Inhalational Agents

Start Studying!

lecture 12-14

Terms

undefined, object

copy deck

What are 3 criteria for development of inhalational anesthetics?: higher potency non-flammability chemical stability
What did fluorination do for inhalational anesthetics?: less potent less soluble in tissues more stable
What state are most agents at room temp? What is an exception?: liquid at atm N20 is gas at atm/room temp
What is Dalton's Law?: total pressure = sum of partial pressures
What is saturated vapor pressure?: maximum possible concentration of molecules in gas phase at certain temperature
If an agent has a HIGH SVP, is the agent more or less volatile? Is the concentration of molecules in gas phase higher or lower?: higher SVP = more volatile and higher concentration of gas molecules (a lot of molecules can be in gas phase before it becomes "saturated")
Which agent has the highest SVP?: Desflurane (681mmHg at 68F)
Which agent has a similar SVP to Halothane so it could used the same vaporizer?: Isoflurane
As temperature increases, what happens to amount of vapor and vapor pressure?: quantity of vapor increases so pressure increases
How do you determine the maximum achievable gas concentration?: sea level pressure/SVP of agent = max concentration %
Which agent requires a special vaporizer due to its boiling point being near room temperature?: Desflurane (74.3F)
What are characteristics of modern vaporizers?: agent specific concentration calibrated temperature compensated flow compensated high resistance to gas flow (VOC-out of circuit)
What are features that prevent accidental filling of vaporizer with incorrect agent?: refill with special tool that matches in color and shape to correct agent
What happens to temperature of liquid agents as they evaporate? So what happens to SVP?: gets cooler (temp decr.) so more to liquid phase -->vapor pressure decreases
What happens to % output in vaporizers that are not temperature compensated? What are ways to compensate for temp in the vaporizer?: % output decreases as temp declines in vaporizer --devices like copper or bimetallic strip, silicone can stabilize temperature and maintain output
What are some things that affect vaporizer performance?: temperature extremes (field anesthesia) fresh gas (O2 alone or O2/N2O) barometric pressure (minimal in clinical practice) filling level (don't overfill) movement/tilting (keep straight) thymol preservative (halothene machines require cleaning)
What are ways to classify vaporizers?: location (VIC/VOC) resistance to carrier flow (high/low) precision (yes/no) temp compensation (yes/no) agent specificity (yes/no)
Will agents achieve equilibrium in tissues based on partial pressure or concentration?: partial pressure (concentrations may be different)
What two things determines volume of gas that will dissolve?: partial pressure and solubility coefficient (Henry's Law)
What indicates an agent's affinity for adjacent tissue at equilibrium?: partition coefficient
do soluble agents have a high or low blood:gas coefficient?: High (more wants to be in blood than in gas)
Do insoluble agents have a partition coefficient greater or less than 1?: less than 1 = insoluble
What are 4 factors that influence rate of the agent from alveolar concentration to blood?: concentration of inhaled agent (partial pressure) alveolar ventilation solubility of agent in blood cardiac output
If a soluble agent is administered to patient with HIGH cardiac output, will onset be faster or slower?: slower/prolonged onset
What does the setting on the vaporizer mean?: % concentration of agent being delivered to patient
What determines speed of anesthesia onset?: delivery of agent to alveoli (FGF and inspired %, ventilation) uptake of agent by blood (solubility, CO, alveolar-venous pp gradient)
If agent is less soluble, will this facilitate or slow onset of anesthesia?: facilitate faster onset (insoluble so doesn't want to stay in blood --> moves into tissues)
Do desflurane, N2O and sevo have high or low solubility coefficients?: low solubility
What is the highest solubility agent? does this facilitate or slow onset of anesthesia?: methoxyflurane very soluble so slow induction (wants to stay in blood rather than shift into tissue/brain)
How does CO effect onset?: increases uptake from alveoli to blood but decreases delivery from blood to tissue/brain (delayed onset)
Is a patient with tachycardia or bradycardia at higher risk of anesthetic overdose?: bradycardia (Fa/Fi rises at faster rate bc Fi is slower to return to lung for exhale)
What does "tension" refer to?: partial pressure of gas dissolved in tissue
What determines uptake into the tissue? What does this mean for uptake in the brain?: blood supply to organ size of organ solubility in tissue brain is small and well perfused --> rapid saturation
When is alveolar - venous gradient the largest? When does gradient disappear?: during induction (high delivery to alveoli but nothing yet returning in venous) diappears when tissues are saturated/venous return equals that of tissue
What can the anesthetist do to speed up wash out?: high FGF and empty reservoir bag through APL valve
Does an insoluble agent speed up or slow rate of recovery?: fast recovery w/insoluble agent
Will increased CO speed or slow rate of recovery? What will slow respiration do?: fast recovery (incr. CO = incr. venous return to alveoli for exhale of agent) slow respiration = slower recovery
What factors affect recovery?: alveolar ventilation solubility CO anesthesia duration metabolism (amt. by liver)
Would a rebreather or nonrebreathing system have faster onset/reach anesthetic saturation faster?: nonrebreather (less volume in apparatus and high FGF so quicker to reach saturation)
What is mechanism of action of inhalational agents? are these affects uniform?: gases interfere with lipid membrane, effecting ion and protein channels enhance GABA and glycine inhibit NMDA and serotonin disrupt synaptic transmission -not uniform
What are CNS effects on brain? Effect on spine?: brain: hypnosis and amnesia spine: immobility in response to pain
What is MAC? How does it relate to potency?: minimum alveolar concentration required to prevent response to stimulus in 50% patients at STP lower mac = more potent (inversely proportional)
what is potency from most to least?: methoxy > halothane > iso> sevo > des >> N2O
What is MAC for halothane? N2O?: halothane = 0.8-0.9 N2O = 7-10
What is MAC for isoflurane and sevoflurane?: iso = 1.3-2.6 sevo = 2.3-2.5
What are some factors that lower MAC?: narcotics/sedatives/analgesics N2O old age hypothermia/hypotension pregnancy severe hypoxemia/hypercapnia
What factors increase MAC?: hyperthermia pediatrics (human) sympathoadrenal stimulation
In practice, what is vaporizer set at to start relative to MAC?: 1.5 x MAC (then adjust as needed)
with monitoring equipment, what does end tidal concentration tell us about patient?: reflects agent's tension in brain
Which is the least soluble inhalational agent? How does this effect recovery?: desflurane least soluble --> fastest recovery
What is MAC of N2O in animals? What is minimum O2% when mixed with N2O?: 200% O2 has to be at least 30%
What are CNS effects of N2O? Respiratory?: increases ICP and CBP (avoid in head trauma) negligable resp. effect
What are cardiovascular effects of N2O? Analgesia?: mild sympathetic stim (maintain HR, BP, CO) mild myocard. depression in vitro yes, analgesia
What is 2nd gas effect?: PP gradient very high for N2O so moves into blood quickly --> incr. PP of 2nd agent in alveoli so it moves into blood = increased speed of induction of 2nd gas
What is concern with N2O and gas filled space?: fills and expands air filled space like rumen, stomach, middle ear, closed pneumothorax, ET tube cuff
what type of breathing system leaves patient at risk for hypoxic gas mixtures?: circle system (closed and low flow)
Diffusion hypoxia at recovery is avoided by doing what for the patient?: provide 100% O2 for several minutes after turning off inhalational agent
Why does Halothane require thymol as a preservative? Is halothane explosive?: unstable in UV light not explosive (ether and chloroform are)
What are halothane's cardiovascular effects (dose dependent)?: depresses myocardial contractility red. CO, SV, MAP (hypotension) arrythmogenic (via catecholemine release) NO vasodilation
Which inhalational agents do not cause vasodilation? Which is the only inhalational agent to cause arrythmias?: halothane and N20 halothane causes arrythmias
What is halothane's effect on blood flow to viscera?: decreases blood flow to organs (can be problematic)
which inhalational agents put patient at risk for malignant hyperthermia? How would you treat this?: all agents can give dantrolene as muscle relaxant
What CNS effects do all inhalational effects share?: increase blood flow to brain (incr. CBF and ICP so avoid in head trauma and surgery) **does NOT include N20
What are respiratory effects of inhalatioal agents (not including N2O)?: bronchodilator ventilatory depression (esp. sevo and des) decreased tidal volume decreased response to hypercapnia
What agent is best choice for sole chamber induction? Why?: sevoflurane insoluble so fast onset; pleasant odor so no catecholemine release
Which agents have pungent odor?: Iso and desflurane
Which agent has highest metabolism in liver? Which has second highest? Lowest?: methoxyflurane (70%) halothane (25%) N20 (0.004%)
What is solubility of desflurane like and how does this effect speed of onset/recovery?: extremely low solubility so rapid onset/recovery
What are some advantages of less soluble agents? which type of patients are these the best option for?: rapid recovery (so ideal for pediatrics, long sx, obese, diabetic and very sick)
Why is fast recovery disadvantageous in horses? How is this avoided?: attempt to stand while still ataxic so sedate w/Romifidine (or xylazine)
What 2 agents do not produce carbon monoxide when reacting with soda lime? How can these products be avoided with agents that do produce CO? Which agent reacts w/soda lime to produce compound A?: halothane and sevo do not cause CO avoid by using fresh soda lime (not dry) and high FGF sevoflurane
Does N2O cause respiratory depression? What is its MAC?: no depression (mild sympathetic stimulation) 200%
What regulatory agencies in US are responsible for anesthetic gas toxicity in personnel?: NIOSH (Nat'l Institute for Occupational Safety and Health) OSHE (Occup. Safety and Health admin.) FDA
What is difference between acute and chronic toxicity?: acute via broken bottle or high exposure for short period chronic via trace levels over career (both are occupational health risks)
what are some signs of acute toxicity?: fatigue, nausea, headache, irritability, diminished motor and judgement making skills
What are ALLEGED risks for chronic toxicity?: abortion, reduced fertility congenital anomalies in offspring carcinogen organ disease (liver/kidney) psychiatric problems
Which gas can impair B12 synthesis that is required for myelin formation and DNA synthesis?: N2O
What are some toxic effects associated with chronic exposure to N2O?: miscarriage, teratogenicity bone marrow depression peripheral neuropathies depr. leukocyte function
What agent is associated w/liver necrosis and death and is an immune mediated reaction?: halothane
What is current consensus based on studies of exposure to gas traces over time?: no evidence of adverse effects (no consensus over acceptable limits) higher incidence of miscarriage w/exposure to unscavenged N2O environments
How much can scavenging systems reduce room pollution?: by half
What are some methods to minimize exposure to gases?: use scavenging system complete air exchange in operating rooms ventilation/filter air minimize mask/chamber induction check equipment for leaks seal airway with cuff refill vaporizor at end of day monitor room's trace gases with device
Which agency assigns each country a yearly quota of controlled drugs?: international narcotics control board
Which agency issues license to clinics for controlled drugs?: Drug Enforcement Agency of US Dept. of Justice
What law initially listed drugs as schedules I-V and is regularly changed by FDA and DEA?: Controlled Substances Act of 1970
What are some drugs listed as schedule I? Schedule II?: I: heroin, cannibis, peyote II: full mu agonist opioids, pentobarbital
What are some drugs listed as sched. III? IV?: III: thiopental, ketamine, telazol, buprenorphine IV: butorphanol, benzodiazepines
Which agency holds you accountable to accurate drug log keeping and investigates records?: DEA

Start Studying!

Deck Info

Number of cards 88