decreased remaining gas due to uptake
The inspiration of anesthetic on the next breath adding more gas
Between more soluble and less soluble which agent washout first
least soluble washout first
what happens as the duration of anesthetics increase with the emergence
Emergence or washout is prolonged
Emergence & Recovery Phase depends on
length of anesthesia depth of anesthesia the solubility of the agent MAC awake What other anesthetic is on board
Stage 1 Gudel level of anesthesia is noted with the following characteristics
is called the stage of analgesia or induction/Amnesia
dizziness, a sense of unreality, and a lessening sensitivity to touch and pain.
sense of hearing is increased, and responses to noises are intensified.
Normal b/p, irregular pulse ..pupils mild constriction
Stage 2 level of anesthesia shows?
Excitement: Delirium, Stimulation, Violent response to stimulation/p and HR elevated, laryngospasm risk…no intubate or extubate here.(Extubate wide awake or deep)
HR irreg and fast/bP HIGH AND pupil constricted
Stage 3 level of anesthesia shows?
is called the surgical or operative stage. four levels of consciousness (planes) within this stage. An anesthetist determines which plane is optimal for the procedure according to the specific tissue sensitivity of the individual and the surgical site. Each successive plane is achieved by increasing the concentration of the anesthetic agent.
Stage 4 ANesthesia is?
is called the toxic or danger stage. Obviously, this is never desired. cardiopulmonary failure and death can occur. The fourth level of consciousness of stage 3 is demonstrated by cardiovascular impairment that results from diaphragmatic paralysis. If this plane is not corrected immediately, stage 4 quickly ensues.
Nitrous oxide CV effects
Stimulates sympathetic nervous system.
Direct myocardial contractility depressant.(affects contractility)
May unmask undiagnosed myocardial depression in CAD, severe hypovolemia, and opioids
Arterial BP, SVR, CO, & HR unchanged or modestly elevated secondary to stimulation of catecholamines (sympathomimetic effect)
Constricts pulmonary vascular smooth muscle and increases PVR, increases RA pressure. Not good for pulmonary htn,sleep apnea as they could have cor pulmonale
Associated with higher incidence of epinephrine induced dysrhythmias
Nitrous oxide pulm effects
Increases respiratory rate.
Decreases VT.
Minimal change in VE and resting CO2 levels.
Hypoxic drive markedly depressed
depression of medullary ventilation center
Diffusion hypoxia
Nitrous oxide cerebral effect
Increases CBF, produces mild elevation of ICP.
Increases CMRO2.
Don’t use for pt;s with increase icp,reduce requirements for oxygen
Nitrous oxide Neuromuscular effect
Does not provide significant muscle relaxation.
May cause skeletal muscle rigidity at >1 MAC.
Not an MH trigger according to MHAUS
Potentiate NMB
NO renal, hepatic,Gi effect
Decreases renal blood flow by increasing renal vascular resistance.
Decreases GFR and urine output.
Hepatic blood flow mildly decreased
Meta-analysis 30 studies suggests postoperative nausea and vomiting risk increased (activation of chemoreceptor trigger zone and vomiting centers in medulla and/or middle ear volume changes).
Causes distention of the bowel- NOT indicated when pt. has bowel obstruction
Nitrous OxideBiotransformation and Toxicity
Almost exclusively eliminated by exhalation.
Biotransformation limited to < 0.01%
Irreversibly oxidizes cobalt atom in vitamin B12 and inhibits vitamin B12 dependent enzymes.
Includes methionine synthetase, necessary for myelin formation and thymidylate synthetase, necessary for DNA synthesis,it inhibits these stuff
Prolonged exposure (>24 hrs) and abuse can result in bone marrow depression (megaloblastic anemia), peripheral neuropathies, and pernicious anemia
Avoid use in pregnant patients
May alter immune response to infection
Nitrous OxideContraindications
Diffuses rapidly into air-containing cavities
Air embolism Pneumothorax Acute intestinal obstruction Intracranial air Pulmonary air cysts Intraoccular air bubbles Tympanic membrane grafting Diffuses into ETT cuff…check cuff pressures regularly,can cause ischemic changes Retinal detachment surgery,air bubble placed,watch for nitrous going into air bubble. Middle ear Surgery Avoid in patients with pulmonary HTN Limited value in patients requiring high FIO2 Can potentiate NMB
Drug interactions
Cannot be used as complete anesthetic (high MAC)
Decreases MAC requirements of other agents
Potentiates neuromuscular blockade
What are the impacts of Flouride in a VA
Fluorine…dec potency ..lower weight
Flourine Reduces Flammability
Flourine renal damage(inhibits sodium reabsorption in the ascending loop
What are the impacts of Chlorine in a VA
Increases potency
More stable
bigger molecular weight
Myocardial depression
Compare chemical structures of NHIDS
H—> Cl,Br ,c, f
I—–> Cl,cc,ff
D—>3c,FFF
s—–>4c,FFF
PP/BG/Mac of Va
Halothane 243 2.3 .74
Enflurane 175 1.8 1.68
Isoflurane 239 1.4 1.15
Desflurane 664 0.42 6.0
Sevoflurane 157 0.69 2.05
N2O 38, 770 0.47 104
The pressure created when gAS MOLECULES BOMBARD THE surface of a liquid and that of the container
Vapor pressure
The boiling point is noted to be the point where?
Vapor pressure equals barometric pressure
How do we vary altitude with Barometric pressure
Increase Altitude, decrease Barometric Pressure
Decrease Altitude, increase Barometric Pressure
what is MaC
The minimum alveolar concentration @ 1 ATM that produces immobility in 50% of patients exposed to noxious stimuli
Measures the anesthetic potency of IA
Inhalation equivalent of ED50
Factors NOT affecting MAC
Stimulus Species Sex PA02 Acid-base Duration
FActors decreasing Mac
Hypothermia Hyponatremia Hypotension (<40mmhg) Hypoxemia Increasing age Pregnancy Benzodiazepines ETOH (acute) A2 agonists Clonidine Ketamine Local Anesthetics Opioids Lithium
HHHHIPBEACKLOL
Factors increasing Mac
Hyperthermia
CNS stimulants
Youth- under one year of age
Increased pheomelanin production (red hair)
what is 1.3 mac
mac where 95% of people won’t move(ED 95)
What is Mac awake?
MAC Awake is the concentration that prevents consciousness in 50% of patients.
its approximately 1/2-1/3 MAC
H 1/2 I 1/3 D 1/3 S 1/3 N 60% for nitrous
What is Mac memory
MAC memory the concentration of anesthetic associated with amnesia in 50% of of patients is significantly less than MAC Awake
Halothane first summary and drug class
Halogenated alkane derivative Vapor Pressure 243 BG Partition Coefficient 2.3 (intermediate solubility) MAC 0.76 (high potency) Nonflammable Sweet, Non-pungent Contains Thymol Thymol is an added preservative to prevent spontaneous oxidative decomposition (also stored in amber bottles) this thymol can can turnstiles and/or temperature compensating devices to malfunction
Halothane Cv Effects
Direct myocardial depressant = BP decrease
Dose dependent decreases in CO (SV decrease 15-30%)
Does not decrease SVR (iso, des, sevo do)
Coronary artery vasodilator, coronary blood flow decreased from drop in systemic BP, can cause ischemia.
Protection from decreased myocardial oxygen demands.
Blunts baroreceptor response to hypotension, no increase in HR. (iso, des, sevo increase HR)
Increased right atrial pressure (CVP)
Increase cutaneous blood flow
Decreased SA node depolarization- prone to junctional rhythm
Decreased conduction AV node/His-Purkinje
Halothane->Arrhythmias
Halothane Resp effects
Increased rate
Decreased VT
Decreased VE, increased resting PACO2
Apneic threshold rises
Hypoxic drive severely depressed (even at low doses 0.1 MAC)
Potent bronchodilator can reverse asthma-induced bronchospasm
Halothane cerebral effects
Uncouples cerebral blood flow and metabolism”
Increases CBF, increases ICP, increases IOP while Modest decrease in CMRO2
Autoregulation blunted.
Can prevent rise in ICP by hyperventilation prior to halothane administration
Cerebral activity decreased
Stay below half mac cos of all these issues
Halothane NM effects
Neuromuscular
Potentiates nondepolarizing NM blocking meds.
Skeletal muscle relaxation 2X less than other volatile agents
Halothane Renal Effects
Reduces RBF, GFR and urine output.
Can limit by pre-op hydration(renal patients)
Halothane Hepatic effects
Decreased hepatic blood flow
Hepatic artery vasoconstriction
Anesthetic induced inhibition of hepatic drug metabolizing enzymes
Metabolism of fentanyl, phenytoin, verapamil may be impaired
Minor liver enzyme elevations
Oxidized metabolite: trifluroracetic acid 20%
Explain Halothane Halothane biotransformation and the 2 types of toxicity
Halothane produces 2 types of hepatotoxicity in susceptible patients.
20% of adult patients develop mild, self-limited post-op hepatotoxicity.
Nausea, lethargy, fever, minor increases in transaminase enzymes.
May be due to non-specific drug effect due to changes in hepatic blood flow that impairs hepatic oxygenation.
Halothane Hepatitis
Occurs in 1 in 10,000 to 1 in 30,000 adults
Extensive hepatic necrosis and death possible
Most likely immune-mediated hepatotoxicity -Immunoglobulin G antibodies present in 70% of those diagnosed
what is the presentation for Volatile Agent Induced Hepatitis
Classic presentation of VA associated hepatitis = fever, anorexia, nausea, chills, myalgias, rash, arthralgia, and eosinophilia followed by jaundice 3-6 days later
Fever Anorexia Nausea Jaundice Arthralgia Myalgia Eosinophillia chills FANJamec
What are the risk factors for Volatile Agent Induced Hepatitis
Risk factors – PRIOR EXPOSURE!, age >40 years old, obesity, female gender, Mexican ethnicity (chromosomal vulnerability), genetic susceptibility, multiple brief procedures within brief duration of time, and enzyme induction
Explain immune theory for Volatile agent-induced hepatitis
Immune theory
Cytochrome P450 2EI oxidizes each anesthetic (except for sevoflurane) to yield highly reactive intermediates that bind covalently (acetylation) to a variety of hepatocellular macromolecules
Altered hepatic proteins may trigger an immunologic response that causes massive hepatic necrosis
volatile agent hepatitis rate of metabolism identify the worst agent
Metabolism of Volatile Agents
Halothane 15-20% metabolized
Enflurane 2.5-3% metabolized
Sevoflurane* 2-5% metabolized(metabolite not toxic
Isoflurane 0.2-2% metabolized
Desflurane 0.02% metabolized
N2O 0.004% (reductive metabolism GI tract)
Why is sevo no an issue with metabolism
chemical structure of sevoflurane prevents metabolism to a acetyl halide
HalothaneDrug Interactions
Myocardial depression exacerbated by Beta-adrenergic blockers and calcium channel blockers.
Tricyclic antidepressants and MAO inhibitors may cause BP instability.(In what way)
Aminophylline use has resulted in serious ventricular dysrhythmias.
HalothaneContraindications
Patients with unexplained liver dysfunction, following halothane exposure
Pre-existing liver disease
Hypovolemia
Aortic stenosis..need to be very cautious with this for any surgery
Patients with pheochromocytoma
Malignant Hyperthermia – Halothane the most potent trigger of all the volatile agents
Face summary of isoflurane and class
Halogenated methyl ethyl ether. Pungent odor-NOT FOR PEDs INDUCTION!!! Nonflammable. MAC – 1.2 (high potency) BG partition coefficient –1.4 (intermediate solubility)
Isoflurane cardiac effects
Mild dose dependent CV depression
Inc Co,Inc HR,(partial preservation of Baroreceptor reflex
Beta adrenergic stim:Decrease SVR,Decrease b/p,Decrease sv 15-30%
Inc RAP(CVp)
If rapid increase in conc..transient inc in Hr AND B/P
FYI
Not recommended during cardiac ablation because it increases the refractoriness of accessory pathways and AV conduction so can interfere with interpretation of electrophysiologic studies
Dilates coronary arteries
Anesthetic Pre-conditioning
Brief exposure to a volatile agent iso/des/sevo can activate KATP channels – hyperpolarizing effect (negative inotropic/relax vascular smooth muscle) which protects the tissue to subsequent ischemic episode(vessels will be dialated and also myocardium ,and the heart does better with subsequent ischemic event .
Coronary steal syndrome
In theory…may cause ischemia in patients with CAD….still use it now
Iso resp effects
Tachypnea less pronounced at >1 MAC compared w/other agents
Decreased tidal volumes and minute ventilation
Increased resting PaCO2
Blunted response to hypoxia and hypercarbia
Bronchodilator
Spontaneously breathing patients
Iso cerebral effects
Increased CBF and ICP at concentrations > 1 MAC (effects less than halothane and Enflurane)
Effects reversed by hyperventilation
Reduces CMRO2, electrically silent EEG at 2 MAC(gets the cerebral met rate down and may also increase cerebral blood flow,thiopental may b used in this case (thought to provide cerebral protection during ischemic periods)
Enhances CSF reabsorption
iso neuromuscular effects
Relaxes skeletal muscle
Hepatic effects of iso
Maintains total hepatic blood flow – vasodilator of hepatic circulation
Has beneficial effects on hepatic oxygen delivery
This is a relatively new finding…some texts will still say that portal vein flow is reduced – 2003 study refutes
Iso renal effect
decrease renal blood flow,gfr and urine output
Iso metabolism
Metabolism & Toxicity
Slowly metabolized 0.2% to Trifluroacetic acid principal end product.
Hepatotoxicity rare
Does not produce fluoride ion at clinically significant levels
Iso contraindication
MH
Des face summary and group structure
Fluorinated methyl ethyl ether
Similar in structure to isoflurane
Pungent odor
Vapor pressure close to atmospheric (681), need special vaporizer.
MAC 6.0 (low potency)
Blood/gas partition coefficient 0.42 (low solubility)
Rapid wash-in (induction) and wash-out (emergence).
May not be good choice for asthmatics cos of pungent odour
Especially in stage 2
Tec 6 vaporizer summary
Electrically heated (to 39 degrees C) and pressurized (to 1520 mmHg) to keep it in the liquid phase vaporizer only for desflurane
Des CV Effects
Similar to isoflurane- Mild dose dependent cardiac depressant effect.
Decrease in SVR and LV stroke volume (15-30%)
Decreased arterial blood pressure due to svr decrease
CO remains unchanged or slightly depressed at 1-2 MAC
Baroreceptor reflex intact, rise in HR
Rapid increases in concentration: transient increase in HR, blood pressure and catecholamine levels (greater than with isoflurane).
Does not increase dilate coronary arterial blood flow.
Increased right atrial pressure (CVP)
Des gives more transient rise per increase in Hr when overpressured than order agents especially sevo
Des resp effects
Increase respiratory rate.
Decreased tidal volume.
Overall decrease in minute ventilation, increased resting PACO2.
Blunts hypercarbic and hypoxic response.
Profound apnea at 1.5-2.0 MAC
>6% Irritating to airways, salivation, breath-holding, coughing, and laryngospasm.
Pt is at risk of laryngospasm,coughing if dose of Des is greater than 6%(stage 2 mostly)
Des Cerebral effects
Increases CBF and Cerebral oxygen consumption decreased.
Effect not usually seen until >1 MAC.
Can lower ICP with hyperventilation.
Des Neuromuscular effect
Dose dependent decrease in response to TOF and tetanic PNS.
Potentiates NM blocking agents
Des Renal Effect
Similar decease in RBF, GFR, and urine output you see with the other agent (r/t decreased CO and BP)
Des hepatic effect
No evidence of hepatic injury
Better with hepatics….liver protective…not a problem…iso,sevo,also good for this
Ds Contraindications
MH
Des Biotransform,Toxicity and Carbon monoxide formation reasoning
0.1% metabolized.
Serum and urine inorganic fluoride levels essentially unchanged from preanesthetic levels.
Carbon monoxide results from degradation of Des by dried out CO2 absorbents
high flows left on all weekend now 1st case on Monday morning.
Carbon Monoxide concentrations
Des>Enf & Iso> Halo & Sevo
Des>enf&Iso>Halo&sevo
DEIHS
Sevo summary and group
Fluorinated methyl isopropyl ether
Non pungent sweet ordor …good for kids
Fast on fast off,good for kids
Sevo CV effects
Mild dose dependent cardiac depressant effect.
SVR, and art BP decline slightly (less than isoflurane or Desflurane).
Stroke volume decrease similar to Iso and Des ( 15-30%)
Little rise in HR (only significantly increases at >1.5 MAC), CO not as well maintained.
No evidence of coronary steal.
Only common agent that does not increase
Also does not cause SNS activation response with increases in concentration
Does not drop bp as much as other agents…
Sevo resp effects
Increased RR and deceased VT
Bronchodilator similar to isoflurane
Minimal airway irritation (best among all current anesthetics)
Decrease in response to carbon dioxide with increased PaCO2
Profound apnea at 1.5-2.0 MAC
Irritates the airway the list,best choice for asthmatics
Sevo Cns effects
Dec. cerebral metabolism O2 consumption > Halothane
Inc. CBF < Halothane
Inc. ICP
Effect not usually seen until >1 MAC.
Response to CO2 & autoregulation maintained at 1.5%
Sevo is the best for brain
Increases these things but less than halothane..
Make list of those that affect the brain the most and the list
Below 1 mac luxury perfusion not an issue
Sevo metabolism and toxicity with comp A production
Compound A is formed when Sevo interacts with soda or baralyme- esp. at low flows (not a metabolite)
Cpd A not nephrotoxic alone but undergoes bioactivation thru glutathione conjugation and metabolism of its conjugates to produce reactive thiol may mediate renal toxicity
COMPOUND A mostly produced by Sevo degradation
Higher concentrations of compound A in presence of Baralyme and/or low flow anesthesia, high sevo concentrations, and anesthetics of long duration.
No clinical evidence of injury
Renal injury demonstrated in rats
Eger et al. demonstrated transient changes in renal function has not been reproduced by subsequent studies
While a level of Compound A exposure at which clinical nephrotoxicity might be expected to occur has not been established, it is prudent to consider all of the factors leading to Compound A exposure in humans, especially duration of exposure, fresh gas flow rate, and concentration of sevoflurane, USP. During sevoflurane, USP anesthesia the clinician should adjust inspired concentration and fresh gas flow rate to minimize exposure to Compound A. To minimize exposure to Compound A, sevoflurane exposure should not exceed 2 MAC∙hours at flow rates of 1 to < 2 L/min. Fresh gas flow rates of <1 L/min are not recommended
Sevo and Free fluoride carbon release
Another concern is production of free fluoride ions = tubular injury and loss of concentrating ability – ARF.
Fluoride levels can rise close to levels associated with risk for kidney– although clinical evidence of injury does not exist
Sevo And Neuromuscular
Dose dependent potentiation of NDMR
Sevo and hepatic blood flow
Hepatic blood flow is maintained similar to isoflurane
Sevo with metabolism and toxicity
inorganic fluoride level increases- no reported nephrotoxicity
metabolized in liver P450 3-5% undergoes biodegradation
Cannot be metabolized to trifluroacetylated liver proteins – 0 risk of “halothane hepatitis”
Sevo Contraindications
Patients with impaired kidney function (relative contraindication) Malignant Hyperthermia (absolute contraindication)
Enflurane summary and class
Halogenated methyl ethyl ether Mild, sweet, ethereal odor Nonflammable MAC 1.7 (high potency) BG partition coefficient 1.9 (intermediate solubility) Vapor Pressure 175 Isomer of Isoflurane
Enflurane cv effcets
Myocardial contractility depression not as bad like iso and halo
Sensitizes heart to dysrhythmic effects of epinephrine
Enflurane Resp effcets
Abolished hypoxic drive.
Marked respiratory depression, at 1 MAC, PACO2 60 mm Hg.
Depressed mucociliary function
Enflurane cns effects
Increases secretion of CSF and resistance to CSF outflow.
EEG changes, tonic-clonic seizures.
Exacerbated by high concentration, hypocapnia, and repetitive auditory stim.
Hyperventilation not recommended.
Enflurane Toxicity and biotransformation
Low metabolism (2-5%). Fluoride production much less than Methoxyflurane. induces defluorination, may be clinically significant in rapid acetylators. Detectable renal dysfunction unlikely
Enflurane Contraindication
Avoid in patients with preexisting kidney disease or impairment
Avoid in patients with known or suspected seizure disorders
Avoid in patients with increased intracranial pressure
Triggering agent for Malignant Hyperthermia
Xenon Summary
Inert gas, odorless, nonexplosive
BG partition coefficient = 0.115
MAC 63-71%
Does expand closed air spaces < N2O though
CV stability, blunt SNS response to pain, analgesia, hypnosis
Costly
Limited experience in patients at this time
Osha and waste Gases standard
No worker should be exposed to more than 2ppm Halogenated agents in O2 or air
No more than 0.55 ppm Halogenated agents if used with Nitrous Oxide
No more than 25ppm of N2O
Highest levels found between anesthesia machine and wall
What is anesthetic preconditioning
Brief exposure to a volatile agent iso/des/sevo can activate KATP channels – hyperpolarizing effect (negative inotropic/relax vascular smooth muscle) which protects the tissue to subsequent ischemic episode(vessels will be dialated and also myocardium ,and the heart does better with subsequent ischemic event
